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"content": "\u003cp>New genetic tools are making it easier and cheaper to engineer viruses and bacteria, and a report commissioned by the Department of Defense has now ranked the top threats posed by the rapidly advancing field of \"synthetic biology.\"[contextly_sidebar id=\"gb9g2YDw6S8Tv2v2EUI0TWtfXV5po4Qp\"]\u003c/p>\n\u003cp>One of the biggest concerns is the ability to recreate known viruses from scratch in the lab. That means a lab could make a deadly virus that is normally kept under lock and key, such as \u003ca href=\"http://www.who.int/csr/disease/smallpox/en/\">smallpox\u003c/a>.\u003c/p>\n\u003cp>\"Right now, recreating pretty much any virus can be done relatively easily. It requires a certain amount of expertise and resources and knowledge,\" says \u003ca href=\"https://medicine.umich.edu/dept/microbiology-immunology/michael-j-imperiale-phd\" target=\"_blank\" rel=\"noopener\">Michael Imperiale\u003c/a>, a microbiologist at the University of Michigan who chaired the committee convened by the \u003ca href=\"http://www.nationalacademies.org/\" target=\"_blank\" rel=\"noopener\">National Academies of Sciences, Engineering, and Medicine\u003c/a> to assess the state of synthetic biology and offer advice to defense officials.\u003c/p>\n\u003cp>As an example of what's possible, Imperiale pointed to the recent and controversial creation of \u003ca href=\"https://www.npr.org/sections/health-shots/2018/02/17/585385308/did-pox-virus-research-put-potential-profits-ahead-of-public-safety\" target=\"_blank\" rel=\"noopener\">horsepox,\u003c/a> a cousin of smallpox, in a Canadian laboratory. \"These things can now be done,\" he said.\u003c/p>\n\u003cp>Another top danger listed in the report, which was released Tuesday, is making existing bacteria or viruses more dangerous. That could happen, by, say, giving them antibiotic resistance or altering them so that they produce toxins or evade vaccines.\u003c/p>\n\u003cp>[ad fullwidth]\u003c/p>\n\u003cp>And one scenario pondered by the experts is the creation of microbes that would produce harmful biochemicals in humans while living on the skin or in the gut. This possibility, the report notes, \"is of high concern because its novelty challenges potential mitigation options.\" Public health officials might not even recognize that they were witnessing a biological attack if the dangerous material was delivered to victims in such an unusual way.\u003c/p>\n\u003cp>All in all, the committee examined about a dozen different synthetic biology technologies that could be potentially misused. For each, they considered how likely it was to be usable as a weapon, how much expertise or resources would be needed, and how well governments would be able to recognize and manage an attack.\u003c/p>\n\u003cp>\"There are certain capabilities that may not be possible now, but in those cases we tried to identify what the bottlenecks or barriers might be that, if overcome, would enable those to be more possible,\" Imperiale says.[contextly_sidebar id=\"hU2ywe0bo5FhMcFg3CwThXSqo89g4izl\"]\u003c/p>\n\u003cp>One of the least concerning possibilities, because of the knowledge and technical barriers, was inventing a brand new pathogen by taking a \"mix and match\" approach to combining genetic parts from multiple organisms, according to the report. It notes that making even simple changes to viruses can produce \"drastic deficiencies\" in key viral properties, \"making any such effort especially difficult,\" and that \"the difficulty increases as the distance from natural pathogens increases.\"\u003c/p>\n\u003cp>But that was exactly the scenario that recently unfolded in a table-top exercise conducted last month by the Johns Hopkins Center for Health Security. During the event, experts in pandemic response and national security grappled with a fictional virus called \"\u003ca href=\"http://www.centerforhealthsecurity.org/about-the-center/pressroom/press_releases/2018-05-15_clade-x-policy-recommendations.html\">Clade X\u003c/a>\" that was created by a terrorist group that inserted genetic elements of deadly \u003ca href=\"https://www.npr.org/2018/05/29/615079779/why-it-s-difficult-for-viruses-to-turn-in-to-deadly-pandemics\" target=\"_blank\" rel=\"noopener\">Nipah\u003c/a> virus into a normally-mild \u003ca href=\"https://www.cdc.gov/parainfluenza/index.html\" target=\"_blank\" rel=\"noopener\">human parainfluenza virus\u003c/a>.\u003c/p>\n\u003cp>The terrorist group in this scenario wanted to depopulate the Earth, and deliberately released the contagious virus at multiple spots around the globe. The resulting pandemic killed 150 million people within a year as officials struggled to contain the social and economic chaos until a vaccine could be made.\u003c/p>\n\u003cp>\"What people don't think about very often is the potential for an engineered organism to become an epidemic or even a pandemic. One of the goals of this exercise was to show that an engineered organism could be the cause of something that we are not really preparing for,\" says \u003ca href=\"http://www.centerforhealthsecurity.org/our-staff/profiles/inglesby/index.html\" target=\"_blank\" rel=\"noopener\">Dr. Tom Inglesby\u003c/a>, director of the Johns Hopkins center. \"What we wanted to show in the exercise was that there are different ways of getting to a pandemic. And we need to be prepared for all of them.\"\u003c/p>\n\u003cp>Much of the public health response to an engineered outbreak would be the same as to a natural outbreak, the exercise showed. That means a possible line of defense is beefing up public health infrastructure such as disease surveillance.\u003c/p>\n\u003cp>And, as the new report notes, the same synthetic biology tools that could be used to harm could also be used to fight this threat, by allowing the rapid creation of better medicines, vaccines, and diagnostics.[contextly_sidebar id=\"9JS7pw28z71O9Hau5X1qfcsxIFZNY5TF\"]\u003c/p>\n\u003cp>\u003ca href=\"https://silver.med.harvard.edu/\">Pamela Silver\u003c/a>, a synthetic biologist at Harvard who was not on the committee but reviewed its report, said that the assessment is \"timely, given that there's a lot of attention being paid to genetic engineering because of \u003ca href=\"https://www.npr.org/sections/health-shots/2015/12/28/460705645/gene-editing-tool-hailed-as-a-breakthrough-and-it-really-is-one\" target=\"_blank\" rel=\"noopener\">CRISPR\u003c/a>,\" the new tool that has made it much easier to edit genes.\u003c/p>\n\u003cp>She does worry, though, that because this report ranked potential threats, \"somebody might say 'oh, here are the three things we have to worry about the most,' and then ignore the others.\"\u003c/p>\n\u003cp>And this assessment was made based on today's technology, she says, but it's clear that biology changes rapidly and is full of surprises. \"So what's the next CRISPR? 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"content": "\u003cdiv class=\"post-body\">\u003cp>\u003cp>New genetic tools are making it easier and cheaper to engineer viruses and bacteria, and a report commissioned by the Department of Defense has now ranked the top threats posed by the rapidly advancing field of \"synthetic biology.\"\u003c/p>\u003cp>\u003c/p>\u003cp>\u003c/p>\n\u003cp>One of the biggest concerns is the ability to recreate known viruses from scratch in the lab. That means a lab could make a deadly virus that is normally kept under lock and key, such as \u003ca href=\"http://www.who.int/csr/disease/smallpox/en/\">smallpox\u003c/a>.\u003c/p>\n\u003cp>\"Right now, recreating pretty much any virus can be done relatively easily. It requires a certain amount of expertise and resources and knowledge,\" says \u003ca href=\"https://medicine.umich.edu/dept/microbiology-immunology/michael-j-imperiale-phd\" target=\"_blank\" rel=\"noopener\">Michael Imperiale\u003c/a>, a microbiologist at the University of Michigan who chaired the committee convened by the \u003ca href=\"http://www.nationalacademies.org/\" target=\"_blank\" rel=\"noopener\">National Academies of Sciences, Engineering, and Medicine\u003c/a> to assess the state of synthetic biology and offer advice to defense officials.\u003c/p>\n\u003cp>As an example of what's possible, Imperiale pointed to the recent and controversial creation of \u003ca href=\"https://www.npr.org/sections/health-shots/2018/02/17/585385308/did-pox-virus-research-put-potential-profits-ahead-of-public-safety\" target=\"_blank\" rel=\"noopener\">horsepox,\u003c/a> a cousin of smallpox, in a Canadian laboratory. \"These things can now be done,\" he said.\u003c/p>\n\u003cp>Another top danger listed in the report, which was released Tuesday, is making existing bacteria or viruses more dangerous. That could happen, by, say, giving them antibiotic resistance or altering them so that they produce toxins or evade vaccines.\u003c/p>\n\u003cp>\u003c/p>\u003c/div>",
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"content": "\u003cdiv class=\"post-body\">\u003cp>\u003c/p>\n\u003cp>And one scenario pondered by the experts is the creation of microbes that would produce harmful biochemicals in humans while living on the skin or in the gut. This possibility, the report notes, \"is of high concern because its novelty challenges potential mitigation options.\" Public health officials might not even recognize that they were witnessing a biological attack if the dangerous material was delivered to victims in such an unusual way.\u003c/p>\n\u003cp>All in all, the committee examined about a dozen different synthetic biology technologies that could be potentially misused. For each, they considered how likely it was to be usable as a weapon, how much expertise or resources would be needed, and how well governments would be able to recognize and manage an attack.\u003c/p>\n\u003cp>\"There are certain capabilities that may not be possible now, but in those cases we tried to identify what the bottlenecks or barriers might be that, if overcome, would enable those to be more possible,\" Imperiale says.\u003c/p>\u003cp>\u003c/p>\u003cp>\u003c/p>\n\u003cp>One of the least concerning possibilities, because of the knowledge and technical barriers, was inventing a brand new pathogen by taking a \"mix and match\" approach to combining genetic parts from multiple organisms, according to the report. It notes that making even simple changes to viruses can produce \"drastic deficiencies\" in key viral properties, \"making any such effort especially difficult,\" and that \"the difficulty increases as the distance from natural pathogens increases.\"\u003c/p>\n\u003cp>But that was exactly the scenario that recently unfolded in a table-top exercise conducted last month by the Johns Hopkins Center for Health Security. During the event, experts in pandemic response and national security grappled with a fictional virus called \"\u003ca href=\"http://www.centerforhealthsecurity.org/about-the-center/pressroom/press_releases/2018-05-15_clade-x-policy-recommendations.html\">Clade X\u003c/a>\" that was created by a terrorist group that inserted genetic elements of deadly \u003ca href=\"https://www.npr.org/2018/05/29/615079779/why-it-s-difficult-for-viruses-to-turn-in-to-deadly-pandemics\" target=\"_blank\" rel=\"noopener\">Nipah\u003c/a> virus into a normally-mild \u003ca href=\"https://www.cdc.gov/parainfluenza/index.html\" target=\"_blank\" rel=\"noopener\">human parainfluenza virus\u003c/a>.\u003c/p>\n\u003cp>The terrorist group in this scenario wanted to depopulate the Earth, and deliberately released the contagious virus at multiple spots around the globe. The resulting pandemic killed 150 million people within a year as officials struggled to contain the social and economic chaos until a vaccine could be made.\u003c/p>\n\u003cp>\"What people don't think about very often is the potential for an engineered organism to become an epidemic or even a pandemic. One of the goals of this exercise was to show that an engineered organism could be the cause of something that we are not really preparing for,\" says \u003ca href=\"http://www.centerforhealthsecurity.org/our-staff/profiles/inglesby/index.html\" target=\"_blank\" rel=\"noopener\">Dr. Tom Inglesby\u003c/a>, director of the Johns Hopkins center. \"What we wanted to show in the exercise was that there are different ways of getting to a pandemic. And we need to be prepared for all of them.\"\u003c/p>\n\u003cp>Much of the public health response to an engineered outbreak would be the same as to a natural outbreak, the exercise showed. That means a possible line of defense is beefing up public health infrastructure such as disease surveillance.\u003c/p>\n\u003cp>And, as the new report notes, the same synthetic biology tools that could be used to harm could also be used to fight this threat, by allowing the rapid creation of better medicines, vaccines, and diagnostics.\u003c/p>\u003cp>\u003c/p>\u003cp>\u003c/p>\n\u003cp>\u003ca href=\"https://silver.med.harvard.edu/\">Pamela Silver\u003c/a>, a synthetic biologist at Harvard who was not on the committee but reviewed its report, said that the assessment is \"timely, given that there's a lot of attention being paid to genetic engineering because of \u003ca href=\"https://www.npr.org/sections/health-shots/2015/12/28/460705645/gene-editing-tool-hailed-as-a-breakthrough-and-it-really-is-one\" target=\"_blank\" rel=\"noopener\">CRISPR\u003c/a>,\" the new tool that has made it much easier to edit genes.\u003c/p>\n\u003cp>She does worry, though, that because this report ranked potential threats, \"somebody might say 'oh, here are the three things we have to worry about the most,' and then ignore the others.\"\u003c/p>\n\u003cp>And this assessment was made based on today's technology, she says, but it's clear that biology changes rapidly and is full of surprises. \"So what's the next CRISPR? What's the next big thing?\" Silver asks. \"We need to anticipate, as well. Biology is a rapidly moving field and we need to stay on top of that.\"\u003c/p>\n\u003cp>\u003c/p>\n\u003cp>She says she just recently was looking at a preprint of a scientific paper about engineering bacteria, \"and I noticed that it was from high school students. That's just amazing to me.\"\u003c/p>\n\u003cdiv class=\"fullattribution\">Copyright 2018 NPR. To see more, visit http://www.npr.org/.\u003cimg src=\"https://www.google-analytics.com/__utm.gif?utmac=UA-5828686-4&utmdt=Report+For+Defense+Department+Ranks+Top+Threats+From+%27Synthetic+Biology%27+&utme=8(APIKey)9(MDAxOTAwOTE4MDEyMTkxMDAzNjczZDljZA004)\">\u003c/div>\n\n\u003c/div>\u003c/p>",
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"content": "\u003cp>Rita Adele Steyn's mother had a double mastectomy in her 40s because she had so many lumps in her breasts. Her first cousin died of breast cancer. And Steyn's sister is going through chemotherapy for the disease now. Steyn worries she might be next.[contextly_sidebar id=\"2jv7QCmynDbyHW9qUVcm6pRU4NOR220R\"]\u003c/p>\n\u003cp>\"Sometimes you feel like you beat the odds. And sometimes you feel like the odds are against you,\" said Steyn, 42, who lives in Tampa, Fla. \"And right now I feel like the odds are against me.\"\u003c/p>\n\u003cp>So Steyn jumped at the chance when she heard about a company offering an inexpensive and easy new way to get her DNA tested for genetic mutations that sharply increase the risk for \u003ca href=\"https://www.cancer.org/cancer/breast-cancer.html\" target=\"_blank\" rel=\"noopener\">breast cancer\u003c/a>.\u003c/p>\n\u003cp>\"I thought it would be good to get tested,\" says Steyn. \"I thought this is something I should know.\"\u003c/p>\n\u003cp>She ordered a $200 testing kit from the company, 23andme, spit into a small plastic tube, sent it back and waited for the results.\u003c/p>\n\u003cp>[ad fullwidth]\u003c/p>\n\u003cp>Genetic testing used to be uncommon and ordered only by doctors. They used it mainly to diagnose rare conditions, to find out whether prospective parents are carrying genetic diseases, or to determine whether patients are at risk for diseases in the future.\u003c/p>\n\u003cp>Now, more people are getting their DNA analyzed for health reasons, in the comfort of their own homes. As genetic testing has gotten easier, faster and more affordable, it has become a multimillion-dollar industry, with many companies aggressively marketing convenient, inexpensive tests directly to consumers. About one-third of Americans say they or a family member have considered getting a genetic test, \u003ca href=\"https://www.npr.org/sections/health-shots/2018/06/01/616126056/poll-genealogical-curiosity-is-a-top-reason-for-dna-tests-privacy-a-concern\" target=\"_blank\" rel=\"noopener\">according to a recent NPR-IBM Watson Health Poll\u003c/a>. And millions of people have gotten them, for a variety of reasons.[contextly_sidebar id=\"5sGM4fbYVp0AOmgc16BrIla2iYM1tjtz\"]\u003c/p>\n\u003cp>\"This health-related testing is probably the next big step in using genomic information in our lives,\" says \u003ca href=\"https://isearch.asu.edu/profile/2783639\" target=\"_blank\" rel=\"noopener\">Robert Cook-Deegan\u003c/a>, who studies health policy at Arizona State University.\u003c/p>\n\u003cp>But others find the trend troubling. The tests have limitations and can be hard to interpret without a doctor or genetic counselor to weigh in.\u003c/p>\n\u003cp>\u003cstrong>Pros and Cons\u003c/strong>\u003c/p>\n\u003cp>The company Steyn used, \u003ca href=\"https://www.23andme.com/\" target=\"_blank\" rel=\"noopener\">23andMe\u003c/a>, recently \u003ca href=\"https://www.npr.org/2018/03/07/591423146/test-for-breast-cancer-gene-will-be-available-in-weeks\" target=\"_blank\" rel=\"noopener\">became the first to win approval\u003c/a> from the Food and Drug Administration to market a genetic test for cancer directly to consumers without a doctor's order. It spent $27.9 million on advertising in the first quarter of 2018, according to the tracking firm Kantar Media. (NPR receives financial support from 23andMe.)\u003c/p>\n\u003cp>The industry is set to grow even more as restrictions on the medical uses of these tests are eased. The Food and Drug Administration recently \u003ca href=\"https://www.fda.gov/NewsEvents/Newsroom/PressAnnouncements/ucm583885.htm\">announced\u003c/a> plans to make it easier for these kinds of tests to win approval.[contextly_sidebar id=\"6BR65Pmc5xtQQjBssPMWnhSlrwXrhHIz\"]\u003c/p>\n\u003cp>Many physicians welcome the trend, saying it's giving people valuable information. Consumers can find out early whether they are at increased risk for cancer, Alzheimer's and other diseases — and take steps to protect themselves. The testing can also sometimes help identify the safest and most effective medications to use.\u003c/p>\n\u003cp>\"Direct-to-consumer genetics companies are leading the way toward democratizing genetics and making it available to more and more people to learn about their risks and intervene in ways to keep themselves healthy,\" says \u003ca href=\"http://personalizedmedicine.partners.org/About/Leadership-Team/Robert%20Green.aspx\" target=\"_blank\" rel=\"noopener\">Robert Green\u003c/a>, a medical geneticist at Harvard.\u003c/p>\n\u003cp>But other genetic specialists, including \u003ca href=\"https://www.med.unc.edu/im/patients/general-medicine-internal-medicine-clinic/james-evans-md-phd\" target=\"_blank\" rel=\"noopener\">James Evans\u003c/a>, a professor of genetics and medicine at the University of North Carolina, Chapel Hill, argue genetic testing is still in its infancy and that the results are often inconclusive and confusing.\u003c/p>\n\u003cp>\"I think that it's an unfortunate development that will likely cause considerable mischief,\" Evans says.\u003c/p>\n\u003cp>One problem is that patients can be easily overwhelmed when results are misleading or murky. Genetic testing is still best done through doctors, he says, working with specially trained genetic counselors who can guide patients every step of the way.[contextly_sidebar id=\"xJAmUsouQpJLM7V2Qt8t7fJx04FgVQwG\"]\u003c/p>\n\u003cp>\"What people deserve is well-thought-out information,\" Evans says. \"The only people who will really benefit are the investors in these companies that market these incomplete and misleading tests.\"\u003c/p>\n\u003cp>Some companies are offering newer forms of genetic testing that decipher and analyze every gene known to carry instructions for producing proteins that might reveal mutations — a process called \u003ca href=\"https://ghr.nlm.nih.gov/primer/testing/sequencing\" target=\"_blank\" rel=\"noopener\">whole exome sequencing\u003c/a>. Still others analyze the entire genetic code, which is called \u003ca href=\"https://www.fda.gov/Food/FoodScienceResearch/WholeGenomeSequencingProgramWGS/\" target=\"_blank\" rel=\"noopener\">whole genome sequencing\u003c/a>, which may find additional clues to disease. They will then analyze customers' genomes for any variations known to be associated with diseases.\u003c/p>\n\u003cp>The approach 23andMe takes is a rapid, but older, process. It analyzes short pieces of DNA for genetic variations known as \u003ca href=\"https://ghr.nlm.nih.gov/primer/genomicresearch/snp\" target=\"_blank\" rel=\"noopener\">single nucleotide variations (SNPs)\u003c/a> associated with specific diseases.\u003c/p>\n\u003cp>Except for 23andMe, all of the companies still require a doctor's order to get this testing. But an increasing number of these companies will find a physician to sign off on that for customers.\u003c/p>\n\u003cp>\"We're all about empowering consumers and making it as easy as possible for people to get these insights,\" says \u003ca href=\"https://www.helix.com/blog/author/elissa-levin/\" target=\"_blank\" rel=\"noopener\">Elissa Levin\u003c/a>, director of policy and clinical services at \u003ca href=\"https://www.helix.com/\">Helix\u003c/a>, a genetic testing company.\u003c/p>\n\u003cp>Dr. \u003ca href=\"https://profiles.stanford.edu/louanne-hudgins\" target=\"_blank\" rel=\"noopener\">Louanne Hudgins\u003c/a>, president of the \u003ca href=\"https://www.acmg.net/\" target=\"_blank\" rel=\"noopener\">American College of Medical Genetics and Genomics\u003c/a>, says she's \"very concerned\" about this.\u003c/p>\n\u003cp>\"Individuals should be evaluated by medical professionals who are not conflicted, meaning they do not somehow work for a company,\" Hudgins says. \"Doctors who are contracted by companies are going to say, 'Do the test' no matter what, even if the test may not be indicated.\"\u003c/p>\n\u003cp>The companies defend the practice, saying the doctors they find for customers may be better suited than the average physician.\u003c/p>\n\u003cp>\"The majority of doctors have had maybe one class in genetics,\" says \u003ca href=\"https://www.color.com/team\" target=\"_blank\" rel=\"noopener\">Othman Laraki\u003c/a>, CEO of Color Genomics, another genetic testing company. \"I think it's much more important to have someone who has a background in genetics than just simply have someone who you can physically meet with.\"[contextly_sidebar id=\"z5IAPc8KdOy51FSsfsI8mbgyU8TgOGr0\"]\u003c/p>\n\u003cp>Privacy is another concern. Genetic testing companies say they have strict policies and procedures to protect customers' information. But some firms provide access to the genetic information they collect on an anonymous basis to drug companies and others to use for research.\u003c/p>\n\u003cp>Recent breaches of privacy by companies that collect information about people, such as Facebook, have underscored the risks of electronic data.