Category Archives: Genetics

Want to help with COVID-19 research? If you tested positive, share your genetic makeup with DNA testing sites – The Union Leader

DNA testing companies like Ancestry.com and 23andMe are using their expertise in the fight against COVID-19.

Ancestry.coms study is available only to its members, but 23andMe is asking past and present COVID-19 patients (customers or not) to take part in a study that will contribute to ongoing research on the new coronavirus.

23andMe asked existing customers in April if they would allow their DNA sample to be used for research aimed at determining if there are genetic factors affecting immune response to the virus. Then the company opened the study to include non-23andMe customers who had been hospitalized with COVID-19.

According to Adam Auton, principal scientist at 23andMe and lead researcher on the study, the testing company is hoping research will offer insight into differences in risk among individuals, and help academic and scientific communities in their efforts to treat the illness.

When the pandemic was getting going, we here at 23andMe were beginning to think through what could we do to really try and help and contribute to the science and understanding of this disease, he said.

Given that we have a very large cohort of people who have had their genomes genotyped, we really felt that we might be able to make an impact on the question of why do some people get very, very sick with a COVID infection whereas other people may have not even noticed that they had an infection at all? And given our expertise in genetics, we wanted to ask the question to what extent genetics plays a role in those outcomes.

Auton said the response has been a positive one. He said hundreds of thousands of people already have completed the survey to participate in the genome study, and of those, over 9,000 individuals said they have tested positive for COVID-19.

Auton is hoping more participants join the study to get a wider spectrum of coronavirus experiences. To join, individuals have to be over 18, live in the United States, be willing to provide a saliva sample for analyzing different parts of your genome, be willing to complete online study surveys, must have tested positive for COVID-19 and must have been hospitalized due to COVID-19 symptoms. Those who qualify will receive the 23andMe Health + Ancestry Service at no cost.

Edgewater resident Judy Schneider, 75, did a 23andMe kit almost 10 years ago. Having rebounded from a COVID-19 diagnosis in March, she was excited to hear about the 23andMe study.

I would participate because Im interested from the point of view that I have asthma and my mother had asthma, she said. Im concerned about being reinfected, so I would participate.

Ashantis Jones, 26, of Lakeview, did a 23andMe kit with her family two Christmases ago. But she said she wouldnt add her genome information to the COVID-19 study.

Theres a cultural implication especially around people of color because weve been tested on since America has become America, she said. So there is a historical context, too, so no. Youre not just going to take my stuff and test. It just starts to get a little bit too Big Brother.

Auton says 23andMe wants to be as transparent as possible with the study, so the studys protocols are overseen by a third-party ethical review board.

I think its super important to emphasize that all of the research that we do is entirely opt-in, Auton said. They can withdraw their consent at any point, and we will stop using their data. We really are very conscious of this. Frankly, we know we couldnt do this research without our participants, so were just extremely grateful to those that have chosen to participate.

Preliminary data shows a variant in the ABO gene (which is associated with blood type) linked to a lower risk, when comparing research participants who reported that they tested positive for COVID-19 with those who tested negative. Auton said data collection will continue through the summer.

We know that genetics is important when determining outcomes across essentially all human diseases, so your genome may have some information in it that confers risks for certain diseases or protection for other diseases, Auton said.

Given that COVID-19 is so new in our lives, I think we just dont know at this stage whether genetics has a really big role to play in determining these outcomes or whether it has a small role. And if we can establish that it has a role, it may be informative about the developments of potential therapies for people who do have these kinds of severe outcomes.

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Want to help with COVID-19 research? If you tested positive, share your genetic makeup with DNA testing sites - The Union Leader

Cancer Genetics CEO "excited about the vision and future" by being highly focused on drug discovery – Proactive Investors USA & Canada

Cancer Genetics, Inc () CEO Jay Roberts tells Proactive the drug discovery and preclinical oncology and immuno-oncology services provider says he's 'excited about the vision and future' of the firm by focusing more on drug discovery and by strengthening its balance sheet.

Roberts says the firm is well positioned to carry through new strategic alternative activities to further strengthen its position in the industry.

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Cancer Genetics CEO "excited about the vision and future" by being highly focused on drug discovery - Proactive Investors USA & Canada

Genetics, profession: Heres the reason why eczema happens – Hindustan Times

Researchers may be getting closer to finding the cure of a chronic skin condition - Eczema, by analysing the cause of the skin disease in a recent study.

An estimated 35 million Americans suffer from eczema, also known as atopic dermatitis. Worldwide, 2 to 5 % of adults and about 15 % of children suffer from symptoms such as dry, inflamed and very itchy skin with open sores.

Although there are myriad treatments for eczema, such as medical creams and natural remedies, the exact causes of the condition remain elusive.

In a new paper, the team -- Associate Professor Guy German and PhD student Zachary W. Lipsky from the Thomas J. Watson School of Engineering and Applied Sciences Department of Biomedical Engineering, and Associate Professor Claudia N.H. Marques of the Harpur College of Arts and Sciences Department of Biological Sciences -- connects two aspects of eczema research that are rarely studied together.