\u003c/p>\n\u003cp>\"I'm really hoping that the security practices associated with genetic information are quite strong,\" says Cook-Deegan. \"The companies say they're strong. Time will tell if that's true.\"\u003c/p>\n\u003cp>A \u003ca href=\"https://www.eeoc.gov/laws/statutes/gina.cfm\">federal law\u003c/a> prohibits the use of genetic information to discriminate against the people for health insurance or jobs. But that law does not protect against the use of genetic information in making decisions about other things, such as life and long-term care insurance.\u003c/p>\n\u003cp>\"These are the types of things you really ought to consider when thinking about doing this kind of genetic testing — not whether there's a special on the testing this week,\" says \u003ca href=\"https://louisville.edu/bioethics/directory/mark-a.-rothstein\" target=\"_blank\" rel=\"noopener\">Mark Rothstein\u003c/a>, a professor of medicine and a bioethicist at the University of Louisville School of Medicine.\u003c/p>\n\u003cp>\u003cstrong>Results — With Limitations\u003c/strong>\u003c/p>\n\u003cp>About a month after sending in her sample, Steyn got a notice that the results of her breast cancer test were ready.\u003c/p>\n\u003cp>\"I'm really nervous,\" she said as she read through the company's explanation of what her results do and do not mean.\u003c/p>\n\u003cp>She paused in silence after she clicked to get the results.\u003c/p>\n\u003cp>\"It says zero variants detected,\" Steyn finally said, meaning the test had not found any mutations that would increase her risk.\u003c/p>\n\u003cp>\"I guess I do feel really relieved. It does make me feel better,\" she said, her voice cracking. \"I guess I just feel my chances are better now, you know?\"\u003c/p>\n\u003cp>Critics worry the testing is misleading — and relying on it could be dangerous. It tests for only three mutations in two genes known as \u003ca href=\"https://www.cancer.gov/about-cancer/causes-prevention/genetics/brca-fact-sheet\" target=\"_blank\" rel=\"noopener\">BRCA1 and BRCA2\u003c/a> that can increase the risk for breast and \u003ca href=\"https://www.cancer.org/cancer/ovarian-cancer.html\" target=\"_blank\" rel=\"noopener\">ovarian cancer\u003c/a>. Women could still have one of the thousands of other mutations that increase the risk, or be at risk for other, nongenetic reasons.[contextly_sidebar id=\"yoPuviqWfqVzH92JGqeNFv9hvL3T9Qlf\"]\u003c/p>\n\u003cp>The concern is that if a woman's 23andMe test shows she's free of the risky mutations, she may think she's in the clear and not do things she should do, such as get regular mammograms or undergo more thorough genetic testing.\u003c/p>\n\u003cp>\"To be very blunt, I worry that women who undertake testing from 23andMe could believe that they do not carry a mutation when in fact they do, and as a consequence could die of breast or ovarian cancer,\" says \u003ca href=\"http://www.gs.washington.edu/faculty/king.htm\" target=\"_blank\" rel=\"noopener\">Mary-Claire King\u003c/a>, a University of Washington geneticist who helped identify the breast cancer genes. \"I do not want to see that happen.\"\u003c/p>\n\u003cp>The company argues that it makes the test's limitations very clear and encourages women to talk to their doctor about the results and possibly seek more extensive genetic testing.\u003c/p>\n\u003cp>For women who discover they have one of the risky gene variants, the information could be crucial, according to \u003ca href=\"https://medical.23andme.com/medical-team/\" target=\"_blank\" rel=\"noopener\">Stacey Detweiller\u003c/a>, a medical affairs associate and genetic counselor at 23andMe.\u003c/p>\n\u003cp>\"Our mission is helping people access, understand and benefit from the human genome,\" Detweiller says. \"There's steps that can be taken from knowing this information that could be life-saving.\"\u003c/p>\n\u003cp>Steyn and the two other women NPR followed through the process of taking the test seemed to understand the test's limitations. They said they knew they couldn't rely on it, but they were curious to see the results.\u003c/p>\n\u003cp>But Steyn admits that she felt somewhat less urgency to get a mammogram or additional testing because of the 23andMe test results, especially since she doesn't have health insurance at the moment.\u003c/p>\n\u003cp>[ad floatright]\u003c/p>\n\u003cp>\"I'm glad I did it, especially in light of the fact that I find myself in a position where I do have to wait to see a doctor now because of the insurance situation I find myself in,\" Steyn says. \"Now I feel a little bit better about waiting. Beforehand, I probably would have not waited and figure out a way to afford this.\"\u003c/p>\n\u003cdiv class=\"fullattribution\">Copyright 2018 NPR. To see more, visit http://www.npr.org/.\u003cimg src=\"https://www.google-analytics.com/__utm.gif?utmac=UA-5828686-4&utmdt=Results+Of+At-Home+Genetic+Tests+For+Health+Can+Be+Hard+To+Interpret+&utme=8(APIKey)9(MDAxOTAwOTE4MDEyMTkxMDAzNjczZDljZA004)\">\u003c/div>\n\n",
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"content": "\u003cdiv class=\"post-body\">\u003cp>\u003cp>Rita Adele Steyn's mother had a double mastectomy in her 40s because she had so many lumps in her breasts. Her first cousin died of breast cancer. And Steyn's sister is going through chemotherapy for the disease now. Steyn worries she might be next.\u003c/p>\u003cp>\u003c/p>\u003cp>\u003c/p>\n\u003cp>\"Sometimes you feel like you beat the odds. And sometimes you feel like the odds are against you,\" said Steyn, 42, who lives in Tampa, Fla. \"And right now I feel like the odds are against me.\"\u003c/p>\n\u003cp>So Steyn jumped at the chance when she heard about a company offering an inexpensive and easy new way to get her DNA tested for genetic mutations that sharply increase the risk for \u003ca href=\"https://www.cancer.org/cancer/breast-cancer.html\" target=\"_blank\" rel=\"noopener\">breast cancer\u003c/a>.\u003c/p>\n\u003cp>\"I thought it would be good to get tested,\" says Steyn. \"I thought this is something I should know.\"\u003c/p>\n\u003cp>She ordered a $200 testing kit from the company, 23andme, spit into a small plastic tube, sent it back and waited for the results.\u003c/p>\n\u003cp>\u003c/p>\u003c/div>",
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"content": "\u003cdiv class=\"post-body\">\u003cp>\u003c/p>\n\u003cp>Genetic testing used to be uncommon and ordered only by doctors. They used it mainly to diagnose rare conditions, to find out whether prospective parents are carrying genetic diseases, or to determine whether patients are at risk for diseases in the future.\u003c/p>\n\u003cp>Now, more people are getting their DNA analyzed for health reasons, in the comfort of their own homes. As genetic testing has gotten easier, faster and more affordable, it has become a multimillion-dollar industry, with many companies aggressively marketing convenient, inexpensive tests directly to consumers. About one-third of Americans say they or a family member have considered getting a genetic test, \u003ca href=\"https://www.npr.org/sections/health-shots/2018/06/01/616126056/poll-genealogical-curiosity-is-a-top-reason-for-dna-tests-privacy-a-concern\" target=\"_blank\" rel=\"noopener\">according to a recent NPR-IBM Watson Health Poll\u003c/a>. And millions of people have gotten them, for a variety of reasons.\u003c/p>\u003cp>\u003c/p>\u003cp>\u003c/p>\n\u003cp>\"This health-related testing is probably the next big step in using genomic information in our lives,\" says \u003ca href=\"https://isearch.asu.edu/profile/2783639\" target=\"_blank\" rel=\"noopener\">Robert Cook-Deegan\u003c/a>, who studies health policy at Arizona State University.\u003c/p>\n\u003cp>But others find the trend troubling. The tests have limitations and can be hard to interpret without a doctor or genetic counselor to weigh in.\u003c/p>\n\u003cp>\u003cstrong>Pros and Cons\u003c/strong>\u003c/p>\n\u003cp>The company Steyn used, \u003ca href=\"https://www.23andme.com/\" target=\"_blank\" rel=\"noopener\">23andMe\u003c/a>, recently \u003ca href=\"https://www.npr.org/2018/03/07/591423146/test-for-breast-cancer-gene-will-be-available-in-weeks\" target=\"_blank\" rel=\"noopener\">became the first to win approval\u003c/a> from the Food and Drug Administration to market a genetic test for cancer directly to consumers without a doctor's order. It spent $27.9 million on advertising in the first quarter of 2018, according to the tracking firm Kantar Media. (NPR receives financial support from 23andMe.)\u003c/p>\n\u003cp>The industry is set to grow even more as restrictions on the medical uses of these tests are eased. The Food and Drug Administration recently \u003ca href=\"https://www.fda.gov/NewsEvents/Newsroom/PressAnnouncements/ucm583885.htm\">announced\u003c/a> plans to make it easier for these kinds of tests to win approval.\u003c/p>\u003cp>\u003c/p>\u003cp>\u003c/p>\n\u003cp>Many physicians welcome the trend, saying it's giving people valuable information. Consumers can find out early whether they are at increased risk for cancer, Alzheimer's and other diseases — and take steps to protect themselves. The testing can also sometimes help identify the safest and most effective medications to use.\u003c/p>\n\u003cp>\"Direct-to-consumer genetics companies are leading the way toward democratizing genetics and making it available to more and more people to learn about their risks and intervene in ways to keep themselves healthy,\" says \u003ca href=\"http://personalizedmedicine.partners.org/About/Leadership-Team/Robert%20Green.aspx\" target=\"_blank\" rel=\"noopener\">Robert Green\u003c/a>, a medical geneticist at Harvard.\u003c/p>\n\u003cp>But other genetic specialists, including \u003ca href=\"https://www.med.unc.edu/im/patients/general-medicine-internal-medicine-clinic/james-evans-md-phd\" target=\"_blank\" rel=\"noopener\">James Evans\u003c/a>, a professor of genetics and medicine at the University of North Carolina, Chapel Hill, argue genetic testing is still in its infancy and that the results are often inconclusive and confusing.\u003c/p>\n\u003cp>\"I think that it's an unfortunate development that will likely cause considerable mischief,\" Evans says.\u003c/p>\n\u003cp>One problem is that patients can be easily overwhelmed when results are misleading or murky. Genetic testing is still best done through doctors, he says, working with specially trained genetic counselors who can guide patients every step of the way.\u003c/p>\u003cp>\u003c/p>\u003cp>\u003c/p>\n\u003cp>\"What people deserve is well-thought-out information,\" Evans says. \"The only people who will really benefit are the investors in these companies that market these incomplete and misleading tests.\"\u003c/p>\n\u003cp>Some companies are offering newer forms of genetic testing that decipher and analyze every gene known to carry instructions for producing proteins that might reveal mutations — a process called \u003ca href=\"https://ghr.nlm.nih.gov/primer/testing/sequencing\" target=\"_blank\" rel=\"noopener\">whole exome sequencing\u003c/a>. Still others analyze the entire genetic code, which is called \u003ca href=\"https://www.fda.gov/Food/FoodScienceResearch/WholeGenomeSequencingProgramWGS/\" target=\"_blank\" rel=\"noopener\">whole genome sequencing\u003c/a>, which may find additional clues to disease. They will then analyze customers' genomes for any variations known to be associated with diseases.\u003c/p>\n\u003cp>The approach 23andMe takes is a rapid, but older, process. It analyzes short pieces of DNA for genetic variations known as \u003ca href=\"https://ghr.nlm.nih.gov/primer/genomicresearch/snp\" target=\"_blank\" rel=\"noopener\">single nucleotide variations (SNPs)\u003c/a> associated with specific diseases.\u003c/p>\n\u003cp>Except for 23andMe, all of the companies still require a doctor's order to get this testing. But an increasing number of these companies will find a physician to sign off on that for customers.\u003c/p>\n\u003cp>\"We're all about empowering consumers and making it as easy as possible for people to get these insights,\" says \u003ca href=\"https://www.helix.com/blog/author/elissa-levin/\" target=\"_blank\" rel=\"noopener\">Elissa Levin\u003c/a>, director of policy and clinical services at \u003ca href=\"https://www.helix.com/\">Helix\u003c/a>, a genetic testing company.\u003c/p>\n\u003cp>Dr. \u003ca href=\"https://profiles.stanford.edu/louanne-hudgins\" target=\"_blank\" rel=\"noopener\">Louanne Hudgins\u003c/a>, president of the \u003ca href=\"https://www.acmg.net/\" target=\"_blank\" rel=\"noopener\">American College of Medical Genetics and Genomics\u003c/a>, says she's \"very concerned\" about this.\u003c/p>\n\u003cp>\"Individuals should be evaluated by medical professionals who are not conflicted, meaning they do not somehow work for a company,\" Hudgins says. \"Doctors who are contracted by companies are going to say, 'Do the test' no matter what, even if the test may not be indicated.\"\u003c/p>\n\u003cp>The companies defend the practice, saying the doctors they find for customers may be better suited than the average physician.\u003c/p>\n\u003cp>\"The majority of doctors have had maybe one class in genetics,\" says \u003ca href=\"https://www.color.com/team\" target=\"_blank\" rel=\"noopener\">Othman Laraki\u003c/a>, CEO of Color Genomics, another genetic testing company. \"I think it's much more important to have someone who has a background in genetics than just simply have someone who you can physically meet with.\"\u003c/p>\u003cp>\u003c/p>\u003cp>\u003c/p>\n\u003cp>Privacy is another concern. Genetic testing companies say they have strict policies and procedures to protect customers' information. But some firms provide access to the genetic information they collect on an anonymous basis to drug companies and others to use for research.\u003c/p>\n\u003cp>Recent breaches of privacy by companies that collect information about people, such as Facebook, have underscored the risks of electronic data.\u003c/p>\n\u003cp>\"I'm really hoping that the security practices associated with genetic information are quite strong,\" says Cook-Deegan. \"The companies say they're strong. Time will tell if that's true.\"\u003c/p>\n\u003cp>A \u003ca href=\"https://www.eeoc.gov/laws/statutes/gina.cfm\">federal law\u003c/a> prohibits the use of genetic information to discriminate against the people for health insurance or jobs. But that law does not protect against the use of genetic information in making decisions about other things, such as life and long-term care insurance.\u003c/p>\n\u003cp>\"These are the types of things you really ought to consider when thinking about doing this kind of genetic testing — not whether there's a special on the testing this week,\" says \u003ca href=\"https://louisville.edu/bioethics/directory/mark-a.-rothstein\" target=\"_blank\" rel=\"noopener\">Mark Rothstein\u003c/a>, a professor of medicine and a bioethicist at the University of Louisville School of Medicine.\u003c/p>\n\u003cp>\u003cstrong>Results — With Limitations\u003c/strong>\u003c/p>\n\u003cp>About a month after sending in her sample, Steyn got a notice that the results of her breast cancer test were ready.\u003c/p>\n\u003cp>\"I'm really nervous,\" she said as she read through the company's explanation of what her results do and do not mean.\u003c/p>\n\u003cp>She paused in silence after she clicked to get the results.\u003c/p>\n\u003cp>\"It says zero variants detected,\" Steyn finally said, meaning the test had not found any mutations that would increase her risk.\u003c/p>\n\u003cp>\"I guess I do feel really relieved. It does make me feel better,\" she said, her voice cracking. \"I guess I just feel my chances are better now, you know?\"\u003c/p>\n\u003cp>Critics worry the testing is misleading — and relying on it could be dangerous. It tests for only three mutations in two genes known as \u003ca href=\"https://www.cancer.gov/about-cancer/causes-prevention/genetics/brca-fact-sheet\" target=\"_blank\" rel=\"noopener\">BRCA1 and BRCA2\u003c/a> that can increase the risk for breast and \u003ca href=\"https://www.cancer.org/cancer/ovarian-cancer.html\" target=\"_blank\" rel=\"noopener\">ovarian cancer\u003c/a>. Women could still have one of the thousands of other mutations that increase the risk, or be at risk for other, nongenetic reasons.\u003c/p>\u003cp>\u003c/p>\u003cp>\u003c/p>\n\u003cp>The concern is that if a woman's 23andMe test shows she's free of the risky mutations, she may think she's in the clear and not do things she should do, such as get regular mammograms or undergo more thorough genetic testing.\u003c/p>\n\u003cp>\"To be very blunt, I worry that women who undertake testing from 23andMe could believe that they do not carry a mutation when in fact they do, and as a consequence could die of breast or ovarian cancer,\" says \u003ca href=\"http://www.gs.washington.edu/faculty/king.htm\" target=\"_blank\" rel=\"noopener\">Mary-Claire King\u003c/a>, a University of Washington geneticist who helped identify the breast cancer genes. \"I do not want to see that happen.\"\u003c/p>\n\u003cp>The company argues that it makes the test's limitations very clear and encourages women to talk to their doctor about the results and possibly seek more extensive genetic testing.\u003c/p>\n\u003cp>For women who discover they have one of the risky gene variants, the information could be crucial, according to \u003ca href=\"https://medical.23andme.com/medical-team/\" target=\"_blank\" rel=\"noopener\">Stacey Detweiller\u003c/a>, a medical affairs associate and genetic counselor at 23andMe.\u003c/p>\n\u003cp>\"Our mission is helping people access, understand and benefit from the human genome,\" Detweiller says. \"There's steps that can be taken from knowing this information that could be life-saving.\"\u003c/p>\n\u003cp>Steyn and the two other women NPR followed through the process of taking the test seemed to understand the test's limitations. They said they knew they couldn't rely on it, but they were curious to see the results.\u003c/p>\n\u003cp>But Steyn admits that she felt somewhat less urgency to get a mammogram or additional testing because of the 23andMe test results, especially since she doesn't have health insurance at the moment.\u003c/p>\n\u003cp>\u003c/p>\u003c/div>",
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"content": "\u003cdiv class=\"post-body\">\u003cp>\u003c/p>\n\u003cp>\"I'm glad I did it, especially in light of the fact that I find myself in a position where I do have to wait to see a doctor now because of the insurance situation I find myself in,\" Steyn says. \"Now I feel a little bit better about waiting. Beforehand, I probably would have not waited and figure out a way to afford this.\"\u003c/p>\n\u003cdiv class=\"fullattribution\">Copyright 2018 NPR. To see more, visit http://www.npr.org/.\u003cimg src=\"https://www.google-analytics.com/__utm.gif?utmac=UA-5828686-4&utmdt=Results+Of+At-Home+Genetic+Tests+For+Health+Can+Be+Hard+To+Interpret+&utme=8(APIKey)9(MDAxOTAwOTE4MDEyMTkxMDAzNjczZDljZA004)\">\u003c/div>\n\n\u003c/div>\u003c/p>",
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"disqusTitle": "UC Berkeley Granted Two CRISPR-Related Patents",
"title": "UC Berkeley Granted Two CRISPR-Related Patents",
"headTitle": "KQED Future of You | KQED Science",
"content": "\u003cp>The University of California will be receiving two CRISPR-related \u003ca href=\"http://patft.uspto.gov/netacgi/nph-Parser?Sect1=PTO1&Sect2=HITOFF&d=PALL&p=1&u=%2Fnetahtml%2FPTO%2Fsrchnum.htm&r=1&f=G&l=50&s1=9,994,831.PN.&OS=PN/9,994,831&RS=PN/9,994,831\" target=\"_blank\" rel=\"noopener\">patents\u003c/a>, marking another step forward in the university's long battle to assert its claims to the revolutionary technology.[contextly_sidebar id=\"HobWula6BihfuZ4zJKYzmOCLk2EeUohl\"]\u003c/p>\n\u003cp>UC Berkeley \u003ca href=\"https://nature1.berkeley.edu/breakthroughs/sp18/genes-to-global-solutions\" target=\"_blank\" rel=\"noopener\">pioneered the technology\u003c/a> in 2012, when a team led by biochemist \u003ca href=\"http://doudnalab.org/\" target=\"_blank\" rel=\"noopener\">Jennifer Doudna\u003c/a> reported that they had successfully developed a “programmable” genome-editing tool that makes highly targeted alterations to the genome of a plant or animal. A team at the \u003ca href=\"https://www.broadinstitute.org/\" target=\"_blank\" rel=\"noopener\">Broad Institute\u003c/a>, owned jointly by Harvard University and the Massachusetts Institute, was also researching the technology during the same period.\u003c/p>\n\u003cp>Commonly known as CRISPR—an acronym for Clustered Regularly Interspaced Short Palindromic Repeats, the groundbreaking technology offers a method to fix genes in living things. It could be used to develop everything from drought-resistant crops, to new treatments for genetic disorders and cancers.\u003c/p>\n\u003cp>UC Berkeley is in a \u003ca href=\"https://www.kqed.org/futureofyou/372137/uc-berkeley-renews-legal-fight-over-crispr-cas9-patent-rights\" target=\"_blank\" rel=\"noopener\">legal fight\u003c/a> with the Broad Institute over the patent rights to CRISPR. UC Berkeley filed its patent application before Broad did, but Broad fast-tracked its application.\u003c/p>\n\u003cp>The United States Patent and Trademark Office in February 2017 \u003ca href=\"https://www.kqed.org/futureofyou/338066/broad-institute-wins-decision-over-uc-berkeley-in-crispr-patent-battle\" target=\"_blank\" rel=\"noopener\">awarded a patent\u003c/a> to Broad for CRISPR's use in plant and animal cells, and a pending patent to UC Berkeley for CRISPR's use in bacterial cells. The UC appealed in April 2017, arguing its scientists were the first inventors of the technology.\u003c/p>\n\u003cp>[ad fullwidth]\u003c/p>\n\u003cp>[contextly_sidebar id=\"dldVTmrihr5ckptkstBunRusJqL7Q1kF\"]The patent granted to UC Berkeley on Tuesday focuses on using the tool to edit single-stranded RNA, according to \u003ca href=\"https://www.statnews.com/2018/06/13/university-of-california-granted-a-key-crispr-patent/\" target=\"_blank\" rel=\"noopener\">a \u003cem>STAT News \u003c/em>report\u003c/a>. The federal agency will reportedly award a second patent next week. That patent, reports STAT, will focus on using the tool to edit regions specifically 10 to 15 base pairs long.\u003c/p>\n\u003cp>Some experts are downplaying the patents' significance.\u003c/p>\n\u003cp>According to New York Law School associate professor Jacob Sherkow, who spoke with\u003ca href=\"https://www.statnews.com/2018/06/13/university-of-california-granted-a-key-crispr-patent/\" target=\"_blank\" rel=\"noopener\">\u003cem> STAT\u003c/em>\u003c/a>, the second patent will likely have “pretty minimal” commercial value.[contextly_sidebar id=\"r1GPWMK2Ali0LLhAqlMmjHyUin6pJWDz\"]\u003c/p>\n\u003cp>The USPTO has so far granted more than \u003ca href=\"https://www.broadinstitute.org/crispr/journalists-statement-and-background-crispr-patent-process\" target=\"_blank\" rel=\"noopener\">60 CRISPR-related patents\u003c/a> to inventors from 18 organizations, according to the Broad Institute.\u003c/p>\n\u003cp>Meanwhile, news of the university's patent awards come as two new \u003ca href=\"https://www.nature.com/articles/s41591-018-0050-6.epdf\" target=\"_blank\" rel=\"noopener\">studies\u003c/a> published on Monday caution that gene cells edited with CRISPR-Cas9 \u003ca href=\"https://www.kqed.org/futureofyou/442526/major-hurdle-for-crispr-edited-cells-might-cause-cancer-find-two-studies\" target=\"_blank\" rel=\"noopener\">may be linked\u003c/a> to cancer.\u003c/p>\n\u003cp>\u003c/p>\n\u003cp> \u003c/p>\n\n",
"disqusIdentifier": "442727 https://ww2.kqed.org/futureofyou/?p=442727",
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"excerpt": "The university is fighting to assert its rights to the revolutionary gene-editing tool known as CRISPR. But some experts are downplaying the patents' significance. ",
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"content": "\u003cdiv class=\"post-body\">\u003cp>\u003cp>The University of California will be receiving two CRISPR-related \u003ca href=\"http://patft.uspto.gov/netacgi/nph-Parser?Sect1=PTO1&Sect2=HITOFF&d=PALL&p=1&u=%2Fnetahtml%2FPTO%2Fsrchnum.htm&r=1&f=G&l=50&s1=9,994,831.PN.&OS=PN/9,994,831&RS=PN/9,994,831\" target=\"_blank\" rel=\"noopener\">patents\u003c/a>, marking another step forward in the university's long battle to assert its claims to the revolutionary technology.\u003c/p>\u003cp>\u003c/p>\u003cp>\u003c/p>\n\u003cp>UC Berkeley \u003ca href=\"https://nature1.berkeley.edu/breakthroughs/sp18/genes-to-global-solutions\" target=\"_blank\" rel=\"noopener\">pioneered the technology\u003c/a> in 2012, when a team led by biochemist \u003ca href=\"http://doudnalab.org/\" target=\"_blank\" rel=\"noopener\">Jennifer Doudna\u003c/a> reported that they had successfully developed a “programmable” genome-editing tool that makes highly targeted alterations to the genome of a plant or animal. A team at the \u003ca href=\"https://www.broadinstitute.org/\" target=\"_blank\" rel=\"noopener\">Broad Institute\u003c/a>, owned jointly by Harvard University and the Massachusetts Institute, was also researching the technology during the same period.\u003c/p>\n\u003cp>Commonly known as CRISPR—an acronym for Clustered Regularly Interspaced Short Palindromic Repeats, the groundbreaking technology offers a method to fix genes in living things. It could be used to develop everything from drought-resistant crops, to new treatments for genetic disorders and cancers.\u003c/p>\n\u003cp>UC Berkeley is in a \u003ca href=\"https://www.kqed.org/futureofyou/372137/uc-berkeley-renews-legal-fight-over-crispr-cas9-patent-rights\" target=\"_blank\" rel=\"noopener\">legal fight\u003c/a> with the Broad Institute over the patent rights to CRISPR. UC Berkeley filed its patent application before Broad did, but Broad fast-tracked its application.\u003c/p>\n\u003cp>The United States Patent and Trademark Office in February 2017 \u003ca href=\"https://www.kqed.org/futureofyou/338066/broad-institute-wins-decision-over-uc-berkeley-in-crispr-patent-battle\" target=\"_blank\" rel=\"noopener\">awarded a patent\u003c/a> to Broad for CRISPR's use in plant and animal cells, and a pending patent to UC Berkeley for CRISPR's use in bacterial cells. The UC appealed in April 2017, arguing its scientists were the first inventors of the technology.\u003c/p>\n\u003cp>\u003c/p>\u003c/div>",
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"content": "\u003cdiv class=\"post-body\">\u003cp>\u003c/p>\n\u003cp>\u003c/p>\u003cp>\u003c/p>\u003cp>The patent granted to UC Berkeley on Tuesday focuses on using the tool to edit single-stranded RNA, according to \u003ca href=\"https://www.statnews.com/2018/06/13/university-of-california-granted-a-key-crispr-patent/\" target=\"_blank\" rel=\"noopener\">a \u003cem>STAT News \u003c/em>report\u003c/a>. The federal agency will reportedly award a second patent next week. That patent, reports STAT, will focus on using the tool to edit regions specifically 10 to 15 base pairs long.\u003c/p>\n\u003cp>Some experts are downplaying the patents' significance.\u003c/p>\n\u003cp>According to New York Law School associate professor Jacob Sherkow, who spoke with\u003ca href=\"https://www.statnews.com/2018/06/13/university-of-california-granted-a-key-crispr-patent/\" target=\"_blank\" rel=\"noopener\">\u003cem> STAT\u003c/em>\u003c/a>, the second patent will likely have “pretty minimal” commercial value.\u003c/p>\u003cp>\u003c/p>\u003cp>\u003c/p>\n\u003cp>The USPTO has so far granted more than \u003ca href=\"https://www.broadinstitute.org/crispr/journalists-statement-and-background-crispr-patent-process\" target=\"_blank\" rel=\"noopener\">60 CRISPR-related patents\u003c/a> to inventors from 18 organizations, according to the Broad Institute.\u003c/p>\n\u003cp>Meanwhile, news of the university's patent awards come as two new \u003ca href=\"https://www.nature.com/articles/s41591-018-0050-6.epdf\" target=\"_blank\" rel=\"noopener\">studies\u003c/a> published on Monday caution that gene cells edited with CRISPR-Cas9 \u003ca href=\"https://www.kqed.org/futureofyou/442526/major-hurdle-for-crispr-edited-cells-might-cause-cancer-find-two-studies\" target=\"_blank\" rel=\"noopener\">may be linked\u003c/a> to cancer.\u003c/p>\n\u003cp>\u003c/p>\n\u003cp> \u003c/p>\n\n\u003c/div>\u003c/p>",
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"disqusTitle": "Stanford Pioneer in Brain Research Wins Prestigious Kyoto Prize",
"title": "Stanford Pioneer in Brain Research Wins Prestigious Kyoto Prize",
"headTitle": "KQED Future of You | KQED Science",
"content": "\u003cp>Karl Deisseroth, a Stanford University professor of bioengineering and psychiatry, has been awarded an international prize worth more than $900,000 for his work in illuminating brain activity with light. The exact amount of the prize was 100 million yen.\u003c/p>\n\u003caside class=\"pullquote alignright\">'Karl has created a revolutionary technology that has broadened our understanding of brain disorders and may one day yield treatments to the millions with these disorders.'\u003ccite>Lloyd Minor, Stanford School of Medicine\u003c/cite>\u003c/aside>\n\u003cp>Deisseroth is receiving the 2018 \u003ca href=\"https://www.kyotoprize.org/en/\" target=\"_blank\" rel=\"noopener\">Kyoto Prize\u003c/a> for advanced technology. Awards are also granted for basic sciences, and arts and philosophy. Some of its recipients have gone on to win the Nobel Prize.\u003c/p>\n\u003cp>\u003ca href=\"https://web.stanford.edu/group/dlab/about_pi.html\" target=\"_blank\" rel=\"noopener\">Deisseroth,\u003c/a> the youngest person to ever receive the prize, is being honored for developing \u003ca href=\"http://web.stanford.edu/group/dlab/optogenetics/\">optogenetics\u003c/a>, a technology that uses light-sensitive proteins to manipulate brain cell activity. The method allows scientists to glean more information about brain disorders and to probe how the nervous system works.\u003c/p>\n\u003cp>\"It is humbling to see all the distinguished people who have won the Kyoto Prize, and to be listed with them. It is wonderful to see pure basic science discoveries recognized in this way,\" said Deisseroth.\u003c/p>\n\u003cp>The technique developed by Deisseroth and his team manipulates cellular activity by delivering a pulse of light to a particular cell through an optical fiber that has been implanted in the animal’s brain. The method yields information on how brain cells give rise to sensations, memories and actions.\u003c/p>\n\u003cfigure id=\"attachment_442697\" class=\"wp-caption alignright\" style=\"max-width: 480px\">\u003cimg class=\"size-full wp-image-442697\" src=\"https://ww2.kqed.org/futureofyou/wp-content/uploads/sites/13/2018/06/image01.jpg\" alt=\"\" width=\"480\" height=\"360\" srcset=\"https://ww2.kqed.org/app/uploads/sites/13/2018/06/image01.jpg 480w, https://ww2.kqed.org/app/uploads/sites/13/2018/06/image01-160x120.jpg 160w, https://ww2.kqed.org/app/uploads/sites/13/2018/06/image01-240x180.jpg 240w, https://ww2.kqed.org/app/uploads/sites/13/2018/06/image01-375x281.jpg 375w\" sizes=\"(max-width: 480px) 100vw, 480px\">\u003cfigcaption class=\"wp-caption-text\">The Kyoto prize medal. \u003ccite>(Inamori Foundation)\u003c/cite>\u003c/figcaption>\u003c/figure>\n\u003cp>“A brilliant and innovative investigator, Karl has created a revolutionary technology that has broadened our understanding of brain disorders and may one day yield treatments to the millions with these disorders,” said Dr. Lloyd Minor, dean of the \u003ca href=\"http://med.stanford.edu/\" target=\"_blank\" rel=\"noopener\">Stanford School of Medicine\u003c/a>, in a statement. “His receipt of the Kyoto Prize is inordinately well-deserved and the product of his unmatched scientific vision.\"\u003c/p>\n\u003cp>[ad fullwidth]\u003c/p>\n\u003cp>Deisseroth has said his research\u003ca href=\"https://www.scientificamerican.com/article/optogenetics-controlling/\" target=\"_blank\" rel=\"noopener\"> was motivated by\u003c/a> a desire to better understand psychiatric disorders, the leading cause of years of life lost to death or disability.\u003c/p>\n\u003cp>Deisseroth’s research, developed between 2004 and 2009, is used by laboratories around the world.\u003c/p>\n\u003cp>\"Thousands of laboratories around the world have used optogenetics to satisfy their own curiosity about the natural world, and to test ideas in a broad range of systems and species,\" he said. \"Many people are also studying brain diseases, and optogenetics-guided clinical trials have already started with some success, bringing a new kind of hope to people affected by these diseases such as substance dependence and depression.\"\u003c/p>\n\u003cp>\u003ciframe width=\"640\" height=\"360\" src=\"https://www.youtube.com/embed/CE6uNFFZ0qc?feature=oembed\" frameborder=\"0\" allow=\"accelerometer; autoplay; encrypted-media; gyroscope; picture-in-picture\" allowfullscreen>\u003c/iframe>\u003c/p>\n\u003cp>What makes optogenetics so groundbreaking is its level of precision in controlling defined activity within specific cells, according to I-Han Chou, senior editor at the journal \"Nature\".[contextly_sidebar id=\"08EVHeybNXS0fTuglKI55A1KVy7EFUpl\"]\u003c/p>\n\u003cp>\"If you imagine the brain as this city, up until now we have been looking at it as if from space,\" Chou\u003ca href=\"https://www.weforum.org/agenda/2016/10/what-is-optogenetics/\" target=\"_blank\" rel=\"noopener\"> told the\u003c/a> World Economic Forum site. \"We haven't had the tools to do anything beyond seeing what the whole city block is doing. What you actually want to know is what the individual components of the city are, what the people are doing, and what's the information being transported from one part of the city to another.\"\u003c/p>\n\u003cp>The technique could transform how neurological disorders such as Parkinson's disease are treated.\u003c/p>\n\u003cp>\"When things go wrong with the brain it is just so devastating. One of the hopes for optogenetics is that if it can work in humans, it might be used as a tool for restoring brain function,\" Chou added.\u003c/p>\n\u003cp>\u003c/p>\n\u003cp> \u003c/p>\n\n",
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"content": "\u003cdiv class=\"post-body\">\u003cp>\u003cp>Karl Deisseroth, a Stanford University professor of bioengineering and psychiatry, has been awarded an international prize worth more than $900,000 for his work in illuminating brain activity with light. The exact amount of the prize was 100 million yen.\u003c/p>\n\u003caside class=\"pullquote alignright\">'Karl has created a revolutionary technology that has broadened our understanding of brain disorders and may one day yield treatments to the millions with these disorders.'\u003ccite>Lloyd Minor, Stanford School of Medicine\u003c/cite>\u003c/aside>\n\u003cp>Deisseroth is receiving the 2018 \u003ca href=\"https://www.kyotoprize.org/en/\" target=\"_blank\" rel=\"noopener\">Kyoto Prize\u003c/a> for advanced technology. Awards are also granted for basic sciences, and arts and philosophy. Some of its recipients have gone on to win the Nobel Prize.\u003c/p>\n\u003cp>\u003ca href=\"https://web.stanford.edu/group/dlab/about_pi.html\" target=\"_blank\" rel=\"noopener\">Deisseroth,\u003c/a> the youngest person to ever receive the prize, is being honored for developing \u003ca href=\"http://web.stanford.edu/group/dlab/optogenetics/\">optogenetics\u003c/a>, a technology that uses light-sensitive proteins to manipulate brain cell activity. The method allows scientists to glean more information about brain disorders and to probe how the nervous system works.\u003c/p>\n\u003cp>\"It is humbling to see all the distinguished people who have won the Kyoto Prize, and to be listed with them. It is wonderful to see pure basic science discoveries recognized in this way,\" said Deisseroth.\u003c/p>\n\u003cp>The technique developed by Deisseroth and his team manipulates cellular activity by delivering a pulse of light to a particular cell through an optical fiber that has been implanted in the animal’s brain. The method yields information on how brain cells give rise to sensations, memories and actions.\u003c/p>\n\u003cfigure id=\"attachment_442697\" class=\"wp-caption alignright\" style=\"max-width: 480px\">\u003cimg class=\"size-full wp-image-442697\" src=\"https://ww2.kqed.org/futureofyou/wp-content/uploads/sites/13/2018/06/image01.jpg\" alt=\"\" width=\"480\" height=\"360\" srcset=\"https://ww2.kqed.org/app/uploads/sites/13/2018/06/image01.jpg 480w, https://ww2.kqed.org/app/uploads/sites/13/2018/06/image01-160x120.jpg 160w, https://ww2.kqed.org/app/uploads/sites/13/2018/06/image01-240x180.jpg 240w, https://ww2.kqed.org/app/uploads/sites/13/2018/06/image01-375x281.jpg 375w\" sizes=\"(max-width: 480px) 100vw, 480px\">\u003cfigcaption class=\"wp-caption-text\">The Kyoto prize medal. \u003ccite>(Inamori Foundation)\u003c/cite>\u003c/figcaption>\u003c/figure>\n\u003cp>“A brilliant and innovative investigator, Karl has created a revolutionary technology that has broadened our understanding of brain disorders and may one day yield treatments to the millions with these disorders,” said Dr. Lloyd Minor, dean of the \u003ca href=\"http://med.stanford.edu/\" target=\"_blank\" rel=\"noopener\">Stanford School of Medicine\u003c/a>, in a statement. “His receipt of the Kyoto Prize is inordinately well-deserved and the product of his unmatched scientific vision.\"\u003c/p>\n\u003cp>\u003c/p>\u003c/div>",
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"content": "\u003cdiv class=\"post-body\">\u003cp>\u003c/p>\n\u003cp>Deisseroth has said his research\u003ca href=\"https://www.scientificamerican.com/article/optogenetics-controlling/\" target=\"_blank\" rel=\"noopener\"> was motivated by\u003c/a> a desire to better understand psychiatric disorders, the leading cause of years of life lost to death or disability.\u003c/p>\n\u003cp>Deisseroth’s research, developed between 2004 and 2009, is used by laboratories around the world.\u003c/p>\n\u003cp>\"Thousands of laboratories around the world have used optogenetics to satisfy their own curiosity about the natural world, and to test ideas in a broad range of systems and species,\" he said. \"Many people are also studying brain diseases, and optogenetics-guided clinical trials have already started with some success, bringing a new kind of hope to people affected by these diseases such as substance dependence and depression.\"\u003c/p>\n\u003cp>\u003ciframe width=\"640\" height=\"360\" src=\"https://www.youtube.com/embed/CE6uNFFZ0qc?feature=oembed\" frameborder=\"0\" allow=\"accelerometer; autoplay; encrypted-media; gyroscope; picture-in-picture\" allowfullscreen>\u003c/iframe>\u003c/p>\n\u003cp>What makes optogenetics so groundbreaking is its level of precision in controlling defined activity within specific cells, according to I-Han Chou, senior editor at the journal \"Nature\".\u003c/p>\u003cp>\u003c/p>\u003cp>\u003c/p>\n\u003cp>\"If you imagine the brain as this city, up until now we have been looking at it as if from space,\" Chou\u003ca href=\"https://www.weforum.org/agenda/2016/10/what-is-optogenetics/\" target=\"_blank\" rel=\"noopener\"> told the\u003c/a> World Economic Forum site. \"We haven't had the tools to do anything beyond seeing what the whole city block is doing. What you actually want to know is what the individual components of the city are, what the people are doing, and what's the information being transported from one part of the city to another.\"\u003c/p>\n\u003cp>The technique could transform how neurological disorders such as Parkinson's disease are treated.\u003c/p>\n\u003cp>\"When things go wrong with the brain it is just so devastating. One of the hopes for optogenetics is that if it can work in humans, it might be used as a tool for restoring brain function,\" Chou added.\u003c/p>\n\u003cp>\u003c/p>\n\u003cp> \u003c/p>\n\n\u003c/div>\u003c/p>",
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"disqusTitle": "Simple Saliva Test Could Identify Men at Greatest Risk of Prostate Cancer",
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"content": "\u003cp>A team of scientists at London's\u003ca href=\"https://www.icr.ac.uk/\" target=\"_blank\" rel=\"noopener\"> Institute of Cancer Research\u003c/a> have developed a \"spit test\" that can be used to identify men most likely to develop prostate cancer, the second leading cause of cancer death in U.S. men.[contextly_sidebar id=\"KO4wdzhP8pt1tRs02KEaCVL4V511U4Nk\"]\u003c/p>\n\u003cp>About 1 in 9 men are diagnosed with prostate cancer at some point, according to the \u003ca href=\"https://www.cancer.org/cancer/prostate-cancer/about/key-statistics.html\" target=\"_blank\" rel=\"noopener\">American Cancer Society. \u003c/a>\u003c/p>\n\u003cp>The study, \u003ca href=\"https://www.nature.com/articles/s41588-018-0142-8\" target=\"_blank\" rel=\"noopener\">published \u003c/a>Monday in the journal Nature Genetics, identified the 1 percent of men with the highest genetic risk for prostate cancer. This group is nearly six times more likely to develop prostate cancer than the general population, according to\u003ca href=\"https://www.eurekalert.org/pub_releases/2018-06/iocr-pcd060818.php\" target=\"_blank\" rel=\"noopener\"> the study.\u003c/a>\u003c/p>\n\u003cp>Researchers, funded in part by the National Institutes of Health, utilized a new DNA analysis method to study the genes of more than 70,000 people. They looked at 150 DNA markers and found that the top 10 percent of men at highest risk for prostate cancer were found to nearly three times the risk of developing the disease. From Gizmodo:\u003c/p>\n\u003cblockquote>\u003cp>Some 45,000 of the subjects had already developed prostate cancer, while 25,000 hadn’t. So the researchers compared the two groups, singling out any inherited genetic variations that might have contributed to their cancer risk.\u003c/p>\u003c/blockquote>\n\u003cp>Based on this data, the study said that researchers discovered 63 new variants that have previously not been associated with prostate cancer. Rosalind Eeles, a geneticist and co-author of the study, said those men found to be at greater genetic risk can receive proper screenings.\u003c/p>\n\u003cp>[ad fullwidth]\u003c/p>\n\u003cp>“The reason we are particularly excited by the test is that this can be offered in general practice as a spit test to really try and identify who is most at risk of prostate cancer so we can offer them targeted screening,” Eeles \u003ca href=\"https://www.theguardian.com/science/2018/jun/11/trials-begin-of-a-saliva-test-for-prostate-cancer\" target=\"_blank\" rel=\"noopener\">told T\u003c/a>\u003ca href=\"https://www.theguardian.com/science/2018/jun/11/trials-begin-of-a-saliva-test-for-prostate-cancer\" target=\"_blank\" rel=\"noopener\">he Guardian.\u003c/a>\u003c/p>\n\u003cp>Most men diagnosed with the disease do not die from it, according to the American Cancer Society. Risk factors include family history, advanced age, and those of African descent.[contextly_sidebar id=\"go4zed6vsFCKAoaAAycufIdrqinev6En\"]\u003c/p>\n\u003cp>\u003c/p>\n\u003cp>About 6 in 10 cases of prostate cancer are diagnosed in men aged 65 or older. From Gizmodo:\u003c/p>\n\u003cblockquote>\u003cp>In the US, people over the age of 50 are \u003ca href=\"https://www.cancer.org/cancer/prostate-cancer/early-detection/acs-recommendations.html\" target=\"_blank\" rel=\"noopener\">generally screened\u003c/a> for prostate cancer via the prostate-specific antigen (PSA) blood test...But the saliva test could reveal especially high-risk people who need annual screening regardless of their PSA level.\u003c/p>\u003c/blockquote>\n\u003cdiv id=\"dfp-ad--inline2\" class=\"js-ad-slot ad-slot ad-slot--inline ad-slot--offset-right ad-slot--inline2 ad-slot--rendered\">\n\u003cdiv class=\"ad-slot__label\">\n\u003cp>Researchers\u003ca href=\"https://www.eurekalert.org/pub_releases/2018-06/iocr-pcd060818.php\" target=\"_blank\" rel=\"noopener\"> now plan a trial\u003c/a> run of the new test at a limited number of clinics to help devise treatments that could reduce cases of prostate cancer among this high-risk group.\u003c/p>\n\u003c/div>\n\u003cdiv>\"We are on the cusp of moving from theory to practice -- from explaining how genetics affect prostate cancer risk, to testing for genetic risk and attempting to prevent the disease,\" Paul Workman, chief executive at The Institute of Cancer Research, said in a \u003ca href=\"https://www.eurekalert.org/pub_releases/2018-06/iocr-pcd060818.php\" target=\"_blank\" rel=\"noopener\">statement\u003c/a>. \"This study also gives us important information about the causes of prostate cancer and the potential role of the immune system, which could ultimately be employed in the design of new treatments.\"\u003c/div>\n\u003c/div>\n\u003cdiv id=\"dfp-ad--inline2\" class=\"js-ad-slot ad-slot ad-slot--inline ad-slot--offset-right ad-slot--inline2 ad-slot--rendered\">\n\u003cdiv id=\"google_ads_iframe_/59666047/theguardian.com/science/article/ng_7__container__\" class=\"ad-slot__content\">\u003c/div>\n\u003c/div>\n\n",
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"excerpt": "Researchers say a promising new saliva test can identify the top 10 percent of men at greatest risk of developing prostate cancer, a leading cause of cancer death in men.",
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"content": "\u003cdiv class=\"post-body\">\u003cp>\u003cp>A team of scientists at London's\u003ca href=\"https://www.icr.ac.uk/\" target=\"_blank\" rel=\"noopener\"> Institute of Cancer Research\u003c/a> have developed a \"spit test\" that can be used to identify men most likely to develop prostate cancer, the second leading cause of cancer death in U.S. men.\u003c/p>\u003cp>\u003c/p>\u003cp>\u003c/p>\n\u003cp>About 1 in 9 men are diagnosed with prostate cancer at some point, according to the \u003ca href=\"https://www.cancer.org/cancer/prostate-cancer/about/key-statistics.html\" target=\"_blank\" rel=\"noopener\">American Cancer Society. \u003c/a>\u003c/p>\n\u003cp>The study, \u003ca href=\"https://www.nature.com/articles/s41588-018-0142-8\" target=\"_blank\" rel=\"noopener\">published \u003c/a>Monday in the journal Nature Genetics, identified the 1 percent of men with the highest genetic risk for prostate cancer. This group is nearly six times more likely to develop prostate cancer than the general population, according to\u003ca href=\"https://www.eurekalert.org/pub_releases/2018-06/iocr-pcd060818.php\" target=\"_blank\" rel=\"noopener\"> the study.\u003c/a>\u003c/p>\n\u003cp>Researchers, funded in part by the National Institutes of Health, utilized a new DNA analysis method to study the genes of more than 70,000 people. They looked at 150 DNA markers and found that the top 10 percent of men at highest risk for prostate cancer were found to nearly three times the risk of developing the disease. From Gizmodo:\u003c/p>\n\u003cblockquote>\u003cp>Some 45,000 of the subjects had already developed prostate cancer, while 25,000 hadn’t. So the researchers compared the two groups, singling out any inherited genetic variations that might have contributed to their cancer risk.\u003c/p>\u003c/blockquote>\n\u003cp>Based on this data, the study said that researchers discovered 63 new variants that have previously not been associated with prostate cancer. Rosalind Eeles, a geneticist and co-author of the study, said those men found to be at greater genetic risk can receive proper screenings.\u003c/p>\n\u003cp>\u003c/p>\u003c/div>",