One result of atopic dermatitis is a decreased level of skin oils known as lipids, particularly one group called ceramides. Lipids on the surface of the skin function to regulate hydration and also help defend the skin from foreign invaders either indirectly through immune signalling or directly through their inherent antimicrobial activity.

Another result of eczema is an increase in staph bacteria in the skin, which can cause irritation and infection.

German said that genetics can play a part in whether someone has eczema, but people in certain occupations have also been shown to be more likely to get the skin condition, such as healthcare professionals, metalworkers, hairdressers, and food processing workers. The connection? An increased amount of handwashing or regular contact with detergents for your job.

What happens if, either through a mutation or through occupational risks, theres a decreased presence of lipids on the skin? he said.

The essence of this study is that in normal, healthy conditions, bacteria do not penetrate the skin barrier. In atopic dermatitis conditions or lipid levels consistent with AD, it does -- and it consistently takes nine days, he added.

Because the staph bacteria are immobile, they need to multiply in number to grow through the protective outer skin layer known as the stratum corneum. The Watson researchers believe the bacteria dont grow around the skin cells but actually through them. With lipid depletion -- either through genetics or occupational risks -- the skin appears to become more vulnerable to bacterial invasion and infection of underlying skin tissue.

When we usually think about the oils in our skin, we think about water retention and moisturizing -- things like that. Now were looking at how these lipids are important for protection against these microorganisms that can come in and cause diseases, Lipsky said.

While this study has not unlocked all the secrets of atopic dermatitis, showing that the bacteria could be the cause rather than the result of the disease is a major step forward. Further research is required, and thats where the Watson team will investigate next.

Now that we know that bacteria can permeate through lipid depleted skin, how does it affect the skin mechanically? Does it make the skin weaker and more likely to crack? Can we figure out how bacteria are moving through different skin layers? Lipsky said.

In scientific research, you get one answer and three additional questions pop up, so were never stuck for things to do, German added.

(This story has been published from a wire agency feed without modifications to the text. Only the headline has been changed.)

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Genetics, profession: Heres the reason why eczema happens - Hindustan Times

New Genetic Mutations Linked to ASD – Technology Networks

Scientists at Sanford Burnham Prebys Medical Discovery Institute and Radboud University Medical Center in the Netherlands have identified mutations in a gene called CNOT1 that affect brain development and impair memory and learning. The study is the first to link neurodevelopmental delays with CNOT1, suggesting that drugs that help restore the genes function may have therapeutic benefit. The research, published in The American Journal of Human Genetics, also revealed that CNOT1 interacts with several known autism spectrum disorder (ASD) genes, opening new research avenues for the condition.Prior to this work, the CNOT1 gene was not on the radar of autism researchers, says Rolf Bodmer, Ph.D., director and professor in the Development, Aging and Regeneration Program at Sanford Burnham Prebys and the studys co-corresponding and co-senior author. This discovery could help us better understand the genetic mechanisms underlying ASD. Our work is also a first step toward exploring drugs that could augment the function of CNOT1 and might be able to help children with neurodevelopmental delays who have these specific mutations.

The cause of developmental disabilities, including ASD, is poorly understood. Research indicates that there may be a genetic component to these conditions, but the precise impact of the genetic variations that have been uncovered to date is unclear. Identifying the underlying cause of developmental disabilities would allow scientists to create diagnostic tests that would provide early diagnoses and potential treatments.

To answer this question, the researchers at Radboud University turned to Bodmer, a world-renowned genetics expert who studies how genes contribute to disease using a fruit fly model. Sreehari Kalvakuri, Ph.D., a postdoctoral researcher in the Bodmer lab, created fruit flies that contained the same CNOT1 variations seen in the patients, including DNA sequences that were misspelled (missense), cut short (truncated) or otherwise altered.

This work identified nine CNOT1 variants that impaired learning and memory, which was measured by several independent approaches including a courtship assay that tested the ability of male fruit flies to remember if their female partners had paired with other males. All of these variants appeared spontaneously (de novo) in the patients, meaning they were not inherited. The scientists also discovered that these CNOT1 mutations interact with known ASD genes revealing a genetic link to ASD that can be further explored.

Fruit flies are a great biological model because we can complete genetic studies very quickly. This work only took a few months instead of the potential decade using a mouse model, says Kalvakuri, the studys co-first author. Additionally, the CNOT1 gene is highly conserved between fruit flies and humans, meaning it does not change much, so we are optimistic these findings can be extrapolated to people.

Next, the scientists plan to identify which molecular components interact with CNOT1, which functions as a scaffold that builds up a larger protein complex. This work might uncover additional potential drug targets for intellectual, learning or memory disorders, including ASD.

The first step toward helping children with neurodevelopmental delays is to determine the cause of the condition, says Bodmer. Our ultimate hope is to find a treatment that could be given as early as possible to help these children stay on track developmentally.

Surprisingly, the findings also have implications for heart disease, the primary focus of Bodmers lab.

A significant fraction of these patients also have cardiac defects, says Bodmer. Conversely, children who are born with heart defects are at a higher risk of developing ASD, too. This study on CNOT1 also provides a previously unknown genetic link between heart function and ASD.