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"content": "\u003cdiv class=\"post-body\">\u003cp>\u003c/p>\n\u003cp>“The reason we are particularly excited by the test is that this can be offered in general practice as a spit test to really try and identify who is most at risk of prostate cancer so we can offer them targeted screening,” Eeles \u003ca href=\"https://www.theguardian.com/science/2018/jun/11/trials-begin-of-a-saliva-test-for-prostate-cancer\" target=\"_blank\" rel=\"noopener\">told T\u003c/a>\u003ca href=\"https://www.theguardian.com/science/2018/jun/11/trials-begin-of-a-saliva-test-for-prostate-cancer\" target=\"_blank\" rel=\"noopener\">he Guardian.\u003c/a>\u003c/p>\n\u003cp>Most men diagnosed with the disease do not die from it, according to the American Cancer Society. Risk factors include family history, advanced age, and those of African descent.\u003c/p>\u003cp>\u003c/p>\u003cp>\u003c/p>\n\u003cp>\u003c/p>\n\u003cp>About 6 in 10 cases of prostate cancer are diagnosed in men aged 65 or older. From Gizmodo:\u003c/p>\n\u003cblockquote>\u003cp>In the US, people over the age of 50 are \u003ca href=\"https://www.cancer.org/cancer/prostate-cancer/early-detection/acs-recommendations.html\" target=\"_blank\" rel=\"noopener\">generally screened\u003c/a> for prostate cancer via the prostate-specific antigen (PSA) blood test...But the saliva test could reveal especially high-risk people who need annual screening regardless of their PSA level.\u003c/p>\u003c/blockquote>\n\u003cdiv id=\"dfp-ad--inline2\" class=\"js-ad-slot ad-slot ad-slot--inline ad-slot--offset-right ad-slot--inline2 ad-slot--rendered\">\n\u003cdiv class=\"ad-slot__label\">\n\u003cp>Researchers\u003ca href=\"https://www.eurekalert.org/pub_releases/2018-06/iocr-pcd060818.php\" target=\"_blank\" rel=\"noopener\"> now plan a trial\u003c/a> run of the new test at a limited number of clinics to help devise treatments that could reduce cases of prostate cancer among this high-risk group.\u003c/p>\n\u003c/div>\n\u003cdiv>\"We are on the cusp of moving from theory to practice -- from explaining how genetics affect prostate cancer risk, to testing for genetic risk and attempting to prevent the disease,\" Paul Workman, chief executive at The Institute of Cancer Research, said in a \u003ca href=\"https://www.eurekalert.org/pub_releases/2018-06/iocr-pcd060818.php\" target=\"_blank\" rel=\"noopener\">statement\u003c/a>. \"This study also gives us important information about the causes of prostate cancer and the potential role of the immune system, which could ultimately be employed in the design of new treatments.\"\u003c/div>\n\u003c/div>\n\u003cdiv id=\"dfp-ad--inline2\" class=\"js-ad-slot ad-slot ad-slot--inline ad-slot--offset-right ad-slot--inline2 ad-slot--rendered\">\n\u003cdiv id=\"google_ads_iframe_/59666047/theguardian.com/science/article/ng_7__container__\" class=\"ad-slot__content\">\u003c/div>\n\u003c/div>\n\n\u003c/div>\u003c/p>",
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"disqusTitle": "A Science Writer Explores The 'Perversions And Potential' Of Genetic Tests",
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"content": "\u003cp>\u003c!-- iframe plugin v.4.3 wordpress.org/plugins/iframe/ -->\u003cbr>\n\u003ciframe src=\"https://www.npr.org/player/embed/618870881/618969757\" width=\"100%\" height=\"290\" frameborder=\"0\" scrolling=\"no\" title=\"NPR embedded audio player\" class=\"iframe-class\">\u003c/iframe>\u003c/p>\n\u003cp>As a science columnist for\u003cem> The New York Times, \u003c/em>Carl Zimmer had reported extensively about genetics and the role gene mutations play in various ailments. After a while, he got to wondering about what secrets his own genetic code holds.[contextly_sidebar id=\"AyWMyOjcCCjd9Wr45bM9omzK5fGeueow\"]\u003c/p>\n\u003cp>\"I wanted to know if there was anything I needed to worry about,\" Zimmer says. \"We all think back to our relatives who got sick and then wonder, 'Is that in me?'\"\u003c/p>\n\u003cp>So Zimmer worked with a genetics counselor to get his entire genome sequenced — an experience he describes as \"very nerve-wracking.\" He worried that he would discover a mutation that would put him on the path for a particular disease.\u003c/p>\n\u003cp>As it turned out, the counselor told Zimmer he has a \"boring genome.\" Though Zimmer initially hoped for a more \"exciting and exotic\" assessment, the counselor reminded him \"A boring genome is a really good genome.\"\u003c/p>\n\u003cp>[ad fullwidth]\u003c/p>\n\u003cp>Zimmer writes about the broader implications of genetic research and testing in his new book, \u003cem>She Has Her Mother's Laugh: The Powers, Perversions and Potential of Heredity\u003c/em>.[contextly_sidebar id=\"YtqF4uhyPE2pCelB55bttG0XpqJfRSq3\"]\u003c/p>\n\u003chr>\n\u003cp>\u003cstrong>Interview Highlights\u003c/strong>\u003c/p>\n\u003cp>\u003cstrong>On how the new genetic editing technology known as \u003ca href=\"https://www.npr.org/tags/419142387/crispr\" target=\"_blank\" rel=\"noopener\">CRISPR\u003c/a> works\u003c/strong>\u003c/p>\n\u003cp>What happens with CRISPR is that scientists will design a molecule — think of it as a probe — and it will search around in the DNA in a cell until if finds a very specific short sequence. And it will grab onto it, and it brings on with it basically molecular scissors, which will then cut the DNA at that spot — kind of like cutting tape. And you can cut out a segment of DNA. And if you just do that, DNA will heal itself. Basically the two loose ends will stitch themselves together, and now that piece is just missing. Or you can add in a little piece of different DNA, and you can actually get the cell to put in that new piece of DNA where you just cut out the old one.\u003c/p>\n\u003cp>\u003cstrong>On whether CRISPR technology could be used to treat diseases in humans\u003c/strong>\u003c/p>\n\u003cp>We're just on the verge of human trials. They will be starting, hopefully very soon, for diseases like sickle-cell anemia. There's actually a lot of research on muscular dystrophy as well. There are a few key diseases where scientists think these would be the best places to start. To basically inject CRISPR molecules into people's bodies; these CRISPR molecules would then go to certain kinds of cells and repair one particular spot in their DNA. And that treats the disease.\u003c/p>\n\u003cp>We shouldn't look at this as a panacea. ... There have been earlier kinds of treatments known as gene therapy, where you basically try to add an extra gene into someone's cells. And that [seemed] like it was just a slam dunk, but then it turned out to not work very well for years and years. ... So CRISPR could be even more exciting and truly revolutionary. We just have to wait and see what this first generation of human clinical trials show us.\u003c/p>\n\u003cp>\u003cstrong>On his visit to an insectarium where a scientist is breeding genetically modified mosquitoes that are resistant to malaria\u003c/strong>\u003c/p>\n\u003cp>First of all, you have to gown up before you go in there. ... And then you go through an air lock, and then you're in this room where there are mosquitoes living in all their different life cycles.\u003c/p>\n\u003cp>So there's a dark room where the female mosquitoes are laying their eggs, because they like to do it in the dark. And then the scientists pull the eggs out from these rooms and they inject DNA into them and then they put them in water, because that's where mosquito larvae like to develop.\u003c/p>\n\u003cp>And so you go into this other room where there are these tubs of water, and these snake-like things are slithering around in there and then they develop into adults. And the females need to drink blood; so [researchers] found that the containers for movie popcorn work really well. What they do is, they basically clamp a warm container of calves' blood on top of them, and then the mosquitoes are underneath — on the underside of the plastic lid — basically poking through and drinking the blood and fattening themselves up. ...\u003c/p>\n\u003cp>You can tell that they've been genetically altered because they have red eyes, which is kind of spooky. But you look at that and you say, well, that means that these could be the cure for malaria. It really could happen. And hundreds of thousands of people die every year of malaria. We've thrown everything we can at it and this parasite is still knocking us down worldwide. So, maybe this could be it – so, that's actually quite exciting.\u003c/p>\n\u003cp>\u003cstrong>On how genetic testing was used in the Golden State Killer case\u003c/strong>\u003c/p>\n\u003cp>For the \u003ca href=\"https://www.npr.org/sections/thetwo-way/2018/04/27/606624218/in-hunt-for-golden-state-killer-investigators-uploaded-his-dna-to-genealogy-site\" target=\"_blank\" rel=\"noopener\">Golden State Killer case\u003c/a>, what somebody decided to do was take the DNA that they had from these crime scenes, and upload it to one of these open-access sites — not a commercial site — and then see if they could find any close matches. And they found that there were some people that looked like they were distant cousins of this person. And they went and did the genealogical research to figure out \"Well, how would they be related?\" And then said \"OK, who are the possible relatives that this person could be, and where do they live?\" And that actually helped narrow down their search until they made an arrest.\u003c/p>\n\u003cp>\u003cstrong>On whether genetic testing companies will protect user privacy\u003c/strong>\u003c/p>\n\u003cp>You can choose different levels of privacy with a lot of these services. So, for example, some people will say \"I want you to look at my DNA. I want you to tell me about my ancestry.\" ... For 23 and Me they'll give you a few bits of information about your medical conditions, and that's it. But they will try to get you to opt in to sharing your data for their own basic research. At 23 and Me, for example, there's a whole team of researchers who are studying all sorts of ... diseases, sleep patterns and so on. And then they will also go into partnerships with drug development companies who will take their data, looking at, say, 50,000 people with lupus and 50,000 people who don't have lupus, and try to look for the genetic differences. Those could point the way toward possible drugs.\u003c/p>\n\u003cp>[ad floatright]\u003c/p>\n\u003cp>\u003cem>Phyllis Myers and Seth Kelley produced and edited the audio of this interview. Bridget Bentz and Seth Kelley adapted it for the Web.\u003c/em>\u003c/p>\n\u003cdiv class=\"fullattribution\">Copyright 2018 Fresh Air. To see more, visit \u003ca href=\"http://www.npr.org/programs/fresh-air/\">Fresh Air\u003c/a>.\u003cimg src=\"https://www.google-analytics.com/__utm.gif?utmac=UA-5828686-4&utmdt=A+Science+Writer+Explores+The+%27Perversions+And+Potential%27+Of+Genetic+Tests&utme=8(APIKey)9(MDAxOTAwOTE4MDEyMTkxMDAzNjczZDljZA004)\">\u003c/div>\n\n",
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"content": "\u003cdiv class=\"post-body\">\u003cp>\u003cp>\u003c!-- iframe plugin v.4.3 wordpress.org/plugins/iframe/ -->\u003cbr>\n\u003ciframe src=\"https://www.npr.org/player/embed/618870881/618969757\" width=\"100%\" height=\"290\" frameborder=\"0\" scrolling=\"no\" title=\"NPR embedded audio player\" class=\"iframe-class\">\u003c/iframe>\u003c/p>\n\u003cp>As a science columnist for\u003cem> The New York Times, \u003c/em>Carl Zimmer had reported extensively about genetics and the role gene mutations play in various ailments. After a while, he got to wondering about what secrets his own genetic code holds.\u003c/p>\u003cp>\u003c/p>\u003cp>\u003c/p>\n\u003cp>\"I wanted to know if there was anything I needed to worry about,\" Zimmer says. \"We all think back to our relatives who got sick and then wonder, 'Is that in me?'\"\u003c/p>\n\u003cp>So Zimmer worked with a genetics counselor to get his entire genome sequenced — an experience he describes as \"very nerve-wracking.\" He worried that he would discover a mutation that would put him on the path for a particular disease.\u003c/p>\n\u003cp>As it turned out, the counselor told Zimmer he has a \"boring genome.\" Though Zimmer initially hoped for a more \"exciting and exotic\" assessment, the counselor reminded him \"A boring genome is a really good genome.\"\u003c/p>\n\u003cp>\u003c/p>\u003c/div>",
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"content": "\u003cdiv class=\"post-body\">\u003cp>\u003c/p>\n\u003cp>Zimmer writes about the broader implications of genetic research and testing in his new book, \u003cem>She Has Her Mother's Laugh: The Powers, Perversions and Potential of Heredity\u003c/em>.\u003c/p>\u003cp>\u003c/p>\u003cp>\u003c/p>\n\u003chr>\n\u003cp>\u003cstrong>Interview Highlights\u003c/strong>\u003c/p>\n\u003cp>\u003cstrong>On how the new genetic editing technology known as \u003ca href=\"https://www.npr.org/tags/419142387/crispr\" target=\"_blank\" rel=\"noopener\">CRISPR\u003c/a> works\u003c/strong>\u003c/p>\n\u003cp>What happens with CRISPR is that scientists will design a molecule — think of it as a probe — and it will search around in the DNA in a cell until if finds a very specific short sequence. And it will grab onto it, and it brings on with it basically molecular scissors, which will then cut the DNA at that spot — kind of like cutting tape. And you can cut out a segment of DNA. And if you just do that, DNA will heal itself. Basically the two loose ends will stitch themselves together, and now that piece is just missing. Or you can add in a little piece of different DNA, and you can actually get the cell to put in that new piece of DNA where you just cut out the old one.\u003c/p>\n\u003cp>\u003cstrong>On whether CRISPR technology could be used to treat diseases in humans\u003c/strong>\u003c/p>\n\u003cp>We're just on the verge of human trials. They will be starting, hopefully very soon, for diseases like sickle-cell anemia. There's actually a lot of research on muscular dystrophy as well. There are a few key diseases where scientists think these would be the best places to start. To basically inject CRISPR molecules into people's bodies; these CRISPR molecules would then go to certain kinds of cells and repair one particular spot in their DNA. And that treats the disease.\u003c/p>\n\u003cp>We shouldn't look at this as a panacea. ... There have been earlier kinds of treatments known as gene therapy, where you basically try to add an extra gene into someone's cells. And that [seemed] like it was just a slam dunk, but then it turned out to not work very well for years and years. ... So CRISPR could be even more exciting and truly revolutionary. We just have to wait and see what this first generation of human clinical trials show us.\u003c/p>\n\u003cp>\u003cstrong>On his visit to an insectarium where a scientist is breeding genetically modified mosquitoes that are resistant to malaria\u003c/strong>\u003c/p>\n\u003cp>First of all, you have to gown up before you go in there. ... And then you go through an air lock, and then you're in this room where there are mosquitoes living in all their different life cycles.\u003c/p>\n\u003cp>So there's a dark room where the female mosquitoes are laying their eggs, because they like to do it in the dark. And then the scientists pull the eggs out from these rooms and they inject DNA into them and then they put them in water, because that's where mosquito larvae like to develop.\u003c/p>\n\u003cp>And so you go into this other room where there are these tubs of water, and these snake-like things are slithering around in there and then they develop into adults. And the females need to drink blood; so [researchers] found that the containers for movie popcorn work really well. What they do is, they basically clamp a warm container of calves' blood on top of them, and then the mosquitoes are underneath — on the underside of the plastic lid — basically poking through and drinking the blood and fattening themselves up. ...\u003c/p>\n\u003cp>You can tell that they've been genetically altered because they have red eyes, which is kind of spooky. But you look at that and you say, well, that means that these could be the cure for malaria. It really could happen. And hundreds of thousands of people die every year of malaria. We've thrown everything we can at it and this parasite is still knocking us down worldwide. So, maybe this could be it – so, that's actually quite exciting.\u003c/p>\n\u003cp>\u003cstrong>On how genetic testing was used in the Golden State Killer case\u003c/strong>\u003c/p>\n\u003cp>For the \u003ca href=\"https://www.npr.org/sections/thetwo-way/2018/04/27/606624218/in-hunt-for-golden-state-killer-investigators-uploaded-his-dna-to-genealogy-site\" target=\"_blank\" rel=\"noopener\">Golden State Killer case\u003c/a>, what somebody decided to do was take the DNA that they had from these crime scenes, and upload it to one of these open-access sites — not a commercial site — and then see if they could find any close matches. And they found that there were some people that looked like they were distant cousins of this person. And they went and did the genealogical research to figure out \"Well, how would they be related?\" And then said \"OK, who are the possible relatives that this person could be, and where do they live?\" And that actually helped narrow down their search until they made an arrest.\u003c/p>\n\u003cp>\u003cstrong>On whether genetic testing companies will protect user privacy\u003c/strong>\u003c/p>\n\u003cp>You can choose different levels of privacy with a lot of these services. So, for example, some people will say \"I want you to look at my DNA. I want you to tell me about my ancestry.\" ... For 23 and Me they'll give you a few bits of information about your medical conditions, and that's it. But they will try to get you to opt in to sharing your data for their own basic research. At 23 and Me, for example, there's a whole team of researchers who are studying all sorts of ... diseases, sleep patterns and so on. And then they will also go into partnerships with drug development companies who will take their data, looking at, say, 50,000 people with lupus and 50,000 people who don't have lupus, and try to look for the genetic differences. Those could point the way toward possible drugs.\u003c/p>\n\u003cp>\u003c/p>\u003c/div>",
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"disqusTitle": "Major CRISPR Hurdle: Edited Cells Might Cause Cancer, Find Studies",
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"content": "\u003cp>Editing cells’ genomes with CRISPR-Cas9 might increase the risk that the altered cells, intended to treat disease, will trigger cancer, two studies published on Monday warn — a potential game-changer for the companies developing CRISPR-based therapies.[contextly_sidebar id=\"Pbm72hAOjQOHNUgNeQaKv0l2d5rX0APO\"]\u003c/p>\n\u003cp>In the studies, published in Nature Medicine, scientists found that cells whose genomes are successfully edited by CRISPR-Cas9 have the potential to seed tumors inside a patient. That could make some CRISPR’d cells ticking time bombs, according to researchers from Sweden’s Karolinska Institute and, separately, Novartis.\u003c/p>\n\u003cp class=\"danger-zone\">\u003ca href=\"https://www.statnews.com/feature/crispr/tracker/\">CRISPR\u003c/a> has already dodged two potentially fatal bullets — a 2017 \u003ca href=\"https://www.nature.com/articles/nmeth.4293.epdf\" target=\"_blank\" rel=\"noopener\">claim\u003c/a> that it causes sky-high numbers of off-target effects was \u003ca href=\"https://www.nature.com/articles/nmeth.4664\" target=\"_blank\" rel=\"noopener\">retracted\u003c/a> in March, and a \u003ca href=\"https://www.biorxiv.org/content/early/2018/01/05/243345\" target=\"_blank\" rel=\"noopener\">report \u003c/a>of human immunity to Cas9 was largely shrugged off as \u003ca href=\"https://www.statnews.com/2018/01/08/immunity-crispr-cas9/\">solvable\u003c/a>. But experts are taking the cancer-risk finding seriously.\u003c/p>\n\u003cp class=\"danger-zone\">The CEO of CRISPR Therapeutics, Sam Kulkarni, told STAT the results are “plausible.” Although they likely apply to one of the main ways that CRISPR edits genomes (replacing disease-causing DNA with healthy versions) more than another (just excising DNA), he said, “it’s something we need to pay attention to, especially as CRISPR expands to more diseases. We need to do the work and make sure edited cells returned to patients don’t become cancerous.”\u003c/p>\n\u003cp class=\"\">Another leading CRISPR scientist, who asked not to be named because of involvement with genome-editing companies, called the new data “pretty striking,” and raised concerns that a potential fatal flaw in some uses of CRISPR had “been missed.”\u003c/p>\n\u003cp>[ad fullwidth]\u003c/p>\n\u003cp>On the other hand, the Novartis paper has been \u003ca href=\"https://www.biorxiv.org/content/early/2017/07/26/168443\" target=\"_blank\" rel=\"noopener\">available\u003c/a> in preliminary form since last summer, and CRISPR experts “haven’t freaked out,” said Erik Sontheimer of the University of Massachusetts Medical School, whose CRISPR research \u003ca href=\"https://www.statnews.com/2018/03/05/crispr-off-target-editing/\">centers\u003c/a> on novel enzymes and off-target effects. “This is something that bears paying attention to, but I don’t think it’s a deal-breaker” for CRISPR therapies.\u003c/p>\n\u003cp>The Karolinska and Novartis groups tested CRISPR on different kinds of human cells — retinal cells and pluripotent stem cells, respectively. But they found essentially the same phenomenon. Standard CRISPR-Cas9 works by cutting both strands of the DNA double helix. That injury causes a cell to activate a biochemical first-aid kit orchestrated by a gene called \u003ca href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4235614/\" target=\"_blank\" rel=\"noopener\">p53,\u003c/a> which either mends the DNA break or makes the cell self-destruct.[contextly_sidebar id=\"X1qu0ifjesXey9YHHpOinoS4KNdNuyur\"]\u003c/p>\n\u003cp>Whichever action p53 takes, the consequence is the same: CRISPR doesn’t work, either because the genome edit is stitched up or the cell is dead. (The Novartis team calculated that p53 reduces CRISPR efficiency in pluripotent stem cells seventeenfold.) That might explain something found over and over: CRISPR is woefully inefficient, with only a small minority of cells into which CRISPR is introduced, usually by a virus, actually having their genomes edited as intended.\u003c/p>\n\u003cp>“We found that cutting the genome with CRISPR-Cas9 induced the activation of … p53,” said Emma Haapaniemi, the lead author of the \u003ca href=\"https://www.nature.com/articles/s41591-018-0049-z\" target=\"_blank\" rel=\"noopener\">Karolinska study\u003c/a>. That “makes editing much more difficult.”\u003c/p>\n\u003cp>The flip side of p53 repairing CRISPR edits, or killing cells that accept the edits, is that cells that survive with the edits do so precisely because they have a dysfunctional p53 and therefore lack this fix-it-or-kill-it mechanism.\u003c/p>\n\u003cp>The reason why that could be a problem is that p53 dysfunction can cause cancer. And not just occasionally. P53 mutations are \u003ca href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2827900/figure/A001008F1/\" target=\"_blank\" rel=\"noopener\">responsible for\u003c/a> nearly half of ovarian cancers; 43 percent of colorectal cancers; 38 percent of lung cancers; nearly one-third of pancreatic, stomach, and liver cancers; and one-quarter of breast cancers, among others.\u003c/p>\n\u003cp>The Novartis team was trying to see how it could increase the efficiency of CRISPR editing of pluripotent stem cells. Because this kind of stem cell can morph into virtually any kind of cell, it might be able to treat a variety of diseases. Neuroscientist Ajamete Kaykas of the company’s Institutes for BioMedical Research in Cambridge, Mass., got CRISPR’s efficiency at inserting or deleting chunks of DNA up to 80 percent. Unfortunately, when CRISPR worked, it was because p53 didn’t, which raises cancer concerns.\u003c/p>\n\u003cp>As a result, the Novartis \u003ca href=\"https://www.nature.com/articles/s41591-018-0050-6\" target=\"_blank\" rel=\"noopener\">paper\u003c/a> concludes that “it will be critical to ensure that [genome-edited cells] have a functional p53 before and after [genome] engineering.” The Karolinska team warns that p53 and related genes “should be monitored when developing cell-based therapies utilizing CRISPR-Cas9.”[contextly_sidebar id=\"f80ZxqMXgIrsBguckwJZNJRkL6wI6fMd\"]\u003c/p>\n\u003cp>The p53 finding doesn’t mean CRISPR is toast. For one thing, “the two papers present preliminary results,” biochemist Bernhard Schmierer of the Karolinska, co-leader of its study, told STAT. “It is unclear if the findings translate into cells actually used in current clinical studies.”\u003c/p>\n\u003cp>For another, the p53 problem might be worse with Cas9 than with other DNA-cutting enzymes used in CRISPR. And, crucially, it probably affects only one avenue of genome-editing.\u003c/p>\n\u003cp>CRISPR edits genomes in either of two ways. It slices out a chunk of disease-causing DNA, in a process called non-homologous end joining (NHEJ), or gene disruption. That’s how CRISPR Therapeutics is going after sickle cell disease. Alternatively, CRISPR both cuts out a disease-causing stretch of DNA and replaces it with healthy nucleotides, in homology-directed repair (HDR), or gene correction. Several university labs are investigating HDR to treat Duchenne \u003ca href=\"https://www.nature.com/articles/s41551-017-0137-2\" target=\"_blank\" rel=\"noopener\">muscular dystrophy,\u003c/a> among many other diseases.\u003c/p>\n\u003cp>In the normal, mature cells she and her team studied, Haapaniemi said, gene disruption “can happen even when p53 is activated.”\u003c/p>\n\u003cp>That’s good news for CRISPR Therapeutics’ sickle-cell and thalassemia \u003ca href=\"http://www.crisprtx.com/our-programs/our-pipeline.php\" target=\"_blank\" rel=\"noopener\">programs \u003c/a>as well as for Editas Medicine’s lead product, targeting a form of blindness, and others in its \u003ca href=\"http://www.editasmedicine.com/pipeline\" target=\"_blank\" rel=\"noopener\">pipeline\u003c/a>, all of which use NHEJ gene disruption. It also should not affect the gene-disruption approach that Intellia Therapeutics and Regeneron are \u003ca href=\"https://www.intelliatx.com/pipeline/\" target=\"_blank\" rel=\"noopener\">taking\u003c/a> to \u003ca href=\"https://ghr.nlm.nih.gov/condition/transthyretin-amyloidosis\" target=\"_blank\" rel=\"noopener\">transthyretin amyloidosis\u003c/a>.\u003c/p>\n\u003cp>CRISPR-based editing of T cells to treat cancer, as scientists at the University of Pennsylvania are studying in a \u003ca href=\"https://www.statnews.com/2016/06/21/crispr-human-trials/\">clinical trial,\u003c/a> should also not have a p53 problem. Nor should any therapy developed with CRISPR base editing, which does not make the double-stranded breaks that trigger p53. Developed by Harvard’s David Liu, base editing replaces a wrong DNA “letter” with the right one, without cutting, and is the basis for startup \u003ca href=\"https://www.statnews.com/2018/05/14/crispr-editas-beam-base-editing/\" target=\"_blank\" rel=\"noopener\">Beam Therapeutics\u003c/a>.\u003c/p>\n\u003cp>The p53 problem, however, might affect other products that companies hope to develop via gene correction, including glycogen storage disease, cystic fibrosis, and severe combined immunodeficiency.\u003c/p>\n\u003cp>It’s also a potential problem for stem cells. There, the Novartis team showed, p53 inactivation seems to be necessary for both NHEJ disruption and HDR correction. (Novartis’ Kaykas said he could not speak to a reporter without clearance from the company’s communications office.) That could be an issue for therapies using CRISPR’d stem cells: The same dysfunctional p53 that allows CRISPR to work its magic also makes cells likely to become cancerous.\u003c/p>\n\u003cp>Which raises an obvious question — if successfully CRISPR’d cells can seed cancers, why hasn’t this been seen before, and why haven’t the many CRISPR’d mice developed tumors?\u003c/p>\n\u003cp>Karolinska’s Haapaniemi said the effect shows up in large-scale experiments like hers and Novartis’ “but can be missed in small-scale studies where people only focus on editing one gene in one cell type.” In speaking to other scientists, she said, “it seems that other teams have noticed the effect of p53 on editing,” but have not highlighted it.\u003c/p>\n\u003cp>Jacob Corn of the University of California, Berkeley, said that although his lab has seen evidence of p53 activation in a few cases, they have “looked hard for growth effects after editing in [human stem cells] and found nothing.”\u003c/p>\n\u003cp>As for why no one has reported CRISPR’d mice getting cancer, Haapaniemi said, “This is a good question.” One reason might be that “laboratory mice are killed early,” perhaps leaving too little time for them to develop cancer.\u003c/p>\n\u003cp>But Corn said he and others “have all been looking for the possibility of cancer. So far, no one has seen evidence of [it] based on p53 status or induced by editing.”\u003c/p>\n\u003cp>Nevertheless, he called the two papers “important, since they remind everyone that genome editing isn’t magic.”\u003c/p>\n\u003cp>[ad floatright]\u003c/p>\n\u003cp>\u003cem>This\u003ca href=\"https://www.statnews.com/2018/06/11/crispr-hurdle-edited-cells-might-cause-cancer/\" target=\"_blank\" rel=\"noopener\"> story\u003c/a> was originally published by STAT, an online publication of Boston Globe Media that covers health, medicine, and scientific discovery.\u003c/em>\u003c/p>\n\n",
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"description": "Editing cells’ genomes with CRISPR-Cas9 might increase the risk that the altered cells, intended to treat disease, will trigger cancer, two studies published on Monday warn — a potential game-changer for the companies developing CRISPR-based therapies. In the studies, published in Nature Medicine, scientists found that cells whose genomes are successfully edited by CRISPR-Cas9 have the",
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"content": "\u003cdiv class=\"post-body\">\u003cp>\u003cp>Editing cells’ genomes with CRISPR-Cas9 might increase the risk that the altered cells, intended to treat disease, will trigger cancer, two studies published on Monday warn — a potential game-changer for the companies developing CRISPR-based therapies.\u003c/p>\u003cp>\u003c/p>\u003cp>\u003c/p>\n\u003cp>In the studies, published in Nature Medicine, scientists found that cells whose genomes are successfully edited by CRISPR-Cas9 have the potential to seed tumors inside a patient. That could make some CRISPR’d cells ticking time bombs, according to researchers from Sweden’s Karolinska Institute and, separately, Novartis.\u003c/p>\n\u003cp class=\"danger-zone\">\u003ca href=\"https://www.statnews.com/feature/crispr/tracker/\">CRISPR\u003c/a> has already dodged two potentially fatal bullets — a 2017 \u003ca href=\"https://www.nature.com/articles/nmeth.4293.epdf\" target=\"_blank\" rel=\"noopener\">claim\u003c/a> that it causes sky-high numbers of off-target effects was \u003ca href=\"https://www.nature.com/articles/nmeth.4664\" target=\"_blank\" rel=\"noopener\">retracted\u003c/a> in March, and a \u003ca href=\"https://www.biorxiv.org/content/early/2018/01/05/243345\" target=\"_blank\" rel=\"noopener\">report \u003c/a>of human immunity to Cas9 was largely shrugged off as \u003ca href=\"https://www.statnews.com/2018/01/08/immunity-crispr-cas9/\">solvable\u003c/a>. But experts are taking the cancer-risk finding seriously.\u003c/p>\n\u003cp class=\"danger-zone\">The CEO of CRISPR Therapeutics, Sam Kulkarni, told STAT the results are “plausible.” Although they likely apply to one of the main ways that CRISPR edits genomes (replacing disease-causing DNA with healthy versions) more than another (just excising DNA), he said, “it’s something we need to pay attention to, especially as CRISPR expands to more diseases. We need to do the work and make sure edited cells returned to patients don’t become cancerous.”\u003c/p>\n\u003cp class=\"\">Another leading CRISPR scientist, who asked not to be named because of involvement with genome-editing companies, called the new data “pretty striking,” and raised concerns that a potential fatal flaw in some uses of CRISPR had “been missed.”\u003c/p>\n\u003cp>\u003c/p>\u003c/div>",
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"content": "\u003cdiv class=\"post-body\">\u003cp>\u003c/p>\n\u003cp>On the other hand, the Novartis paper has been \u003ca href=\"https://www.biorxiv.org/content/early/2017/07/26/168443\" target=\"_blank\" rel=\"noopener\">available\u003c/a> in preliminary form since last summer, and CRISPR experts “haven’t freaked out,” said Erik Sontheimer of the University of Massachusetts Medical School, whose CRISPR research \u003ca href=\"https://www.statnews.com/2018/03/05/crispr-off-target-editing/\">centers\u003c/a> on novel enzymes and off-target effects. “This is something that bears paying attention to, but I don’t think it’s a deal-breaker” for CRISPR therapies.\u003c/p>\n\u003cp>The Karolinska and Novartis groups tested CRISPR on different kinds of human cells — retinal cells and pluripotent stem cells, respectively. But they found essentially the same phenomenon. Standard CRISPR-Cas9 works by cutting both strands of the DNA double helix. That injury causes a cell to activate a biochemical first-aid kit orchestrated by a gene called \u003ca href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4235614/\" target=\"_blank\" rel=\"noopener\">p53,\u003c/a> which either mends the DNA break or makes the cell self-destruct.\u003c/p>\u003cp>\u003c/p>\u003cp>\u003c/p>\n\u003cp>Whichever action p53 takes, the consequence is the same: CRISPR doesn’t work, either because the genome edit is stitched up or the cell is dead. (The Novartis team calculated that p53 reduces CRISPR efficiency in pluripotent stem cells seventeenfold.) That might explain something found over and over: CRISPR is woefully inefficient, with only a small minority of cells into which CRISPR is introduced, usually by a virus, actually having their genomes edited as intended.\u003c/p>\n\u003cp>“We found that cutting the genome with CRISPR-Cas9 induced the activation of … p53,” said Emma Haapaniemi, the lead author of the \u003ca href=\"https://www.nature.com/articles/s41591-018-0049-z\" target=\"_blank\" rel=\"noopener\">Karolinska study\u003c/a>. That “makes editing much more difficult.”\u003c/p>\n\u003cp>The flip side of p53 repairing CRISPR edits, or killing cells that accept the edits, is that cells that survive with the edits do so precisely because they have a dysfunctional p53 and therefore lack this fix-it-or-kill-it mechanism.\u003c/p>\n\u003cp>The reason why that could be a problem is that p53 dysfunction can cause cancer. And not just occasionally. P53 mutations are \u003ca href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2827900/figure/A001008F1/\" target=\"_blank\" rel=\"noopener\">responsible for\u003c/a> nearly half of ovarian cancers; 43 percent of colorectal cancers; 38 percent of lung cancers; nearly one-third of pancreatic, stomach, and liver cancers; and one-quarter of breast cancers, among others.\u003c/p>\n\u003cp>The Novartis team was trying to see how it could increase the efficiency of CRISPR editing of pluripotent stem cells. Because this kind of stem cell can morph into virtually any kind of cell, it might be able to treat a variety of diseases. Neuroscientist Ajamete Kaykas of the company’s Institutes for BioMedical Research in Cambridge, Mass., got CRISPR’s efficiency at inserting or deleting chunks of DNA up to 80 percent. Unfortunately, when CRISPR worked, it was because p53 didn’t, which raises cancer concerns.\u003c/p>\n\u003cp>As a result, the Novartis \u003ca href=\"https://www.nature.com/articles/s41591-018-0050-6\" target=\"_blank\" rel=\"noopener\">paper\u003c/a> concludes that “it will be critical to ensure that [genome-edited cells] have a functional p53 before and after [genome] engineering.” The Karolinska team warns that p53 and related genes “should be monitored when developing cell-based therapies utilizing CRISPR-Cas9.”\u003c/p>\u003cp>\u003c/p>\u003cp>\u003c/p>\n\u003cp>The p53 finding doesn’t mean CRISPR is toast. For one thing, “the two papers present preliminary results,” biochemist Bernhard Schmierer of the Karolinska, co-leader of its study, told STAT. “It is unclear if the findings translate into cells actually used in current clinical studies.”\u003c/p>\n\u003cp>For another, the p53 problem might be worse with Cas9 than with other DNA-cutting enzymes used in CRISPR. And, crucially, it probably affects only one avenue of genome-editing.\u003c/p>\n\u003cp>CRISPR edits genomes in either of two ways. It slices out a chunk of disease-causing DNA, in a process called non-homologous end joining (NHEJ), or gene disruption. That’s how CRISPR Therapeutics is going after sickle cell disease. Alternatively, CRISPR both cuts out a disease-causing stretch of DNA and replaces it with healthy nucleotides, in homology-directed repair (HDR), or gene correction. Several university labs are investigating HDR to treat Duchenne \u003ca href=\"https://www.nature.com/articles/s41551-017-0137-2\" target=\"_blank\" rel=\"noopener\">muscular dystrophy,\u003c/a> among many other diseases.\u003c/p>\n\u003cp>In the normal, mature cells she and her team studied, Haapaniemi said, gene disruption “can happen even when p53 is activated.”\u003c/p>\n\u003cp>That’s good news for CRISPR Therapeutics’ sickle-cell and thalassemia \u003ca href=\"http://www.crisprtx.com/our-programs/our-pipeline.php\" target=\"_blank\" rel=\"noopener\">programs \u003c/a>as well as for Editas Medicine’s lead product, targeting a form of blindness, and others in its \u003ca href=\"http://www.editasmedicine.com/pipeline\" target=\"_blank\" rel=\"noopener\">pipeline\u003c/a>, all of which use NHEJ gene disruption. It also should not affect the gene-disruption approach that Intellia Therapeutics and Regeneron are \u003ca href=\"https://www.intelliatx.com/pipeline/\" target=\"_blank\" rel=\"noopener\">taking\u003c/a> to \u003ca href=\"https://ghr.nlm.nih.gov/condition/transthyretin-amyloidosis\" target=\"_blank\" rel=\"noopener\">transthyretin amyloidosis\u003c/a>.\u003c/p>\n\u003cp>CRISPR-based editing of T cells to treat cancer, as scientists at the University of Pennsylvania are studying in a \u003ca href=\"https://www.statnews.com/2016/06/21/crispr-human-trials/\">clinical trial,\u003c/a> should also not have a p53 problem. Nor should any therapy developed with CRISPR base editing, which does not make the double-stranded breaks that trigger p53. Developed by Harvard’s David Liu, base editing replaces a wrong DNA “letter” with the right one, without cutting, and is the basis for startup \u003ca href=\"https://www.statnews.com/2018/05/14/crispr-editas-beam-base-editing/\" target=\"_blank\" rel=\"noopener\">Beam Therapeutics\u003c/a>.\u003c/p>\n\u003cp>The p53 problem, however, might affect other products that companies hope to develop via gene correction, including glycogen storage disease, cystic fibrosis, and severe combined immunodeficiency.\u003c/p>\n\u003cp>It’s also a potential problem for stem cells. There, the Novartis team showed, p53 inactivation seems to be necessary for both NHEJ disruption and HDR correction. (Novartis’ Kaykas said he could not speak to a reporter without clearance from the company’s communications office.) That could be an issue for therapies using CRISPR’d stem cells: The same dysfunctional p53 that allows CRISPR to work its magic also makes cells likely to become cancerous.\u003c/p>\n\u003cp>Which raises an obvious question — if successfully CRISPR’d cells can seed cancers, why hasn’t this been seen before, and why haven’t the many CRISPR’d mice developed tumors?\u003c/p>\n\u003cp>Karolinska’s Haapaniemi said the effect shows up in large-scale experiments like hers and Novartis’ “but can be missed in small-scale studies where people only focus on editing one gene in one cell type.” In speaking to other scientists, she said, “it seems that other teams have noticed the effect of p53 on editing,” but have not highlighted it.\u003c/p>\n\u003cp>Jacob Corn of the University of California, Berkeley, said that although his lab has seen evidence of p53 activation in a few cases, they have “looked hard for growth effects after editing in [human stem cells] and found nothing.”\u003c/p>\n\u003cp>As for why no one has reported CRISPR’d mice getting cancer, Haapaniemi said, “This is a good question.” One reason might be that “laboratory mice are killed early,” perhaps leaving too little time for them to develop cancer.\u003c/p>\n\u003cp>But Corn said he and others “have all been looking for the possibility of cancer. So far, no one has seen evidence of [it] based on p53 status or induced by editing.”\u003c/p>\n\u003cp>Nevertheless, he called the two papers “important, since they remind everyone that genome editing isn’t magic.”\u003c/p>\n\u003cp>\u003c/p>\u003c/div>",
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"title": "Parenting of the Future: Converting Ordinary Cells Into Sperm and Eggs",
"headTitle": "Future of You | KQED Future of You | KQED Science",
"content": "\u003cp>So you want to have a baby.\u003c/p>\n\u003cp>Would you like a dark-haired girl with a high risk of someday getting colon cancer, but a good chance of above-average music ability?[contextly_sidebar id=\"hGdwiHda2M4gvFM3sXPeB5lpQehOV9JO\"]\u003c/p>\n\u003cp>Or would you prefer a girl with a good prospect for high SAT scores and a good shot at being athletic, but who also is likely to run an above-average risk of bipolar disorder and lupus as an adult?\u003c/p>\n\u003cp>How about a boy with a good shot at having musical ability and dodging asthma, but who also would be predisposed to cataracts and type 2 diabetes?\u003c/p>\n\u003cp>Confused? You’re just getting started. There are dozens more choices for which of your embryos should be placed in the womb to become your child.\u003c/p>\n\u003cp>[ad fullwidth]\u003c/p>\n\u003cp>That’s the future a biomedical ethics expert envisions for 20 to 40 years from now — soon enough that today’s children may face it when they start their own families.\u003c/p>\n\u003cp>“The majority of babies of people who have good health coverage will be conceived this way,” predicts Henry Greely, a Stanford University law professor who works in bioethics.\u003c/p>\n\u003cp>You’ve probably read about concerns over “designer babies,” whose DNA is shaped by gene editing. Greely is focused on a different technology that has gotten much less attention: In a startling bit of biological alchemy, scientists have shown that in mice, they can turn ordinary cells into sperm and eggs.\u003c/p>\n\u003cp class=\"caption\">[contextly_sidebar id=\"eTManZd4WaqVP8G2asFbvl91UNkETnUW\"]A prominent biomedical ethics expert says that in 20 to 40 years, many prospective parents may choose from dozens of embryos to become their babies and would be provided with genetic information about each embryo to help make the choice. (April 18)\u003c/p>\n\u003cp>It’s too soon to know if it could be done in people. But if it can, it could become a powerful infertility treatment, permitting genetic parenthood for people who can’t make their own sperm or eggs.\u003c/p>\n\u003cp>It also would mean that a woman who wants to get pregnant could produce dozens more eggs per attempt than with the current procedure of harvesting some from her ovaries.\u003c/p>\n\u003cp>And that means a lot of choices.\u003c/p>\n\u003cp>\u003cstrong>An Array of Embryos\u003c/strong>\u003cbr>\nHere’s what Greely envisions: A man and woman walk into a fertility clinic. The man drops off some sperm. The woman leaves some skin cells, which are turned into eggs and fertilized with the man’s sperm.\u003c/p>\n\u003cp>Unlike in vitro fertilization today, which typically yields around eight eggs per try, the new method could result in 100 embryos.\u003c/p>\n\u003cp>The embryos’ complete library of DNA would be decoded and analyzed to reveal genetic predispositions, both for disease and personal traits. The man and woman would get dossiers on the embryos that pass minimum tests for suitability.\u003c/p>\n\u003cp>Out of, say, 80 suitable embryos, the couple would then choose one or two to implant.\u003c/p>\n\u003cp>The possibilities don’t stop there. The technology might also help open the door to same-sex couples having children genetically related to both of them, though the additional twist of making eggs from men or sperm from women would be a huge biological challenge.[contextly_sidebar id=\"SrDdSI0zE6VxuvIcDgGVohz7igj80GaU\"]\u003c/p>\n\u003cp>More worrisome is the so-called Brad Pitt scenario: We all shed a bit of sloughed-off DNA every day, like on the lip of a coffee cup. Such discarded material could be secretly snatched up to turn an unwitting celebrity into a genetic parent.\u003c/p>\n\u003cp>It is a long way in the future, but real life is already creeping toward it. Some scientists are trying to make human eggs and sperm in the lab. They are working with “iPS cells,” which are ordinary body cells that have been morphed into a malleable state.\u003c/p>\n\u003cp>Amander Clark of the University of California, Los Angeles, says her goal is to aid basic research into why some people are infertile. She acknowledges the technique might itself be used to treat some infertility, particularly in young people made sterile by cancer treatments.\u003c/p>\n\u003cp>As for decoding the complete DNA library of embryos, Dr. Louanne Hudgins, who studies prenatal genetic screening and diagnosis at Stanford, says some pregnant patients there say they’ve already had fertility clinics do that. They didn’t reveal why, Hudgins said.\u003c/p>\n\u003cp>Hudgins, who’s president of the American College of Medical Genetics and Genomics, said no national medical association has endorsed decoding all the DNA of an embryo, which is called its genome. So she believes no insurance company would pay for that now.\u003c/p>\n\u003cp>\u003cstrong>‘Easy' Prenatal Diagnosis\u003c/strong>\u003cbr>\nGreely, who lays out his ideas in a book called “The End of Sex and the Future of Human Reproduction,” calls his vision “easy PGD,” or prenatal genetic diagnosis.\u003c/p>\n\u003cp>Ordinary PGD has been done for decades. When a couple is known to be at risk for having a child with a specific genetic disorder, such as cystic fibrosis or sickle cell anemia, the woman undergoes a procedure to remove some eggs. After fertilization, some cells are plucked from the embryos and examined to identify those without carry the disease-causing abnormality.\u003c/p>\n\u003cp>That procedure looks for a specific problem in a few embryos, not entire genomes from dozens of them. If a couple wants to select a “super baby,” says Dr. Richard Scott Jr., a founding partner of Reproductive Medicine Associates of New Jersey, “we tell them we can’t do it.”