This article has been republished from the following materials. Note: material may have been edited for length and content. For further information, please contact the cited source.

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New Genetic Mutations Linked to ASD - Technology Networks

Open Rank Faculty Positions in Plant Quantitative Genetics and Breeding job with SKOLKOVO INSTITUTE OF SCIENCE AND TECHNOLOGY | 211940 – Times Higher…

Skoltech is seeking application for tenure track faculty at Assistant Professor or Associate Professor position to its newly createdDigital Agriculture Laboratory.Thecandidate should hold a PhD degree (or equivalent) inbiology, genetics, biotechnology.He/she should have substantial expertise inplant genetics, genomics or other related disciplines, proven experience of establishing independent sustainable research, educational and innovation programs, in conjunction with established MS and PhD programs in Life Sciences. Of particular interest are those candidates with proven expertise in plant quantitative genetics, plant breeding and agrobiotech.

The Skolkovo Institute of Science and Technologyis an English-speaking international graduate research university in Moscow, Russia. Established in 2011 in collaboration with MIT, Skoltech advances scientific knowledge, educates global leaders in innovation and fosters new technologies to address critical issues facing Russia and the world. Skoltech is an integral part of theSkolkovo Innovation Centerthat comprises a complete high-tech city with a number of international R&D centers and start-up incubators.

The mission of the Digital Agriculture Laboratory is to conduct research, education, and innovation activities to provide new tools and techniques for implementing modern breeding techniques in plants and animals and to address the question of digital agriculture. We aim to establish at Skoltech a highly impactful interdisciplinary center of fundamental and problem-driven research aimed at advancing our knowledge and innovations in the agriculture sector, with particular dedication to the relationships with industrial partners.

How to apply:

To apply, please go to our application website: http://join.skoltech.ru/how-to-apply/ and follow the instructions or send an e-mail tofacultysearch@skoltech.ru.

Review of applications will continue until the position has been filled. Applicants should submit the following documents: (1) cover letter, (2) curriculum vitae, (3) two-page statement of teaching interests and philosophy, (4) statement of research plans, (5) innovation statement, and (6) the names and contact information of at least three professional references.

The application submission deadline isSeptember 1st. The selection of candidates for the position starts immediately until the position is filled.

Skoltech offers:

Skoltech is committed to diversity and equality, and all applicants are invited to apply regardless of their gender, race or nationality.

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Open Rank Faculty Positions in Plant Quantitative Genetics and Breeding job with SKOLKOVO INSTITUTE OF SCIENCE AND TECHNOLOGY | 211940 - Times Higher...

Seattle Genetics Announces Positive Topline Results from Phase 2 Clinical Trial of Tisotumab Vedotin in Recurrent or Metastatic Cervical Cancer -…

BOTHELL, Wash.--(BUSINESS WIRE)--Seattle Genetics, Inc. (Nasdaq:SGEN) today announced positive topline results from the phase 2 single-arm clinical trial known as innovaTV 204 evaluating tisotumab vedotin administered every three weeks for the treatment of patients who have relapsed or progressed on or after prior treatment for recurrent or metastatic cervical cancer. Results from the trial showed a 24 percent confirmed objective response rate (ORR) by independent central review [95% Confidence Interval: 15.9%-33.3%] with a median duration of response (DOR) of 8.3 months. The most common treatment-related adverse events (greater than or equal to 20 percent) included alopecia, epistaxis (nose bleeds), nausea, conjunctivitis, fatigue and dry eye. The data will be submitted for presentation at an upcoming medical meeting.

Tisotumab vedotin is an investigational antibody-drug conjugate (ADC) directed to tissue factor, which is expressed on cervical cancer and can promote tumor growth, angiogenesis and metastases.1 Standard therapies for previously treated recurrent and/or metastatic cervical cancer generally result in limited objective response rates of typically less than 15 percent with median overall survival ranging from 6.0 to 9.4 months, in an all-comers population.1-8 Tisotumab vedotin is being developed by Seattle Genetics in collaboration with Genmab.

Available therapies upon progression after first line chemotherapy in recurrent or metastatic cervical cancer are limited, and there is a significant unmet need for new treatment options, said Roger Dansey, M.D., Chief Medical Officer at Seattle Genetics. Tisotumab vedotin has demonstrated clinically meaningful and durable objective responses with a manageable safety profile, and we look forward to discussing with the FDA the potential submission of a Biologics License Application to support an accelerated approval.

Cervical cancer originates in the cells lining the cervix. Over 13,500 women are expected to be diagnosed with cervical cancer in the U.S. in 2020, with approximately 4,200 deaths.9 Cervical cancer remains one of the leading causes of cancer death in women globally, with over 311,000 women dying annually; the vast majority of these women being in the developing world.10 Routine medical examinations and the human papillomavirus (HPV) vaccine have lowered the incidence of cervical cancer in the developed world. Despite these advances, women are still diagnosed with cervical cancer, which often recurs or becomes metastatic.

Additional clinical trials of tisotumab vedotin are currently enrolling patients, including in combination with pembrolizumab, carboplatin or bevacizumab, and with a weekly dosing schedule in patients with locally advanced or metastatic cervical cancer. Tisotumab vedotin is also being evaluated in other tissue factor expressing tumor types, including ovarian and other solid tumors.

About innovaTV 204 Trial

The innovaTV 204 trial (also known as GCT1015-04 or innovaTV 204/GOG-3023/ENGOT-cx6) is an ongoing single-arm, global, multicenter study of tisotumab vedotin for patients with recurrent or metastatic cervical cancer who were previously treated with doublet chemotherapy with or without bevacizumab. Additionally, patients were eligible if they had received up to two prior lines of therapy in the metastatic setting. In the study, 101 patients were treated with tisotumab vedotin at multiple centers in the U.S. and Europe. The primary endpoint of the trial was confirmed objective response rate per Response Evaluation Criteria in Solid Tumors (RECIST) v1.1 as assessed by independent central review. Key secondary endpoints included duration of response, progression-free survival, overall survival, safety and tolerability.

The study was conducted in collaboration with European Network of Gynaecological Oncological Trial Groups (ENGOT) and Gynecologic Oncology Group (GOG). For more information about the phase 2 innovaTV 204 clinical trial and other clinical trials with tisotumab vedotin, please visit http://www.clinicaltrials.gov.

About Tisotumab Vedotin

Tisotumab vedotin is an investigational antibody-drug conjugate (ADC) composed of Genmabs fully human monoclonal antibody specific for tissue factor and Seattle Genetics ADC technology that utilizes a protease-cleavable linker that covalently attaches the microtubule-disrupting agent monomethyl auristatin E (MMAE) to the antibody and releases it upon internalization, inducing target cell death. In cancer biology, tissue factor is a protein that can promote tumor growth, angiogenesis and metastases.1 Based on its high expression on many solid tumors and its rapid internalization, tissue factor was selected as a target for an ADC approach. Tisotumab vedotin is being co-developed by Genmab and Seattle Genetics, under an agreement in which the companies share all costs and profits for the product on a 50:50 basis.

Tisotumab vedotin is being evaluated in ongoing clinical trials as monotherapy in a range of solid tumors, including recurrent and/or metastatic cervical cancer, ovarian cancer and in combination with other commonly used therapies in recurrent or metastatic cervical cancer. These trials are evaluating tisotumab vedotin on a weekly or every three weeks dosing schedule.

About Seattle Genetics

Seattle Genetics, Inc. is a global biotechnology company that discovers, develops and commercializes transformative cancer medicines to make a meaningful difference in peoples lives. ADCETRIS (brentuximab vedotin) and PADCEVTM (enfortumab vedotin-ejfv) use the companys industry-leading antibody-drug conjugate (ADC) technology. ADCETRIS is approved in certain CD30-expressing lymphomas, and PADCEV is approved in certain metastatic urothelial cancers. TUKYSATM (tucatinib), a small molecule tyrosine kinase inhibitor, is approved in certain HER2-positive metastatic breast cancers. The company is headquartered in the Seattle, Washington area, with locations in California, Switzerland and the European Union. For more information on our robust pipeline, visit http://www.seattlegenetics.com and follow @SeattleGenetics on Twitter.

Forward Looking Statements

Certain of the statements made in this press release are forward looking, such as those, among others, relating to the potential submission of a BLA to the FDA under the FDAs accelerated approval program and the potential for regulatory approval of tisotumab vedotin based on the innovaTV 204 trial; the therapeutic potential of tisotumab vedotin, its possible benefits and uses, including as monotherapy or in combination with other agents, and in other tumor types or with a weekly dosing regimen, and the tisotumab vedotin future development program. Actual results or developments may differ materially from those projected or implied in these forward-looking statements. Factors that may cause such a difference include the possibility that the data from innovaTV 204 may not be sufficient to support accelerated approval; the possibility of impediments or delays in the submission of a potential BLA to the FDA; the risk of adverse events, including the potential for newly-emerging safety signals; delays, setbacks or failures in clinical development activities for a variety of reasons, including the difficulty and uncertainty of pharmaceutical product development, adverse regulatory action, possible required modifications to clinical trials, failure to properly conduct or manage clinical trials and failure of clinical results to support continued development or regulatory approvals. More information about the risks and uncertainties faced by Seattle Genetics is contained under the caption Risk Factors included in the companys Quarterly Report on Form 10-Q for the quarter ended March 31, 2020 filed with the Securities and Exchange Commission. Seattle Genetics disclaims any intention or obligation to update or revise any forward-looking statements, whether as a result of new information, future events or otherwise, except as required by law.

References:

1 Van de Berg YW et al. Blood 2012;119:924.2 Miller et al., Gynecol Oncol 2008; 110:65.3 Bookman et al., Gynecol Oncol 2000; 77:446.4 Garcia et al., Am J Clin Oncol 2007; 30:428.5 Monk et al., J Clin Oncol 2009; 27:1069.6 Santin et al., Gynecol Oncol 2011; 122:495.7 Schilder et al., Gynecol Oncol 2005; 96:1038 Chung HC et al. J Clin Oncol 2019; 37:1470.9 National Cancer Institute SEER. Cancer Stat Facts: Cervix Uteri Cancer. Available at https://seer.cancer.gov/statfacts/html/cervix.html. Last accessed April 2020.10 Global Cancer Statistics 2018: GLOBOCAN Estimates of Incidence and Mortality Worldwide for 36 Cancers in 185 countries https://www.iarc.fr/news-events/global-cancer-statistics-2018-globocan-estimates-of-incidence-and-mortality-worldwide-for-36-cancers-in-185-countries/.