\u003c/p>\n\u003cp>In fact, Scott and others say, even wide-ranging analysis would not provide a precise forecast of how a child will turn out.\u003c/p>\n\u003cp>[contextly_sidebar id=\"izPvBHygWyTNurqnYm1uuauGvc2JdDjo\"]If DNA is the hardware, there’s also the software: chemical modifications that determine when and where particular genes turn on and off. Much of this “epigenome” would develop after an embryo’s genes are sampled, Scott said.\u003c/p>\n\u003cp>“Your child may not turn out to be the three-sport All-American at Stanford,” because “the epigenome didn’t work out,” Scott said.\u003c/p>\n\u003cp>Greely agrees that predictions about behavioral traits like intelligence and athletic ability will be imprecise, because of epigenetics and because of basic uncertainties about what genes are involved and how they interact. And a person’s upbringing and life experiences have a big effect.\u003c/p>\n\u003cp>\u003cstrong>What Would Couples Do?\u003cbr>\n\u003c/strong>Even if the predictions aren’t perfect, would couples want to take steps to control their child’s genetics? Many experts doubt it.\u003c/p>\n\u003cp>Only a “very small minority” seek a perfect baby, says Stanford’s Hudgins. In her practice, she said she often finds women pass up all screening because they figure the baby’s fate is “in God’s hands.”\u003c/p>\n\u003cp>Dr. James Grifo of the New York University Fertility Center also questions how popular the idea would be.\u003c/p>\n\u003cp>“No patient has ever came to me and said, ’I want a designer baby,’” said Grifo, who’s performed in vitro fertilization since 1988.\u003c/p>\n\u003cp>[contextly_sidebar id=\"hN50KvG8BIKoBQkiV9DDiJW3PjvffZIF\"]Greely doubts that influencing brainpower or athleticism would be a major draw for parents. Instead, he thinks they would care most about avoiding awful diseases that strike in infancy or childhood. They’ll probably be less concerned about illnesses that might show up later in life, such as Alzheimer’s or Parkinson’s. For one thing, he says, parents-to-be may see them as becoming treatable by the time a child becomes vulnerable.\u003c/p>\n\u003cp>He thinks easy PGD is coming, and it would be better if properly handled. He says it should be proven safe, subsidized, monitored for long-term effects, and regulated so that parents can choose whether to use it and decide what embryonic traits to focus on. And he’d outlaw stealing somebody’s DNA and unwittingly making them a parent.\u003c/p>\n\u003cp>\u003cstrong>Others See Pitfalls\u003c/strong>\u003cbr>\nOnce the genetic profile is done, could it come back to haunt a child if, say, a life insurer or nursing home demanded to see it to assess disease risk? How would the large number of rejected embryos be handled ethically and politically?\u003c/p>\n\u003cp>Perhaps future regulation could limit the number of embryos created, as well as what traits a couple could select for, said I. Glenn Cohen, a Harvard law professor.\u003c/p>\n\u003cp>Lori B. Andrews, a professor at the Chicago-Kent College of Law, summed up her views in a review of Greely’s book.\u003c/p>\n\u003cp>“The idea of easy PGD,” she wrote, “should make us uneasy indeed.”\u003c/p>\n\u003cp>Still, even some who doubt the idea’s feasibility say Greely is right to raise the issue.\u003c/p>\n\u003cp>[ad floatright]\u003c/p>\n\u003cp>“It’s certainly something we have to take seriously and think through now,” said Marcy Darnovsky, who writes on the politics of human biotechnology as executive director of the Center for Genetics and Society in Berkeley, California. “This is not just a technical or science question.”\u003cbr>\n__\u003cbr>\nThis Associated Press \u003ca href=\"https://apnews.com/tag/GeneticFrontiers\" target=\"_blank\" rel=\"noopener\">series\u003c/a> was produced in \u003ca href=\"https://www.ap.org/press-releases/2018/ap-hhmi-expand-collaboration-to-bolster-health-science-coverage\" target=\"_blank\" rel=\"noopener\">partnership\u003c/a> with the Howard Hughes Medical Institute’s Department of Science Education. The AP is solely responsible for all content.\u003c/p>\n\n",
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"content": "\u003cdiv class=\"post-body\">\u003cp>\u003cp>So you want to have a baby.\u003c/p>\n\u003cp>Would you like a dark-haired girl with a high risk of someday getting colon cancer, but a good chance of above-average music ability?\u003c/p>\u003cp>\u003c/p>\u003cp>\u003c/p>\n\u003cp>Or would you prefer a girl with a good prospect for high SAT scores and a good shot at being athletic, but who also is likely to run an above-average risk of bipolar disorder and lupus as an adult?\u003c/p>\n\u003cp>How about a boy with a good shot at having musical ability and dodging asthma, but who also would be predisposed to cataracts and type 2 diabetes?\u003c/p>\n\u003cp>Confused? You’re just getting started. There are dozens more choices for which of your embryos should be placed in the womb to become your child.\u003c/p>\n\u003cp>\u003c/p>\u003c/div>",
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"content": "\u003cdiv class=\"post-body\">\u003cp>\u003c/p>\n\u003cp>That’s the future a biomedical ethics expert envisions for 20 to 40 years from now — soon enough that today’s children may face it when they start their own families.\u003c/p>\n\u003cp>“The majority of babies of people who have good health coverage will be conceived this way,” predicts Henry Greely, a Stanford University law professor who works in bioethics.\u003c/p>\n\u003cp>You’ve probably read about concerns over “designer babies,” whose DNA is shaped by gene editing. Greely is focused on a different technology that has gotten much less attention: In a startling bit of biological alchemy, scientists have shown that in mice, they can turn ordinary cells into sperm and eggs.\u003c/p>\n\u003cp class=\"caption\">\u003c/p>\u003cp>\u003c/p>\u003cp>A prominent biomedical ethics expert says that in 20 to 40 years, many prospective parents may choose from dozens of embryos to become their babies and would be provided with genetic information about each embryo to help make the choice. (April 18)\u003c/p>\n\u003cp>It’s too soon to know if it could be done in people. But if it can, it could become a powerful infertility treatment, permitting genetic parenthood for people who can’t make their own sperm or eggs.\u003c/p>\n\u003cp>It also would mean that a woman who wants to get pregnant could produce dozens more eggs per attempt than with the current procedure of harvesting some from her ovaries.\u003c/p>\n\u003cp>And that means a lot of choices.\u003c/p>\n\u003cp>\u003cstrong>An Array of Embryos\u003c/strong>\u003cbr>\nHere’s what Greely envisions: A man and woman walk into a fertility clinic. The man drops off some sperm. The woman leaves some skin cells, which are turned into eggs and fertilized with the man’s sperm.\u003c/p>\n\u003cp>Unlike in vitro fertilization today, which typically yields around eight eggs per try, the new method could result in 100 embryos.\u003c/p>\n\u003cp>The embryos’ complete library of DNA would be decoded and analyzed to reveal genetic predispositions, both for disease and personal traits. The man and woman would get dossiers on the embryos that pass minimum tests for suitability.\u003c/p>\n\u003cp>Out of, say, 80 suitable embryos, the couple would then choose one or two to implant.\u003c/p>\n\u003cp>The possibilities don’t stop there. The technology might also help open the door to same-sex couples having children genetically related to both of them, though the additional twist of making eggs from men or sperm from women would be a huge biological challenge.\u003c/p>\u003cp>\u003c/p>\u003cp>\u003c/p>\n\u003cp>More worrisome is the so-called Brad Pitt scenario: We all shed a bit of sloughed-off DNA every day, like on the lip of a coffee cup. Such discarded material could be secretly snatched up to turn an unwitting celebrity into a genetic parent.\u003c/p>\n\u003cp>It is a long way in the future, but real life is already creeping toward it. Some scientists are trying to make human eggs and sperm in the lab. They are working with “iPS cells,” which are ordinary body cells that have been morphed into a malleable state.\u003c/p>\n\u003cp>Amander Clark of the University of California, Los Angeles, says her goal is to aid basic research into why some people are infertile. She acknowledges the technique might itself be used to treat some infertility, particularly in young people made sterile by cancer treatments.\u003c/p>\n\u003cp>As for decoding the complete DNA library of embryos, Dr. Louanne Hudgins, who studies prenatal genetic screening and diagnosis at Stanford, says some pregnant patients there say they’ve already had fertility clinics do that. They didn’t reveal why, Hudgins said.\u003c/p>\n\u003cp>Hudgins, who’s president of the American College of Medical Genetics and Genomics, said no national medical association has endorsed decoding all the DNA of an embryo, which is called its genome. So she believes no insurance company would pay for that now.\u003c/p>\n\u003cp>\u003cstrong>‘Easy' Prenatal Diagnosis\u003c/strong>\u003cbr>\nGreely, who lays out his ideas in a book called “The End of Sex and the Future of Human Reproduction,” calls his vision “easy PGD,” or prenatal genetic diagnosis.\u003c/p>\n\u003cp>Ordinary PGD has been done for decades. When a couple is known to be at risk for having a child with a specific genetic disorder, such as cystic fibrosis or sickle cell anemia, the woman undergoes a procedure to remove some eggs. After fertilization, some cells are plucked from the embryos and examined to identify those without carry the disease-causing abnormality.\u003c/p>\n\u003cp>That procedure looks for a specific problem in a few embryos, not entire genomes from dozens of them. If a couple wants to select a “super baby,” says Dr. Richard Scott Jr., a founding partner of Reproductive Medicine Associates of New Jersey, “we tell them we can’t do it.”\u003c/p>\n\u003cp>In fact, Scott and others say, even wide-ranging analysis would not provide a precise forecast of how a child will turn out.\u003c/p>\n\u003cp>\u003c/p>\u003cp>\u003c/p>\u003cp>If DNA is the hardware, there’s also the software: chemical modifications that determine when and where particular genes turn on and off. Much of this “epigenome” would develop after an embryo’s genes are sampled, Scott said.\u003c/p>\n\u003cp>“Your child may not turn out to be the three-sport All-American at Stanford,” because “the epigenome didn’t work out,” Scott said.\u003c/p>\n\u003cp>Greely agrees that predictions about behavioral traits like intelligence and athletic ability will be imprecise, because of epigenetics and because of basic uncertainties about what genes are involved and how they interact. And a person’s upbringing and life experiences have a big effect.\u003c/p>\n\u003cp>\u003cstrong>What Would Couples Do?\u003cbr>\n\u003c/strong>Even if the predictions aren’t perfect, would couples want to take steps to control their child’s genetics? Many experts doubt it.\u003c/p>\n\u003cp>Only a “very small minority” seek a perfect baby, says Stanford’s Hudgins. In her practice, she said she often finds women pass up all screening because they figure the baby’s fate is “in God’s hands.”\u003c/p>\n\u003cp>Dr. James Grifo of the New York University Fertility Center also questions how popular the idea would be.\u003c/p>\n\u003cp>“No patient has ever came to me and said, ’I want a designer baby,’” said Grifo, who’s performed in vitro fertilization since 1988.\u003c/p>\n\u003cp>\u003c/p>\u003cp>\u003c/p>\u003cp>Greely doubts that influencing brainpower or athleticism would be a major draw for parents. Instead, he thinks they would care most about avoiding awful diseases that strike in infancy or childhood. They’ll probably be less concerned about illnesses that might show up later in life, such as Alzheimer’s or Parkinson’s. For one thing, he says, parents-to-be may see them as becoming treatable by the time a child becomes vulnerable.\u003c/p>\n\u003cp>He thinks easy PGD is coming, and it would be better if properly handled. He says it should be proven safe, subsidized, monitored for long-term effects, and regulated so that parents can choose whether to use it and decide what embryonic traits to focus on. And he’d outlaw stealing somebody’s DNA and unwittingly making them a parent.\u003c/p>\n\u003cp>\u003cstrong>Others See Pitfalls\u003c/strong>\u003cbr>\nOnce the genetic profile is done, could it come back to haunt a child if, say, a life insurer or nursing home demanded to see it to assess disease risk? How would the large number of rejected embryos be handled ethically and politically?\u003c/p>\n\u003cp>Perhaps future regulation could limit the number of embryos created, as well as what traits a couple could select for, said I. Glenn Cohen, a Harvard law professor.\u003c/p>\n\u003cp>Lori B. Andrews, a professor at the Chicago-Kent College of Law, summed up her views in a review of Greely’s book.\u003c/p>\n\u003cp>“The idea of easy PGD,” she wrote, “should make us uneasy indeed.”\u003c/p>\n\u003cp>Still, even some who doubt the idea’s feasibility say Greely is right to raise the issue.\u003c/p>\n\u003cp>\u003c/p>\u003c/div>",
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"content": "\u003cdiv class=\"post-body\">\u003cp>\u003c/p>\n\u003cp>“It’s certainly something we have to take seriously and think through now,” said Marcy Darnovsky, who writes on the politics of human biotechnology as executive director of the Center for Genetics and Society in Berkeley, California. “This is not just a technical or science question.”\u003cbr>\n__\u003cbr>\nThis Associated Press \u003ca href=\"https://apnews.com/tag/GeneticFrontiers\" target=\"_blank\" rel=\"noopener\">series\u003c/a> was produced in \u003ca href=\"https://www.ap.org/press-releases/2018/ap-hhmi-expand-collaboration-to-bolster-health-science-coverage\" target=\"_blank\" rel=\"noopener\">partnership\u003c/a> with the Howard Hughes Medical Institute’s Department of Science Education. The AP is solely responsible for all content.\u003c/p>\n\n\u003c/div>\u003c/p>",
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"disqusTitle": "Biologists Trace Genetic Roots Of Evolution, One Cell at a Time",
"title": "Biologists Trace Genetic Roots Of Evolution, One Cell at a Time",
"headTitle": "Future of You | KQED Future of You | KQED Science",
"content": "\u003cp>Genetic mutations are the driving force of evolution, and now scientists have managed to study the effect of mutations in exquisite detail by watching what happens as they pop up in single cells.\u003c/p>\n\u003cp>Only about one percent of mutations were bad enough to kill off the cell, according to a \u003ca href=\"http://science.sciencemag.org/cgi/doi/10.1126/science.aan0797\" target=\"_blank\" rel=\"noopener\">report\u003c/a> published Thursday in \u003cem>Science\u003c/em>. Most of the time, these small changes in its DNA appeared to have no effect at all.[contextly_sidebar id=\"kvnKbnjyKwJnWuLsgRUewEIFcd5eTbqG\"]\u003c/p>\n\u003cp>Mutations have been studied for centuries, says \u003ca href=\"https://www.micalis.fr/micalis_eng/Poles-and-teams/Pole-Biosys/AJ-Aymerich-Jules/SyBER-group-Jules/SyBER-members/Lydia-Robert\" target=\"_blank\" rel=\"noopener\">Lydia Robert\u003c/a>, a researcher at INRA, an agricultural research institute in Paris, France, who notes that they can have medical impacts ranging from antibiotic resistance to cancer.\u003c/p>\n\u003cp>But research on mutations basically has focused on large-scale effects in populations.\u003c/p>\n\u003cp>\"You have a test tube with millions of bacteria, for instance, and you try to measure some property which is an average of all the cells in the population,\" says Robert.[contextly_sidebar id=\"B1EJ5qXFqZz59odJ0F4Nzqz7Z0w5fjPW\"]\u003c/p>\n\u003cp>[ad fullwidth]\u003c/p>\n\u003cp>In contrast, she and her colleagues wanted to study mutations in single cells.\u003c/p>\n\u003cp>So they turned to a so-called \"mother machine\" — a microfluidics device equipped with hundreds of tiny tubes, each no wider than a single E. coli bacterium.\u003c/p>\n\u003cp>\u003cstrong>'Mother Machine'\u003c/strong>\u003cbr>\nThey trapped a single bacterial cell in each tube, and spied on them with a microscope. Every time the bacterial cell divided into two, to reproduce itself, its genetic material got copied. If that copying process went awry and made a mistake, producing a mutation, this error got flagged by a fluorescent tag. The research team tracked about 20,000 mutations over hundreds of generations.\u003c/p>\n\u003cp>The researchers first checked to see if some cells might have an increased mutation rate compared to others.\u003c/p>\n\u003cp>\"We were surprised that in fact it was not the case,\" says Robert, explaining that, under their experimental conditions, all the cells seemed to share the same probability of acquiring mutations, and these genetic changes seemed to occur at a steady rate.\u003c/p>\n\u003cp>\"Many, many of them had no effect at all. This was a bit of a surprise to me,\" Robert says. \"I would have expected a lot of mutations to be slightly bad, and they are not even bad at all.\"\u003c/p>\n\u003cp>Just one percent of the time, a mutation killed the cell outright. And a mutation was very harmful to a cell (but not lethal) about 0.2 percent of the time.\u003c/p>\n\u003cp>\"Most of the time it's really neutral. The cell gets a mutation but it does nothing to the cell,\" says Robert.\u003c/p>\n\u003cp>\u003cstrong>Study Conditions\u003c/strong>\u003cbr>\nIn this study, the bacteria in the little tubes were living under good conditions and weren't exposed to any natural selection or competition—so the researchers could not determine how often mutations produced a beneficial effect that enhanced the bacterial cells' growth and survival.\u003c/p>\n\u003cp>Future studies could start to explore that. \"We're going to change, basically, the environment and see what it changes,\" Robert says. \"What happens if the environment is harsher? Is it going to change the way mutations occur, or are they going to kill more of the cells or less of the cells?\"\u003c/p>\n\u003cp>Already, what the researchers have observed so far confirms a lot of the core thinking that goes into evolutionary biology, says \u003ca href=\"http://myxo.css.msu.edu/\">Richard Lenski\u003c/a>, a biologist at Michigan State University who has spent the last three decades following the evolution of bacteria populations living in flasks in his lab.\u003c/p>\n\u003cp>\"What's exciting about this paper is the technical elegance of it, the rigorous quantification,\" says Lenski, \"This is another nice demonstration that random mutation really has this kind of clock-like dynamic, and that, absent natural selection, populations will, in fact, not only not be able to hold their own, but will tend to decay over time,\" because most mutations are either neutral or deleterious.[contextly_sidebar id=\"KsUxGvhivFMcATApHvyB6fQZaguGW0J5\"]\u003c/p>\n\u003cp>Looking at mutations without any natural selection is very artificial, Lenski says, \"but that allows them to really focus on the underlying process of mutation.\"\u003c/p>\n\u003cp>Some people study evolution in the real world, in all its gory detail, he says. But there's also value in studying genetic changes in this kind of controlled setting that can give a cleaner answers.\u003c/p>\n\u003cp>\u003c/p>\n\u003cp>\"Fitting those two together is always a challenge,\" says Lenski, \"but that's the way science works.\"\u003c/p>\n\u003cdiv class=\"fullattribution\">Copyright 2018 NPR. To see more, visit http://www.npr.org/.\u003cimg src=\"https://www.google-analytics.com/__utm.gif?utmac=UA-5828686-4&utmdt=Biologists+Trace+Genetic+Roots+Of+Evolution%2C+One+Cell+At+A+Time&utme=8(APIKey)9(MDAxOTAwOTE4MDEyMTkxMDAzNjczZDljZA004)\">\u003c/div>\n\n",
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"content": "\u003cdiv class=\"post-body\">\u003cp>\u003cp>Genetic mutations are the driving force of evolution, and now scientists have managed to study the effect of mutations in exquisite detail by watching what happens as they pop up in single cells.\u003c/p>\n\u003cp>Only about one percent of mutations were bad enough to kill off the cell, according to a \u003ca href=\"http://science.sciencemag.org/cgi/doi/10.1126/science.aan0797\" target=\"_blank\" rel=\"noopener\">report\u003c/a> published Thursday in \u003cem>Science\u003c/em>. Most of the time, these small changes in its DNA appeared to have no effect at all.\u003c/p>\u003cp>\u003c/p>\u003cp>\u003c/p>\n\u003cp>Mutations have been studied for centuries, says \u003ca href=\"https://www.micalis.fr/micalis_eng/Poles-and-teams/Pole-Biosys/AJ-Aymerich-Jules/SyBER-group-Jules/SyBER-members/Lydia-Robert\" target=\"_blank\" rel=\"noopener\">Lydia Robert\u003c/a>, a researcher at INRA, an agricultural research institute in Paris, France, who notes that they can have medical impacts ranging from antibiotic resistance to cancer.\u003c/p>\n\u003cp>But research on mutations basically has focused on large-scale effects in populations.\u003c/p>\n\u003cp>\"You have a test tube with millions of bacteria, for instance, and you try to measure some property which is an average of all the cells in the population,\" says Robert.\u003c/p>\u003cp>\u003c/p>\u003cp>\u003c/p>\n\u003cp>\u003c/p>\u003c/div>",
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"content": "\u003cdiv class=\"post-body\">\u003cp>\u003c/p>\n\u003cp>In contrast, she and her colleagues wanted to study mutations in single cells.\u003c/p>\n\u003cp>So they turned to a so-called \"mother machine\" — a microfluidics device equipped with hundreds of tiny tubes, each no wider than a single E. coli bacterium.\u003c/p>\n\u003cp>\u003cstrong>'Mother Machine'\u003c/strong>\u003cbr>\nThey trapped a single bacterial cell in each tube, and spied on them with a microscope. Every time the bacterial cell divided into two, to reproduce itself, its genetic material got copied. If that copying process went awry and made a mistake, producing a mutation, this error got flagged by a fluorescent tag. The research team tracked about 20,000 mutations over hundreds of generations.\u003c/p>\n\u003cp>The researchers first checked to see if some cells might have an increased mutation rate compared to others.\u003c/p>\n\u003cp>\"We were surprised that in fact it was not the case,\" says Robert, explaining that, under their experimental conditions, all the cells seemed to share the same probability of acquiring mutations, and these genetic changes seemed to occur at a steady rate.\u003c/p>\n\u003cp>\"Many, many of them had no effect at all. This was a bit of a surprise to me,\" Robert says. \"I would have expected a lot of mutations to be slightly bad, and they are not even bad at all.\"\u003c/p>\n\u003cp>Just one percent of the time, a mutation killed the cell outright. And a mutation was very harmful to a cell (but not lethal) about 0.2 percent of the time.\u003c/p>\n\u003cp>\"Most of the time it's really neutral. The cell gets a mutation but it does nothing to the cell,\" says Robert.\u003c/p>\n\u003cp>\u003cstrong>Study Conditions\u003c/strong>\u003cbr>\nIn this study, the bacteria in the little tubes were living under good conditions and weren't exposed to any natural selection or competition—so the researchers could not determine how often mutations produced a beneficial effect that enhanced the bacterial cells' growth and survival.\u003c/p>\n\u003cp>Future studies could start to explore that. \"We're going to change, basically, the environment and see what it changes,\" Robert says. \"What happens if the environment is harsher? Is it going to change the way mutations occur, or are they going to kill more of the cells or less of the cells?\"\u003c/p>\n\u003cp>Already, what the researchers have observed so far confirms a lot of the core thinking that goes into evolutionary biology, says \u003ca href=\"http://myxo.css.msu.edu/\">Richard Lenski\u003c/a>, a biologist at Michigan State University who has spent the last three decades following the evolution of bacteria populations living in flasks in his lab.\u003c/p>\n\u003cp>\"What's exciting about this paper is the technical elegance of it, the rigorous quantification,\" says Lenski, \"This is another nice demonstration that random mutation really has this kind of clock-like dynamic, and that, absent natural selection, populations will, in fact, not only not be able to hold their own, but will tend to decay over time,\" because most mutations are either neutral or deleterious.\u003c/p>\u003cp>\u003c/p>\u003cp>\u003c/p>\n\u003cp>Looking at mutations without any natural selection is very artificial, Lenski says, \"but that allows them to really focus on the underlying process of mutation.\"\u003c/p>\n\u003cp>Some people study evolution in the real world, in all its gory detail, he says. But there's also value in studying genetic changes in this kind of controlled setting that can give a cleaner answers.\u003c/p>\n\u003cp>\u003c/p>\n\u003cp>\"Fitting those two together is always a challenge,\" says Lenski, \"but that's the way science works.\"\u003c/p>\n\u003cdiv class=\"fullattribution\">Copyright 2018 NPR. To see more, visit http://www.npr.org/.\u003cimg src=\"https://www.google-analytics.com/__utm.gif?utmac=UA-5828686-4&utmdt=Biologists+Trace+Genetic+Roots+Of+Evolution%2C+One+Cell+At+A+Time&utme=8(APIKey)9(MDAxOTAwOTE4MDEyMTkxMDAzNjczZDljZA004)\">\u003c/div>\n\n\u003c/div>\u003c/p>",
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"content": "\u003cp>It might seem that scientists have never met a chunk of DNA they couldn’t edit in mice or isolated cells using\u003c/p>\n\u003cp>CRISPR\u003cstrong> —\u003c/strong> from mutations causing \u003ca href=\"https://www.nature.com/articles/nature25164\" target=\"_blank\" rel=\"noopener\">deafness\u003c/a> to those for \u003ca href=\"http://advances.sciencemag.org/content/4/1/eaap9004\" target=\"_blank\" rel=\"noopener\">Duchenne muscular dystrophy.\u003c/a> In fact, they are learning what every pencil- or Word-wielding editor knows: It’s much easier to improve something that’s in terrible shape than writing that’s near perfect.\u003c/p>\n\u003cp>In genome-editing, the challenge for CRISPR-wielding scientists is to edit only one of the two copies, or alleles, of every gene that people have, repairing the ever-so-slightly broken one and leaving the healthy one alone.\u003c/p>\n\u003cp>Now, in one of the first research papers scheduled for publication in the first journal dedicated to research on CRISPR, scientists in Boston \u003ca href=\"https://www.biorxiv.org/content/early/2018/01/29/197962\" target=\"_blank\" rel=\"noopener\">report\u003c/a> “allele specific” editing of a gene that, when mutated, destroys the eye’s photoreceptors and causes the form of blindness called retinitis pigmentosa.\u003c/p>\n\u003cp>[contextly_sidebar id=\"4VdUEhIyuniYpIiGF8VW99wqTQ1JaiBO\"]The achievement might one day help people with retinitis pigmentosa, which affects about 100,000 people in the U.S. But its greater significance is as a proof-of-concept. The hope is that the same trick might work in the hundreds of diseases, including Huntington’s disease and Marfan syndrome, where inheriting a single mutated gene (from mom \u003cem>or\u003c/em> dad) is enough to cause problems despite the presence of a healthy copy, too.\u003c/p>\n\u003cp>[ad fullwidth]\u003c/p>\n\u003cp>“You want to target only the mutant allele without messing up the healthy one,” said Linzhao Cheng, of Johns Hopkins University School of Medicine, who is \u003ca href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4351458/\" target=\"_blank\" rel=\"noopener\">developing\u003c/a> allele-specific techniques for blood disorders. “But the alleles might differ in only one nucleotide,” one of the molecular “letters” that spell out the genetic code. “That makes allele-specific editing probably the most challenging situation for CRISPR.”\u003c/p>\n\u003cp>The Boston scientists, led by Dr. Qin Liu of the Ocular Genomics Institute at Massachusetts Eye & Ear Infirmary, aimed to remove the misspelled copy of the gene for rhodopsin, which makes up the rods (of rods and cones fame) in the eye. The misspelling consisted of a single wrong nucleotide. That seemingly minor glitch, called P23H, is enough to produce a rogue rhodopsin that is toxic to the healthy rhodopsins produced by the healthy copy.\u003c/p>\n\u003cp>“It just kills the photoreceptors,” said Dr. Stephen Rose, chief research officer at the Foundation Fighting Blindness, which helped fund Liu’s research. “But what if you could repair that one mutation and turn it back to the normal form? That’s the holy grail, to wave a magic wand and change a single wrong nucleotide to the right one.”\u003c/p>\n\u003caside class=\"pullquote alignright\">“You want to target only the mutant allele without messing up the healthy one.”\u003ccite>Linzhao Cheng, Johns Hopkins University.\u003c/cite>\u003c/aside>\n\u003cp>That’s what Liu and her colleagues report doing in the paper to be published in\u003cstrong> \u003c/strong>\u003ca href=\"http://online.liebertpub.com/toc/crispr/0/0\" target=\"_blank\" rel=\"noopener\">The CRISPR Journal\u003c/a>, whose first issue is due this month. They built standard CRISPR molecules: a target-finding molecule called a guide RNA and a snip-the-nucleotide enzyme, in this case a version of Cas9. They injected their CRISPR molecules under the retinas of days-old mice bred to have one good rhodopsin gene and one mutated copy.\u003c/p>\n\u003cp>The editing flopped. The target-finding molecule couldn’t tell the healthy gene from the one-letter-off copy.\u003c/p>\n\u003cp>Back at the drawing board, the scientists, who included Editas Medicine co-founder J. Keith Joung of Massachusetts General Hospital, created target-finding molecules that looked for shorter regions of DNA, hoping to avoid editing the healthy gene. That produced better results: Cas9 edited only the mutant allele. But it did so in very few of the cells. As long as there is a lot of mutant rhodopsin compared to healthy rhodopsin, the mutant proteins will kill the eyes’ rods.\u003c/p>\n\u003cp>The third time was the charm.\u003c/p>\n\u003cp>In addition to using the short target-finding molecules, the scientists also tweaked Cas9 so it made a beeline for tiny DNA mile markers (called PAMs). The mile markers nearest the disease-causing allele are, luckily, different from those near the healthy one. Including the go-to-PAM instruction in their CRISPR produced accurate editing and a lot of it: There were nearly three times as many healthy rhodopsin molecules as mutant ones, compared to similar numbers of healthy and mutant rhodopsin in cells that had not been CRISPR’d. That translated into healthier eyes, with treated mice having five or six rows of photoreceptors compared with three or four in untreated mice. (The mice were not tested for eyesight, however.)\u003c/p>\n\u003cp>[contextly_sidebar id=\"sdpN9QvSR4CNAVKzz3djOr9Ogv4R5axT\"]As always with CRISPR, there is a danger of editing unintended regions of DNA. The scientists checked potential “off target” sites; nine were fine, and one was inadvertently edited in 3 percent of treated cells, though with no apparent ill effects.\u003c/p>\n\u003cp>“It’s nice work,” said biologist Tara Moore of Ulster University, who is \u003ca href=\"https://www.nature.com/articles/s41598-017-16279-4\" target=\"_blank\" rel=\"noopener\">developing\u003c/a> allele-specific CRISPR editing for eye diseases. Exploiting DNA’s tiny mile markers, the PAMs, offers the best shot at allele-specific editing, she said: “Otherwise it’s “a challenge,” and the chance of hitting the disease-causing DNA but sparing the healthy copy “is low.”\u003c/p>\n\u003cp>The mouse study raises hopes that allele-specific editing might work not only for the mutation in retinitis pigmentosa but also “for most, if not all, human dominant alleles,” the scientists wrote.\u003c/p>\n\u003cp>Liu said she was not permitted to speak to reporters about the paper until The CRISPR Journal published it. The study was also funded by the National Institutes of Health and Mass. General.\u003c/p>\n\u003cp>\u003c/p>\n\u003cp>\u003cem>This \u003ca href=\"https://www.statnews.com/2018/02/02/crispr-blindness-retinitis-pigmentosa/\" target=\"_blank\" rel=\"noopener\">story\u003c/a> was originally published by STAT, an online publication of Boston Globe Media that covers health, medicine, and scientific discovery.\u003c/em>\u003c/p>\n\n",
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"content": "\u003cdiv class=\"post-body\">\u003cp>\u003cp>It might seem that scientists have never met a chunk of DNA they couldn’t edit in mice or isolated cells using\u003c/p>\n\u003cp>CRISPR\u003cstrong> —\u003c/strong> from mutations causing \u003ca href=\"https://www.nature.com/articles/nature25164\" target=\"_blank\" rel=\"noopener\">deafness\u003c/a> to those for \u003ca href=\"http://advances.sciencemag.org/content/4/1/eaap9004\" target=\"_blank\" rel=\"noopener\">Duchenne muscular dystrophy.\u003c/a> In fact, they are learning what every pencil- or Word-wielding editor knows: It’s much easier to improve something that’s in terrible shape than writing that’s near perfect.\u003c/p>\n\u003cp>In genome-editing, the challenge for CRISPR-wielding scientists is to edit only one of the two copies, or alleles, of every gene that people have, repairing the ever-so-slightly broken one and leaving the healthy one alone.\u003c/p>\n\u003cp>Now, in one of the first research papers scheduled for publication in the first journal dedicated to research on CRISPR, scientists in Boston \u003ca href=\"https://www.biorxiv.org/content/early/2018/01/29/197962\" target=\"_blank\" rel=\"noopener\">report\u003c/a> “allele specific” editing of a gene that, when mutated, destroys the eye’s photoreceptors and causes the form of blindness called retinitis pigmentosa.\u003c/p>\n\u003cp>\u003c/p>\u003cp>\u003c/p>\u003cp>The achievement might one day help people with retinitis pigmentosa, which affects about 100,000 people in the U.S. But its greater significance is as a proof-of-concept. The hope is that the same trick might work in the hundreds of diseases, including Huntington’s disease and Marfan syndrome, where inheriting a single mutated gene (from mom \u003cem>or\u003c/em> dad) is enough to cause problems despite the presence of a healthy copy, too.\u003c/p>\n\u003cp>\u003c/p>\u003c/div>",
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"content": "\u003cdiv class=\"post-body\">\u003cp>\u003c/p>\n\u003cp>“You want to target only the mutant allele without messing up the healthy one,” said Linzhao Cheng, of Johns Hopkins University School of Medicine, who is \u003ca href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4351458/\" target=\"_blank\" rel=\"noopener\">developing\u003c/a> allele-specific techniques for blood disorders. “But the alleles might differ in only one nucleotide,” one of the molecular “letters” that spell out the genetic code. “That makes allele-specific editing probably the most challenging situation for CRISPR.”\u003c/p>\n\u003cp>The Boston scientists, led by Dr. Qin Liu of the Ocular Genomics Institute at Massachusetts Eye & Ear Infirmary, aimed to remove the misspelled copy of the gene for rhodopsin, which makes up the rods (of rods and cones fame) in the eye. The misspelling consisted of a single wrong nucleotide. That seemingly minor glitch, called P23H, is enough to produce a rogue rhodopsin that is toxic to the healthy rhodopsins produced by the healthy copy.\u003c/p>\n\u003cp>“It just kills the photoreceptors,” said Dr. Stephen Rose, chief research officer at the Foundation Fighting Blindness, which helped fund Liu’s research. “But what if you could repair that one mutation and turn it back to the normal form? That’s the holy grail, to wave a magic wand and change a single wrong nucleotide to the right one.”\u003c/p>\n\u003caside class=\"pullquote alignright\">“You want to target only the mutant allele without messing up the healthy one.”\u003ccite>Linzhao Cheng, Johns Hopkins University.\u003c/cite>\u003c/aside>\n\u003cp>That’s what Liu and her colleagues report doing in the paper to be published in\u003cstrong> \u003c/strong>\u003ca href=\"http://online.liebertpub.com/toc/crispr/0/0\" target=\"_blank\" rel=\"noopener\">The CRISPR Journal\u003c/a>, whose first issue is due this month. They built standard CRISPR molecules: a target-finding molecule called a guide RNA and a snip-the-nucleotide enzyme, in this case a version of Cas9. They injected their CRISPR molecules under the retinas of days-old mice bred to have one good rhodopsin gene and one mutated copy.\u003c/p>\n\u003cp>The editing flopped. The target-finding molecule couldn’t tell the healthy gene from the one-letter-off copy.\u003c/p>\n\u003cp>Back at the drawing board, the scientists, who included Editas Medicine co-founder J. Keith Joung of Massachusetts General Hospital, created target-finding molecules that looked for shorter regions of DNA, hoping to avoid editing the healthy gene. That produced better results: Cas9 edited only the mutant allele. But it did so in very few of the cells. As long as there is a lot of mutant rhodopsin compared to healthy rhodopsin, the mutant proteins will kill the eyes’ rods.\u003c/p>\n\u003cp>The third time was the charm.\u003c/p>\n\u003cp>In addition to using the short target-finding molecules, the scientists also tweaked Cas9 so it made a beeline for tiny DNA mile markers (called PAMs). The mile markers nearest the disease-causing allele are, luckily, different from those near the healthy one. Including the go-to-PAM instruction in their CRISPR produced accurate editing and a lot of it: There were nearly three times as many healthy rhodopsin molecules as mutant ones, compared to similar numbers of healthy and mutant rhodopsin in cells that had not been CRISPR’d. That translated into healthier eyes, with treated mice having five or six rows of photoreceptors compared with three or four in untreated mice. (The mice were not tested for eyesight, however.)\u003c/p>\n\u003cp>\u003c/p>\u003cp>\u003c/p>\u003cp>As always with CRISPR, there is a danger of editing unintended regions of DNA. The scientists checked potential “off target” sites; nine were fine, and one was inadvertently edited in 3 percent of treated cells, though with no apparent ill effects.\u003c/p>\n\u003cp>“It’s nice work,” said biologist Tara Moore of Ulster University, who is \u003ca href=\"https://www.nature.com/articles/s41598-017-16279-4\" target=\"_blank\" rel=\"noopener\">developing\u003c/a> allele-specific CRISPR editing for eye diseases. Exploiting DNA’s tiny mile markers, the PAMs, offers the best shot at allele-specific editing, she said: “Otherwise it’s “a challenge,” and the chance of hitting the disease-causing DNA but sparing the healthy copy “is low.”\u003c/p>\n\u003cp>The mouse study raises hopes that allele-specific editing might work not only for the mutation in retinitis pigmentosa but also “for most, if not all, human dominant alleles,” the scientists wrote.\u003c/p>\n\u003cp>Liu said she was not permitted to speak to reporters about the paper until The CRISPR Journal published it. The study was also funded by the National Institutes of Health and Mass. General.\u003c/p>\n\u003cp>\u003c/p>\n\u003cp>\u003cem>This \u003ca href=\"https://www.statnews.com/2018/02/02/crispr-blindness-retinitis-pigmentosa/\" target=\"_blank\" rel=\"noopener\">story\u003c/a> was originally published by STAT, an online publication of Boston Globe Media that covers health, medicine, and scientific discovery.\u003c/em>\u003c/p>\n\n\u003c/div>\u003c/p>",
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"content": "\u003cp>Why has the human race been unable to prevent wars over long periods of time?\u003c/p>\n\u003cp>It's a complicated question. But one part of the answer may be rooted in our genetic lineage.\u003c/p>\n\u003cp>We share more than 98 percent of our genes with both chimpanzees and bonobos, which possess contrasting genetic instincts for the treatment of outsiders.\u003c/p>\n\u003cp>When alpha male chimpanzees from two different groups collide they usually fight. Chimps are aggressively xenophobic. But bonobos are usually led by alpha females who tend toward cooperation. When groups of bonobos intersect, they usually hang out, groom each other and have sex.\u003c/p>\n\u003caside class=\"pullquote alignright\">'We are basically making variations on primate patterns. We have a primate psychology, and that has implications.'\u003ccite>Frans de Waal, Emory University\u003c/cite>\u003c/aside>\n\u003cp>For more than four decades, primatologist \u003ca href=\"http://www.emory.edu/LIVING_LINKS/people/dewaal.shtml\" target=\"_blank\" rel=\"noopener\">Frans de Waal\u003c/a> has studied the parallels between primate and human behavior. He's written best-selling books like \"\u003ca href=\"http://geni.us/chimpanzeepolitics\" target=\"_blank\" rel=\"noopener\">Chimpanzee Politics\u003c/a>,\" which analyzes how chimpanzees schmooze their way to the top, not unlike human politicians. De Waal's latest books are\u003cem> \u003c/em>\"\u003ca rel=\"noopener\">Our Inner Ape\u003c/a>\" and \"\u003ca href=\"http://www.emory.edu/LIVING_LINKS/empathy/\" target=\"_blank\" rel=\"noopener\">The Age of Empathy\u003c/a>\u003cem>.\"\u003c/em>\u003c/p>\n\u003cp>[ad fullwidth]\u003c/p>\n\u003cp>De Waal spoke recently at \u003ca href=\"http://www.tedmed.com/\" target=\"_blank\" rel=\"noopener\">TEDMED\u003c/a> in Palm Springs. I caught up with him to find out what apes can teach us about leadership. The following has been edited for length and clarity.\u003c/p>\n\u003cp>[audio src=https://www.kqed.org/.stream/anon/radio/science/2017/11/WEBBullyorAlphaMcClurg171113.mp3 program=\"KQED Future of You\" title=\"The Difference Between a Bully and a True Alpha Male\" ]\u003c/p>\n\u003cp>\u003cb>On the history of the term 'alpha male'\u003c/b>\u003c/p>\n\u003cp>The term goes back to the '40s and '50s, in wolf research, to describe the highest-ranking male or the highest-ranking female.\u003c/p>\n\u003cp>There's a very simplistic view of an alpha male in today's literature, and I object to that. Today an alpha male is usually thought to be strong, bullying and intimidating. The term actually became popular after my book \"Chimpanzee Politics. \" Since then they use it in Washington D.C., but I don't agree with the way they use it.\u003c/p>\n\u003cp>\u003cstrong>On the attributes of an alpha male\u003c/strong>\u003c/p>\n\u003cp>I divide them into two categories. One are the bullies. That's the minority and they usually don't last very long. They last a couple of years and then they are ousted, or killed sometimes, or kicked out of the group.\u003c/p>\n\u003cp>The other category has leadership capacities. They're not just bullies -- they break up fights, keep the peace in the group and defend the underdog, as when the pope or the president visits the sites of earthquakes and hurricanes to provide comfort.\u003c/p>\n\u003cp>\u003cem>TEDMED will post De Waal's most recent talk later this year. Here is his previous TED talk.\u003c/em>\u003c/p>\n\u003cp>https://www.ted.com/talks/frans_de_waal_do_animals_have_morals\u003c/p>\n\u003cp>\u003cstrong>On the alpha versus bully distinction and its relationship to the current political situation\u003c/strong>\u003c/p>\n\u003cp>I am struck by the fact that our current president is so often called an alpha male, which started in the elections. People were boasting about what an alpha male he was. I'm still waiting to see the leadership capacities that I so much value in chimpanzees.\u003c/p>\n\u003cp>The rise to the top can be done with intimidation and bluffing, but what happens after that when they are in the top position, they sometimes become very cocky. They think they can do anything. The group usually puts an end to that.\u003c/p>\n\u003cp>\u003cstrong>On empathy and building alliances\u003cbr>\n\u003c/strong>\u003c/p>\n\u003cp>Alliances are always necessary. It's very unusual that a male completely rises to the top on his own. He needs to have a few buddies and female support. Then you need keep the ones who brought you to power, happy.\u003c/p>\n\u003cp>On empathy, I call the chimpanzee males at the top the consolers-in-chief. This consolation behavior that males show is actually very unique because females usually do much more of it than males. Females are more empathetic in all mammals. Males who are very good at that are very much valued by the community.\u003c/p>\n\u003cdiv class=\"mceTemp\">\u003c/div>\n\u003cp>\u003cstrong>On the desire to vote for the alpha male in the presidential election \u003c/strong>\u003c/p>\n\u003cp>It was clear that Donald J. Trump, who had defeated many male candidates just by being tall and lowering his voice and insulting them in their faces, didn't know what to do with Clinton. He much preferred attacking Obama and Clinton's husband, which in fact he did right before the second debate by dragging up some sex accusations. Trump loomed large behind Clinton but also knew that his usual tactics would not work against a woman.\u003c/p>\n\u003cp>This dynamic was very interesting, because also among chimpanzees, the males know how to handle each other, which is all bluff and vigor, but usually cannot fight a female the same way as a male. After all, their competition is all about females, so harming them, or even killing them, is one of the worst things they can do. Attacks on females also may trigger defensive responses. In human politics, this might apply even more.\u003c/p>\n\u003cp>\u003cstrong>Lessons for humans?\u003c/strong>\u003c/p>\n\u003cp>What I've learned is that a lot of things that we think are uniquely human are not. We tend to exaggerate these things -- that morality and culture are uniquely human. Now we know from primate studies that we are not inventing so much.\u003c/p>\n\u003cp>\u003c/p>\n\u003cp>We have a primate psychology, and that has implications. It's not so much practical implications. People sometimes ask me how do we resolve the Palestinian conflict if it's based on chimpanzee behavior. I don't think that's going to happen, but we do learn that the way we look at our own species is erroneous.\u003c/p>\n\n",