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Seattle Genetics Announces Positive Topline Results from Phase 2 Clinical Trial of Tisotumab Vedotin in Recurrent or Metastatic Cervical Cancer -...

Race Is Real, But It’s Not Genetic – Discover Magazine

A friend of mine with Central American, Southern European and West African ancestry islactose intolerant. Drinking milk products upsets her stomach, and so she avoids them. About a decade ago, because of her low dairy intake, she feared that she might not be getting enough calcium, so she asked her doctor for abone density test. He responded that she didnt need one because blacks do not get osteoporosis.

My friend is not alone. The view that black people dont need a bone density test is a longstanding and common myth. A2006 studyin North Carolina found that out of 531 African American and Euro-American women screened for bone mineral density, only 15 percent were African American women despite the fact that African American women made up almost half of that clinical population. A health fair in Albany, New York, in 2000,turned into a ruckuswhen black women were refused free osteoporosis screening. The situationhasnt changed muchin more recent years.

Meanwhile,FRAX, a widely used calculatorthat estimates ones risk of osteoporotic fractures, is based on bone density combined with age, sex and, yes, race. Race, even though it is never defined or demarcated, is baked into the fracture risk algorithms.

Lets break down the problem.

First, presumably based on appearances, doctors placed my friend and others into a socially defined race box called black, which is a tenuous way to classify anyone.

Race is a highly flexible way in which societies lump people into groups based on appearance that is assumed to be indicative of deeper biological or cultural connections. As a cultural category, the definitions and descriptions of races vary. Color lines based on skin tone can shift, which makes sense, but the categories are problematic for making any sort of scientific pronouncements.

Second, these medical professionals assumed that there was a firm genetic basis behind this racial classification, which there isnt.

Third, they assumed that this purported racially defined genetic difference would protect these women from osteoporosis and fractures.

Some studies suggestthat African American women meaning women whose ancestry ties back to Africa may indeed reach greater bone density than other women, which could be protective against osteoporosis. But that does not mean being black that is, possessing an outward appearance that is socially defined as black prevents someone from getting osteoporosis or bone fractures. Indeed, this same research also reports that African American women are more likely to die after a hip fracture. The link between osteoporosis risk and certain racial populations may be due to lived differencessuch as nutritionandactivity levels, both of which affect bone density.

But more important:Geographicancestry is not the same thing as race. African ancestry, for instance, does not tidily map onto being black (or vice versa). In fact, a2016 studyfound wide variation in osteoporosis risk among women living in different regions within Africa. Their genetic risks have nothing to do with their socially defined race.

When medical professionals or researchers look for ageneticcorrelateto race, they are falling into a trap: They assume thatgeographic ancestry, which does indeed matter to genetics, can be conflated with race, which does not. Sure, different human populations living in distinct places may statistically have different genetic traits such as sickle cell trait (discussed below) but such variation is aboutlocal populations(people in a specific region), not race.

Like a fish in water, weve all been engulfed by the smog of thinking that race is biologically real. Thus, it is easy to incorrectly conclude that racial differences in health, wealth and all manner of other outcomes are the inescapable result of genetic differences.

The reality is that socially defined racial groups in the U.S. and most everywhere else do differ in outcomes. But thats not due to genes. Rather, it is due to systemic differences in lived experience and institutional racism.

Communities of color in the United States, for example, often have reduced access to medical care, well-balanced diets andhealthy environments. They are often treated more harshly in their interactions withlaw enforcement and the legal system. Studies show that they experience greater social stress, includingendemic racism, that adversely affects all aspects of health. For example, babies born to African American women are more thantwice as likely to diein their first year than babies born to non-Hispanic Euro-American women.

Systemic racism leads to different health outcomes for various populations. The infant mortality rate, for example, for African American infants is double that for European Americans. (Credit: Kelly Lacy/Pexels)

As a professor of biological anthropology, I teach and advise college undergraduates. While my students are aware of inequalities in the life experiences of different socially delineated racial groups, most of them also think that biological races are real things. Indeed, more than half of Americans still believe that their racial identity is determined byinformation contained in their DNA.

For the longest time, Europeans thought that the sun revolved around the Earth. Their culturally attuned eyes saw this as obvious and unquestionably true. Just as astronomers now know thats not true,nearly all population geneticistsknow that dividing people into races neither explains nor describes human genetic variation.

Yet this idea of race-as-genetics will not die. For decades, it has been exposed to the sunlight of facts, but, like a vampire, it continues to suck blood not only surviving but causing harm in how it can twist science to support racist ideologies. With apologies for the grisly metaphor, it is time to put a wooden stake through the heart of race-as-genetics. Doing so will make for better science and a fairer society.

In 1619, the first people from Africa arrived in Virginia and became integrated into society. Only after African and European bond laborers unified in various rebellions did colony leaders recognize the need to separate laborers.Race dividedindentured Irish and other Europeans from enslaved Africans, and reduced opposition by those of European descent to the intolerable conditions of enslavement. What made race different from other prejudices, including ethnocentrism (the idea that a given culture is superior), is that it claimed that differences were natural, unchanging and God-given. Eventually, race also received the stamp of science.

Over the next decades, Euro-American natural scientists debated the details of race, asking questions such as how often the races were created (once, as stated in the Bible, or many separate times), the number of races and their defining, essential characteristics. But they did not question whether races were natural things. They reified race, making the idea of race real by unquestioning, constant use.

In the 1700s, Carl Linnaeus, the father of modern taxonomy and someone not without ego, liked to imagine himself asorganizing what God created. Linnaeus famously classified ourown species into racesbased on reports from explorers and conquerors.

The race categories he created includedAmericanus,Africanus, and evenMonstrosus(for wild and feral individuals and those with birth defects), and their essential defining traits included a biocultural mlange of color, personality and modes of governance. Linnaeus describedEuropeausas white, sanguine and governed by law, andAsiaticusas yellow, melancholic and ruled by opinion. These descriptions highlight just how much ideas of race are formulated by social ideas of the time.

Swedish taxonomist Carl Linnaeus divided humanity up into racial categories according to his notion of shared essences among populations, a concept researchers now recognize has no scientific basis. (Credit: Wikimedia Commons/Public Domain)

In line with early Christian notions, these racial types were arranged in a hierarchy:a great chain of being, from lower forms to higher forms that are closer to God. Europeans occupied the highest rungs, and other races were below, just above apes and monkeys.

So, the first big problems with the idea of race are that members of a racial group do not share essences, Linnaeus idea of some underlying spirit that unified groups, nor are races hierarchically arranged. A related fundamental flaw is that races were seen to be static and unchanging. There is no allowance for a process of change or what we now call evolution.

There have been lots of efforts since Charles Darwins time to fashion the typological and static concept of race into an evolutionary concept. For example, Carleton Coon, a former president of the American Association of Physical Anthropologists, argued inThe Origin of Races(1962) that five racesevolved separatelyand became modern humans at different times.

One nontrivial problem with Coons theory, and all attempts to make race into an evolutionary unit, is that there is no evidence. Rather, all the archaeological and genetic data point to abundant flows of individuals, ideas and genes across continents, withmodern humansevolving at the same time, together.

Afew pundits such asCharles Murrayof the American Enterprise Institute and science writers such asNicholas Wade, formerly ofThe New York Times, still argue that even though humans dont come in fixed, color-coded races, dividing us into races still does a decent job ofdescribinghuman genetic variation. Their position is shockingly wrong. Weve known for almost 50 years that race does not describe human genetic variation.

In 1972, Harvard evolutionary biologist Richard Lewontinhad the idea to testhow much human genetic variation could be attributed to racial groupings. He famously assembled genetic data from around the globe and calculated how much variation was statistically apportioned within versus among races. Lewontin found that only about 6 percent of genetic variation in humans could be statistically attributed to race categorizations. Lewontin showed that the social category of race explains very little of the genetic diversity among us.

Furthermore, recent studies reveal that the variation between any two individuals isverysmall, on the order of onesingle nucleotide polymorphism(SNP), or single letter change in our DNA, per 1,000. That means that racial categorization could, at most, relate to 6 percent of the variation found in 1 in 1,000 SNPs. Put simply, race fails to explain much.

In addition, genetic variation can be greaterwithingroups that societies lump together as one race than it is between races. To understand how that can be true, first imagine six individuals: two each from the continents of Africa, Asia and Europe. Again, all of these individuals will be remarkably the same: On average, only about 1 out of 1,000 of their DNA letters will be different. A study by Ning Yu and colleaguesplaces the overall difference more precisely at 0.88 per 1,000.

The researchers further found that people in Africa had less in common with one another than they did with people in Asia or Europe. Lets repeat that: On average, two individuals in Africa aremoregenetically dissimilar from each other than either one of them is from an individual in Europe or Asia.

Homo sapiensevolved in Africa; the groups that migrated out likely did not include all of the genetic variation that built up in Africa. Thats an example of what evolutionary biologists call thefounder effect, where migrant populations who settle in a new region have less variation than the population where they came from.

Genetic variation across Europe and Asia, and the Americas and Australia, is essentially a subset of the genetic variation in Africa. If genetic variation were a set of Russian nesting dolls, all of the other continental dolls pretty much fit into the African doll.

What all these data show is that the variation that scientists from Linnaeus to Coon to the contemporary osteoporosis researcher think is race is actually much better explained by a populationslocation. Genetic variation is highly correlated togeographic distance. Ultimately, the farther apart groups of people are from one another geographically, and, secondly, the longer they have been apart, can together explain groups genetic distinctions from one another. Compared to race, those factors not only better describe human variation, they invoke evolutionary processes to explain variation.

Those osteoporosis doctors might argue that even though socially defined race poorly describes human variation, it still could be a useful classification tool in medicine and other endeavors. When the rubber of actual practice hits the road, is race a useful way to make approximations about human variation?