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"content": "\u003cdiv class=\"post-body\">\u003cp>\u003cp>Why has the human race been unable to prevent wars over long periods of time?\u003c/p>\n\u003cp>It's a complicated question. But one part of the answer may be rooted in our genetic lineage.\u003c/p>\n\u003cp>We share more than 98 percent of our genes with both chimpanzees and bonobos, which possess contrasting genetic instincts for the treatment of outsiders.\u003c/p>\n\u003cp>When alpha male chimpanzees from two different groups collide they usually fight. Chimps are aggressively xenophobic. But bonobos are usually led by alpha females who tend toward cooperation. When groups of bonobos intersect, they usually hang out, groom each other and have sex.\u003c/p>\n\u003caside class=\"pullquote alignright\">'We are basically making variations on primate patterns. We have a primate psychology, and that has implications.'\u003ccite>Frans de Waal, Emory University\u003c/cite>\u003c/aside>\n\u003cp>For more than four decades, primatologist \u003ca href=\"http://www.emory.edu/LIVING_LINKS/people/dewaal.shtml\" target=\"_blank\" rel=\"noopener\">Frans de Waal\u003c/a> has studied the parallels between primate and human behavior. He's written best-selling books like \"\u003ca href=\"http://geni.us/chimpanzeepolitics\" target=\"_blank\" rel=\"noopener\">Chimpanzee Politics\u003c/a>,\" which analyzes how chimpanzees schmooze their way to the top, not unlike human politicians. De Waal's latest books are\u003cem> \u003c/em>\"\u003ca rel=\"noopener\">Our Inner Ape\u003c/a>\" and \"\u003ca href=\"http://www.emory.edu/LIVING_LINKS/empathy/\" target=\"_blank\" rel=\"noopener\">The Age of Empathy\u003c/a>\u003cem>.\"\u003c/em>\u003c/p>\n\u003cp>\u003c/p>\u003c/div>",
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"content": "\u003cdiv class=\"post-body\">\u003cp>\u003c/p>\n\u003cp>\u003cb>On the history of the term 'alpha male'\u003c/b>\u003c/p>\n\u003cp>The term goes back to the '40s and '50s, in wolf research, to describe the highest-ranking male or the highest-ranking female.\u003c/p>\n\u003cp>There's a very simplistic view of an alpha male in today's literature, and I object to that. Today an alpha male is usually thought to be strong, bullying and intimidating. The term actually became popular after my book \"Chimpanzee Politics. \" Since then they use it in Washington D.C., but I don't agree with the way they use it.\u003c/p>\n\u003cp>\u003cstrong>On the attributes of an alpha male\u003c/strong>\u003c/p>\n\u003cp>I divide them into two categories. One are the bullies. That's the minority and they usually don't last very long. They last a couple of years and then they are ousted, or killed sometimes, or kicked out of the group.\u003c/p>\n\u003cp>The other category has leadership capacities. They're not just bullies -- they break up fights, keep the peace in the group and defend the underdog, as when the pope or the president visits the sites of earthquakes and hurricanes to provide comfort.\u003c/p>\n\u003cp>\u003cem>TEDMED will post De Waal's most recent talk later this year. Here is his previous TED talk.\u003c/em>\u003c/p>\n\u003cp>https://www.ted.com/talks/frans_de_waal_do_animals_have_morals\u003c/p>\n\u003cp>\u003cstrong>On the alpha versus bully distinction and its relationship to the current political situation\u003c/strong>\u003c/p>\n\u003cp>I am struck by the fact that our current president is so often called an alpha male, which started in the elections. People were boasting about what an alpha male he was. I'm still waiting to see the leadership capacities that I so much value in chimpanzees.\u003c/p>\n\u003cp>The rise to the top can be done with intimidation and bluffing, but what happens after that when they are in the top position, they sometimes become very cocky. They think they can do anything. The group usually puts an end to that.\u003c/p>\n\u003cp>\u003cstrong>On empathy and building alliances\u003cbr>\n\u003c/strong>\u003c/p>\n\u003cp>Alliances are always necessary. It's very unusual that a male completely rises to the top on his own. He needs to have a few buddies and female support. Then you need keep the ones who brought you to power, happy.\u003c/p>\n\u003cp>On empathy, I call the chimpanzee males at the top the consolers-in-chief. This consolation behavior that males show is actually very unique because females usually do much more of it than males. Females are more empathetic in all mammals. Males who are very good at that are very much valued by the community.\u003c/p>\n\u003cdiv class=\"mceTemp\">\u003c/div>\n\u003cp>\u003cstrong>On the desire to vote for the alpha male in the presidential election \u003c/strong>\u003c/p>\n\u003cp>It was clear that Donald J. Trump, who had defeated many male candidates just by being tall and lowering his voice and insulting them in their faces, didn't know what to do with Clinton. He much preferred attacking Obama and Clinton's husband, which in fact he did right before the second debate by dragging up some sex accusations. Trump loomed large behind Clinton but also knew that his usual tactics would not work against a woman.\u003c/p>\n\u003cp>This dynamic was very interesting, because also among chimpanzees, the males know how to handle each other, which is all bluff and vigor, but usually cannot fight a female the same way as a male. After all, their competition is all about females, so harming them, or even killing them, is one of the worst things they can do. Attacks on females also may trigger defensive responses. In human politics, this might apply even more.\u003c/p>\n\u003cp>\u003cstrong>Lessons for humans?\u003c/strong>\u003c/p>\n\u003cp>What I've learned is that a lot of things that we think are uniquely human are not. We tend to exaggerate these things -- that morality and culture are uniquely human. Now we know from primate studies that we are not inventing so much.\u003c/p>\n\u003cp>\u003c/p>\n\u003cp>We have a primate psychology, and that has implications. It's not so much practical implications. People sometimes ask me how do we resolve the Palestinian conflict if it's based on chimpanzee behavior. I don't think that's going to happen, but we do learn that the way we look at our own species is erroneous.\u003c/p>\n\n\u003c/div>\u003c/p>",
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"airtime": "FRI 4:30pm-5pm, 6:30pm-7pm, 11pm-11:30pm",
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"officialWebsiteLink": "/californiareportmagazine",
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"order": 10
},
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"google": "https://podcasts.google.com/feed/aHR0cHM6Ly9mZWVkcy5tZWdhcGhvbmUuZm0vS1FJTkM3NjkwNjk1OTAz",
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},
"city-arts": {
"id": "city-arts",
"title": "City Arts & Lectures",
"info": "A one-hour radio program to hear celebrated writers, artists and thinkers address contemporary ideas and values, often discussing the creative process. Please note: tapes or transcripts are not available",
"imageSrc": "https://ww2.kqed.org/radio/wp-content/uploads/sites/50/2018/05/cityartsandlecture-300x300.jpg",
"officialWebsiteLink": "https://www.cityarts.net/",
"airtime": "SUN 1pm-2pm, TUE 10pm, WED 1am",
"meta": {
"site": "news",
"source": "City Arts & Lectures"
},
"link": "https://www.cityarts.net",
"subscribe": {
"tuneIn": "https://tunein.com/radio/City-Arts-and-Lectures-p692/",
"rss": "https://www.cityarts.net/feed/"
}
},
"closealltabs": {
"id": "closealltabs",
"title": "Close All Tabs",
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"info": "Close All Tabs breaks down how digital culture shapes our world through thoughtful insights and irreverent humor.",
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"officialWebsiteLink": "/podcasts/closealltabs",
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"order": 1
},
"link": "/podcasts/closealltabs",
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"title": "Code Switch / Life Kit",
"info": "\u003cem>Code Switch\u003c/em>, which listeners will hear in the first part of the hour, has fearless and much-needed conversations about race. Hosted by journalists of color, the show tackles the subject of race head-on, exploring how it impacts every part of society — from politics and pop culture to history, sports and more.\u003cbr />\u003cbr />\u003cem>Life Kit\u003c/em>, which will be in the second part of the hour, guides you through spaces and feelings no one prepares you for — from finances to mental health, from workplace microaggressions to imposter syndrome, from relationships to parenting. The show features experts with real world experience and shares their knowledge. Because everyone needs a little help being human.\u003cbr />\u003cbr />\u003ca href=\"https://www.npr.org/podcasts/510312/codeswitch\">\u003cem>Code Switch\u003c/em> offical site and podcast\u003c/a>\u003cbr />\u003ca href=\"https://www.npr.org/lifekit\">\u003cem>Life Kit\u003c/em> offical site and podcast\u003c/a>\u003cbr />",
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"meta": {
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"google": "https://podcasts.google.com/feed/aHR0cHM6Ly93d3cubnByLm9yZy9yc3MvcG9kY2FzdC5waHA_aWQ9NTEwMzEy",
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"id": "commonwealth-club",
"title": "Commonwealth Club of California Podcast",
"info": "The Commonwealth Club of California is the nation's oldest and largest public affairs forum. As a non-partisan forum, The Club brings to the public airwaves diverse viewpoints on important topics. The Club's weekly radio broadcast - the oldest in the U.S., dating back to 1924 - is carried across the nation on public radio stations and is now podcasting. Our website archive features audio of our recent programs, as well as selected speeches from our long and distinguished history. This podcast feed is usually updated twice a week and is always un-edited.",
"airtime": "THU 10pm, FRI 1am",
"imageSrc": "https://cdn.kqed.org/wp-content/uploads/2024/04/Commonwealth-Club-Podcast-Tile-360x360-1.jpg",
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"meta": {
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"source": "Commonwealth Club of California"
},
"link": "/radio/program/commonwealth-club",
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"google": "https://podcasts.google.com/feed/aHR0cDovL3d3dy5jb21tb253ZWFsdGhjbHViLm9yZy9hdWRpby9wb2RjYXN0L3dlZWtseS54bWw",
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}
},
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"id": "forum",
"title": "Forum",
"tagline": "The conversation starts here",
"info": "KQED’s live call-in program discussing local, state, national and international issues, as well as in-depth interviews.",
"airtime": "MON-FRI 9am-11am, 10pm-11pm",
"imageSrc": "https://cdn.kqed.org/wp-content/uploads/2024/04/Forum-Podcast-Tile-703x703-1.jpg",
"imageAlt": "KQED Forum with Mina Kim and Alexis Madrigal",
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"source": "kqed",
"order": 9
},
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"google": "https://podcasts.google.com/feed/aHR0cHM6Ly9mZWVkcy5tZWdhcGhvbmUuZm0vS1FJTkM5NTU3MzgxNjMz",
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"id": "freakonomics-radio",
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"info": "Freakonomics Radio is a one-hour award-winning podcast and public-radio project hosted by Stephen Dubner, with co-author Steve Levitt as a regular guest. It is produced in partnership with WNYC.",
"imageSrc": "https://ww2.kqed.org/news/wp-content/uploads/sites/10/2018/05/freakonomicsRadio.png",
"officialWebsiteLink": "http://freakonomics.com/",
"airtime": "SUN 1am-2am, SAT 3pm-4pm",
"meta": {
"site": "radio",
"source": "WNYC"
},
"link": "/radio/program/freakonomics-radio",
"subscribe": {
"npr": "https://rpb3r.app.goo.gl/4s8b",
"apple": "https://itunes.apple.com/us/podcast/freakonomics-radio/id354668519",
"tuneIn": "https://tunein.com/podcasts/WNYC-Podcasts/Freakonomics-Radio-p272293/",
"rss": "https://feeds.feedburner.com/freakonomicsradio"
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},
"fresh-air": {
"id": "fresh-air",
"title": "Fresh Air",
"info": "Hosted by Terry Gross, \u003cem>Fresh Air from WHYY\u003c/em> is the Peabody Award-winning weekday magazine of contemporary arts and issues. One of public radio's most popular programs, Fresh Air features intimate conversations with today's biggest luminaries.",
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"link": "/radio/program/fresh-air",
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"apple": "https://itunes.apple.com/WebObjects/MZStore.woa/wa/viewPodcast?s=143441&mt=2&id=214089682&at=11l79Y&ct=nprdirectory",
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"rss": "https://feeds.npr.org/381444908/podcast.xml"
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"info": "A live production of NPR and WBUR Boston, in collaboration with stations across the country, Here & Now reflects the fluid world of news as it's happening in the middle of the day, with timely, in-depth news, interviews and conversation. Hosted by Robin Young, Jeremy Hobson and Tonya Mosley.",
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"rss": "https://feeds.npr.org/510051/podcast.xml"
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},
"hidden-brain": {
"id": "hidden-brain",
"title": "Hidden Brain",
"info": "Shankar Vedantam uses science and storytelling to reveal the unconscious patterns that drive human behavior, shape our choices and direct our relationships.",
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"officialWebsiteLink": "https://www.npr.org/series/423302056/hidden-brain",
"airtime": "SUN 7pm-8pm",
"meta": {
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"source": "NPR"
},
"link": "/radio/program/hidden-brain",
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},
"how-i-built-this": {
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"title": "How I Built This with Guy Raz",
"info": "Guy Raz dives into the stories behind some of the world's best known companies. How I Built This weaves a narrative journey about innovators, entrepreneurs and idealists—and the movements they built.",
"imageSrc": "https://ww2.kqed.org/news/wp-content/uploads/sites/10/2018/05/howIBuiltThis.png",
"officialWebsiteLink": "https://www.npr.org/podcasts/510313/how-i-built-this",
"airtime": "SUN 7:30pm-8pm",
"meta": {
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"source": "npr"
},
"link": "/radio/program/how-i-built-this",
"subscribe": {
"npr": "https://rpb3r.app.goo.gl/3zxy",
"apple": "https://itunes.apple.com/us/podcast/how-i-built-this-with-guy-raz/id1150510297?mt=2",
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"rss": "https://feeds.npr.org/510313/podcast.xml"
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},
"hyphenacion": {
"id": "hyphenacion",
"title": "Hyphenación",
"tagline": "Where conversation and cultura meet",
"info": "What kind of no sabo word is Hyphenación? For us, it’s about living within a hyphenation. Like being a third-gen Mexican-American from the Texas border now living that Bay Area Chicano life. Like Xorje! Each week we bring together a couple of hyphenated Latinos to talk all about personal life choices: family, careers, relationships, belonging … everything is on the table. ",
"imageSrc": "https://cdn.kqed.org/wp-content/uploads/2025/03/Hyphenacion_FinalAssets_PodcastTile.png",
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"officialWebsiteLink": "/podcasts/hyphenacion",
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"order": 15
},
"link": "/podcasts/hyphenacion",
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"spotify": "https://open.spotify.com/show/2p3Fifq96nw9BPcmFdIq0o?si=39209f7b25774f38",
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},
"jerrybrown": {
"id": "jerrybrown",
"title": "The Political Mind of Jerry Brown",
"tagline": "Lessons from a lifetime in politics",
"info": "The Political Mind of Jerry Brown brings listeners the wisdom of the former Governor, Mayor, and presidential candidate. Scott Shafer interviewed Brown for more than 40 hours, covering the former governor's life and half-century in the political game – and Brown has some lessons he'd like to share. ",
"imageSrc": "https://cdn.kqed.org/wp-content/uploads/2024/04/The-Political-Mind-of-Jerry-Brown-Podcast-Tile-703x703-1.jpg",
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"officialWebsiteLink": "/podcasts/jerrybrown",
"meta": {
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"source": "kqed",
"order": 18
},
"link": "/podcasts/jerrybrown",
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}
},
"latino-usa": {
"id": "latino-usa",
"title": "Latino USA",
"airtime": "MON 1am-2am, SUN 6pm-7pm",
"info": "Latino USA, the radio journal of news and culture, is the only national, English-language radio program produced from a Latino perspective.",
"imageSrc": "https://ww2.kqed.org/radio/wp-content/uploads/sites/50/2018/04/latinoUsa.jpg",
"officialWebsiteLink": "http://latinousa.org/",
"meta": {
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},
"link": "/radio/program/latino-usa",
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"apple": "https://itunes.apple.com/WebObjects/MZStore.woa/wa/viewPodcast?s=143441&mt=2&id=79681317&at=11l79Y&ct=nprdirectory",
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"rss": "https://feeds.npr.org/510016/podcast.xml"
}
},
"marketplace": {
"id": "marketplace",
"title": "Marketplace",
"info": "Our flagship program, helmed by Kai Ryssdal, examines what the day in money delivered, through stories, conversations, newsworthy numbers and more. Updated Monday through Friday at about 3:30 p.m. PT.",
"airtime": "MON-FRI 4pm-4:30pm, MON-WED 6:30pm-7pm",
"imageSrc": "https://cdn.kqed.org/wp-content/uploads/2024/04/Marketplace-Podcast-Tile-360x360-1.jpg",
"officialWebsiteLink": "https://www.marketplace.org/",
"meta": {
"site": "news",
"source": "American Public Media"
},
"link": "/radio/program/marketplace",
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"rss": "https://feeds.publicradio.org/public_feeds/marketplace-pm/rss/rss"
}
},
"masters-of-scale": {
"id": "masters-of-scale",
"title": "Masters of Scale",
"info": "Masters of Scale is an original podcast in which LinkedIn co-founder and Greylock Partner Reid Hoffman sets out to describe and prove theories that explain how great entrepreneurs take their companies from zero to a gazillion in ingenious fashion.",
"airtime": "Every other Wednesday June 12 through October 16 at 8pm (repeats Thursdays at 2am)",
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"officialWebsiteLink": "https://mastersofscale.com/",
"meta": {
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"source": "WaitWhat"
},
"link": "/radio/program/masters-of-scale",
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"apple": "http://mastersofscale.app.link/",
"rss": "https://rss.art19.com/masters-of-scale"
}
},
"mindshift": {
"id": "mindshift",
"title": "MindShift",
"tagline": "A podcast about the future of learning and how we raise our kids",
"info": "The MindShift podcast explores the innovations in education that are shaping how kids learn. Hosts Ki Sung and Katrina Schwartz introduce listeners to educators, researchers, parents and students who are developing effective ways to improve how kids learn. We cover topics like how fed-up administrators are developing surprising tactics to deal with classroom disruptions; how listening to podcasts are helping kids develop reading skills; the consequences of overparenting; and why interdisciplinary learning can engage students on all ends of the traditional achievement spectrum. This podcast is part of the MindShift education site, a division of KQED News. KQED is an NPR/PBS member station based in San Francisco. You can also visit the MindShift website for episodes and supplemental blog posts or tweet us \u003ca href=\"https://twitter.com/MindShiftKQED\">@MindShiftKQED\u003c/a> or visit us at \u003ca href=\"/mindshift\">MindShift.KQED.org\u003c/a>",
"imageSrc": "https://cdn.kqed.org/wp-content/uploads/2024/04/Mindshift-Podcast-Tile-703x703-1.jpg",
"imageAlt": "KQED MindShift: How We Will Learn",
"officialWebsiteLink": "/mindshift/",
"meta": {
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"source": "kqed",
"order": 12
},
"link": "/podcasts/mindshift",
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"google": "https://podcasts.google.com/feed/aHR0cHM6Ly9mZWVkcy5tZWdhcGhvbmUuZm0vS1FJTkM1NzY0NjAwNDI5",
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"stitcher": "https://www.stitcher.com/podcast/kqed/stories-teachers-share",
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}
},
"morning-edition": {
"id": "morning-edition",
"title": "Morning Edition",
"info": "\u003cem>Morning Edition\u003c/em> takes listeners around the country and the world with multi-faceted stories and commentaries every weekday. Hosts Steve Inskeep, David Greene and Rachel Martin bring you the latest breaking news and features to prepare you for the day.",
"airtime": "MON-FRI 3am-9am",
"imageSrc": "https://cdn.kqed.org/wp-content/uploads/2024/04/Morning-Edition-Podcast-Tile-360x360-1.jpg",
"officialWebsiteLink": "https://www.npr.org/programs/morning-edition/",
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"link": "/radio/program/morning-edition"
},
"onourwatch": {
"id": "onourwatch",
"title": "On Our Watch",
"tagline": "Deeply-reported investigative journalism",
"info": "For decades, the process for how police police themselves has been inconsistent – if not opaque. In some states, like California, these proceedings were completely hidden. After a new police transparency law unsealed scores of internal affairs files, our reporters set out to examine these cases and the shadow world of police discipline. On Our Watch brings listeners into the rooms where officers are questioned and witnesses are interrogated to find out who this system is really protecting. Is it the officers, or the public they've sworn to serve?",
"imageSrc": "https://cdn.kqed.org/wp-content/uploads/2024/04/On-Our-Watch-Podcast-Tile-703x703-1.jpg",
"imageAlt": "On Our Watch from NPR and KQED",
"officialWebsiteLink": "/podcasts/onourwatch",
"meta": {
"site": "news",
"source": "kqed",
"order": 11
},
"link": "/podcasts/onourwatch",
"subscribe": {
"apple": "https://podcasts.apple.com/podcast/id1567098962",
"google": "https://podcasts.google.com/feed/aHR0cHM6Ly9mZWVkcy5ucHIub3JnLzUxMDM2MC9wb2RjYXN0LnhtbD9zYz1nb29nbGVwb2RjYXN0cw",
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"rss": "https://feeds.npr.org/510360/podcast.xml"
}
},
"on-the-media": {
"id": "on-the-media",
"title": "On The Media",
"info": "Our weekly podcast explores how the media 'sausage' is made, casts an incisive eye on fluctuations in the marketplace of ideas, and examines threats to the freedom of information and expression in America and abroad. For one hour a week, the show tries to lift the veil from the process of \"making media,\" especially news media, because it's through that lens that we see the world and the world sees us",
"airtime": "SUN 2pm-3pm, MON 12am-1am",
"imageSrc": "https://ww2.kqed.org/radio/wp-content/uploads/sites/50/2018/04/onTheMedia.png",
"officialWebsiteLink": "https://www.wnycstudios.org/shows/otm",
"meta": {
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"source": "wnyc"
},
"link": "/radio/program/on-the-media",
"subscribe": {
"apple": "https://itunes.apple.com/us/podcast/on-the-media/id73330715?mt=2",
"tuneIn": "https://tunein.com/radio/On-the-Media-p69/",
"rss": "http://feeds.wnyc.org/onthemedia"
}
},
"pbs-newshour": {
"id": "pbs-newshour",
"title": "PBS NewsHour",
"info": "Analysis, background reports and updates from the PBS NewsHour putting today's news in context.",
"airtime": "MON-FRI 3pm-4pm",
"imageSrc": "https://cdn.kqed.org/wp-content/uploads/2024/04/PBS-News-Hour-Podcast-Tile-360x360-1.jpg",
"officialWebsiteLink": "https://www.pbs.org/newshour/",
"meta": {
"site": "news",
"source": "pbs"
},
"link": "/radio/program/pbs-newshour",
"subscribe": {
"apple": "https://itunes.apple.com/us/podcast/pbs-newshour-full-show/id394432287?mt=2",
"tuneIn": "https://tunein.com/radio/PBS-NewsHour---Full-Show-p425698/",
"rss": "https://www.pbs.org/newshour/feeds/rss/podcasts/show"
}
},
"perspectives": {
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