When Ive lectured at medical schools, my most commonly asked question concerns sickle cell trait. Writer Sherman Alexie, a member of the Spokane-Coeur dAlene tribes, put the question this wayin a 1998 interview: If race is not real, explain sickle cell anemia to me.

OK! Sickle cell is a genetic trait: It is the result of an SNP that changes the amino acid sequence of hemoglobin, the protein that carries oxygen in red blood cells. When someone carries two copies of the sickle cell variant, they will have the disease. In the U.S., sickle cell disease is most prevalent in people who identify as African American, creating the impression that it is a black disease.

(Credit: SciePro/Shutterstock)

Yet scientists have known about the much more complexgeographic distributionof sickle cell mutation since the 1950s. It is almost nonexistent in the Americas, most parts of Europe and Asia and also in large swaths of Northern and Southern Africa. On the other hand, it is common in West-Central Africa and also parts of the Mediterranean, Arabian Peninsula, and India. Globally, it does not correlate with continents or socially defined races.

Inone of the most widely citedpapers in anthropology, American biological anthropologist Frank Livingstone helped to explain the evolution of sickle cell. He showed that places with a long history of agriculture and endemic malaria have a high prevalence of sickle cell trait (a single copy of the allele). He put this information together with experimental and clinical studies that showed how sickle cell trait helped people resist malaria, and made a compelling case for sickle cell trait being selected for in those areas.Evolution and geography, not race, explain sickle cell anemia.

What about forensic scientists: Are they good at identifying race? In the U.S., forensic anthropologists are typically employed by law enforcement agencies to help identify skeletons, including inferences about sex, age, height and race. The methodological gold standards for estimating race are algorithms based on a series of skull measurements, such as widest breadth and facial height. Forensic anthropologists assume these algorithms work.

The origin of the claim that forensic scientists are good at ascertaining race comes from a 1962 study of black, white and Native American skulls, which claimed an 8090 percent success rate. That forensic scientists are good at telling race from a skull is a standard trope of both thescientific literatureandpopular portrayals.But my analysisof four later tests showed that the correct classification of Native American skulls from other contexts and locations averaged about two incorrect for every correct identification. The results are no better than a random assignment of race.

Thats because humans are not divisible into biological races. On top of that, human variation does not stand still. Race groups are impossible to define in any stable or universal way. It cannot be done based on biology not by skin color, bone measurements or genetics. It cannot be done culturally: Race groupings have changed over time and place throughout history.

Science 101: If you cannot define groups consistently, then you cannot make scientific generalizations about them.

Skull measurements are a longstanding tool in forensic anthropology. (Credit: Internet Archive Book Images/Flickr/Public Domain)

Wherever one looks, race-as-genetics is bad science. Moreover, when society continues to chase genetic explanations, it misses the larger societal causes underlying racial inequalities in health, wealth and opportunity.

To be clear, what I am saying is that human biogenetic variation is real. Lets just continue to study human genetic variation free of the utterly constraining idea of race. When researchers want to discuss genetic ancestry or biological risks experienced by people in certain locations, they can do so without conflating these human groupings withracial categories. Lets be clear that genetic variation is an amazingly complex result of evolution and mustnt ever be reduced to race.

Similarly, race is real, it just isnt genetic. Its a culturally created phenomenon. We ought to know much more about the process of assigning individuals to a race group, including the category white. And we especially need to know more about the effects of living in a racialized world: for example, how a societys categoriesand prejudiceslead to health inequalities. Lets be clear that race is a purely sociopolitical construction with powerful consequences.

It is hard to convince people of the dangers of thinking race is based on genetic differences. Like climate change, the structure of human genetic variation isnt something we can see and touch, so it is hard to comprehend. And our culturally trained eyes play a trick on us by seeming to see race as obviously real. Race-as-genetics is even more deeply ideologically embedded than humanitys reliance on fossil fuels and consumerism. For these reasons, racial ideas will prove hard to shift, but it is possible.

Over 13,000 scientistshave come together to form and publicize a consensus statement about the climate crisis, and that has surely moved public opinion to align with science. Geneticists and anthropologists need to do the same for race-as-genetics. The recent American Association of Physical AnthropologistsStatement on Race & Racismis a fantastic start.

In the U.S., slavery ended over 150 years ago and the Civil Rights Law of 1964 passed half a century ago, but the ideology of race-as-genetics remains. It is time to throw race-as-genetics on the scrapheap of ideas that are no longer useful.

We can start by getting my friend and anyone else who has been denied that long-overdue bone density test.

Alan Goodmanis a professor of biological anthropology at Hampshire College in Massachusetts. This story was originally posted onSAPIENS. Read the original articlehere.

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Race Is Real, But It's Not Genetic - Discover Magazine

BRIEF-Seattle Genetics Announces Positive Topline Results From Phase 2 Clinical Trial Of Tisotumab Vedotin – Reuters

June 29 (Reuters) - Seattle Genetics Inc:

* SEATTLE GENETICS ANNOUNCES POSITIVE TOPLINE RESULTS FROM PHASE 2 CLINICAL TRIAL OF TISOTUMAB VEDOTIN IN RECURRENT OR METASTATIC CERVICAL CANCER

* SEATTLE GENETICS - LOOK FORWARD TO DISCUSSING WITH FDA POTENTIAL SUBMISSION OF BLA TO SUPPORT ACCELERATED APPROVAL OF TISOTUMAB VEDOTIN Source text for Eikon: Further company coverage:

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BRIEF-Seattle Genetics Announces Positive Topline Results From Phase 2 Clinical Trial Of Tisotumab Vedotin - Reuters

University of East London lecturer says PHE report fails to address genetics – Newham Recorder

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PUBLISHED: 10:00 29 June 2020

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Dr Winston Morgan, Reader in Toxicology and Clinical Biochemistry at the University of East London, says race and genetics are key omissions from the PHE report on coronavirus. Picture: University of East London

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Dr Morgan a reader in toxicology and clinical biochemistry at the university commended the report for properly addressing the structural problems linked to racism which have caused Covid-19 to disproportionately impact BAME communities.

However, the lecturer criticised the complete lack of consideration given to the issue of genetics, and specifically to answering the question as to whether certain traits increase virus susceptibility.

Failing to adequately address this subject leaves the door open for continued speculation around race and genetics, said Dr Morgan.

This report was an opportunity to knock the speculation on its head, and allow for focus to be appropriately shifted to dealing with the damaging structural problems within society.

A spokesperson for PHE said: The review was not able to look at genetic factors and more research in this area is needed.

To complement the review, a research call by the National Institute for Health Research (NIHR) and UK Research and Innovation (UKRI) has jointly called for research proposals to investigate emerging evidence of an association between ethnicity and COVID-19 incidence and adverse health outcomes.

Dr Morgan also queried how the report framed its discussion of the relationship between the BAME community and the NHS: The report missed a number of opportunities, such as not to consider that historical racism will impact on both the speed and level of treatment BAME groups are likely to receive when they interact with the NHS.

Instead, it focused on the fact that as a result of historical racism BAME groups are less likely to seek care when needed.

Both arguments are underpinned by historical racism, and should have been given equal weight in the report: By omitting the former it has the feel of blaming the victims for not complaining.

PHE conceded that the report did not consider every issue: There are many impacts of systemic racism and PHEs qualitative report identified the issues that were raised repeatedly by stakeholders.

This does not mean that other factors are not relevant and confirms the need for further more detailed research studies on these issues.

Dr Morgan concluded that despite reservations over the lack of wider recommendation about tackling structural racism in wider society, all seven recommendations should be implemented.

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University of East London lecturer says PHE report fails to address genetics - Newham Recorder

Coronavirus’s Genetics Not Changing Much, And That Bodes Well For A Vaccine : Shots – Health News – NPR

Internationally, scientists now have on file the genomes of more than 47,000 different samples of the virus that causes COVID-19 up from just one in January. Here's a transmission electron micrograph of SARS-CoV-2 virus particles (orange) isolated from a patient. National Institute of Allergy and Infectious Diseases/National Institutes of Health hide caption

Internationally, scientists now have on file the genomes of more than 47,000 different samples of the virus that causes COVID-19 up from just one in January. Here's a transmission electron micrograph of SARS-CoV-2 virus particles (orange) isolated from a patient.

Scientists are monitoring the virus that causes COVID-19 for genetic changes that could make a vaccine ineffective. But so far, they're not seeing any.

"There's nothing alarming about the way the coronavirus is mutating or the speed at which it's mutating," says Emma Hodcroft, a molecular epidemiologist at the University of Basel in Switzerland. "We don't think this will be a problem [for vaccines] in the short term."

"To date, there have been very few mutations observed," says Peter Thielen, a senior scientist at Johns Hopkins Applied Physics Laboratory. "And any mutations that we do see are likely not having an effect on the function of the virus itself."

That's good news for scientists working to produce an effective vaccine by the end of the year. And it reflects the enormous quantity of genetic information on SARS-CoV-2, the virus that causes COVID-19, that researchers have amassed since the virus appeared in China late last year.

In January, scientists were limited to just one whole genome sequence of the virus. "Today we have over 47,000 coronavirus genomes that have been submitted to international databases," Thielen says.

New genomes are added every day by teams of scientists from around the world. And each time a new one arrives, it gets a close examination, Thielen says.

"What we're looking for in the data is similarity between the virus that first emerged and the genome that had been deposited and any changes that have occurred in the virus," he says. And overall, the viruses circulating today look remarkably similar to the ones first identified in China.

There had been concern about mutations because SARS-CoV-2 is a type of virus capable of quickly changing its genes. But unlike many similar viruses, the coronavirus uses a proofreading system to catch any errors in the genetic code when it begins generating copies of itself.

"The targets for vaccine design today remain the same as we would have designed them in January."

Peter Thielen, Johns Hopkins Applied Physics Laboratory

"So if there's a change, it will actually make a correction at a specific location," Thielen says.

Vaccine developers have been especially concerned about genetic locations that affect something called a spike protein. It's a structure on the surface of the coronavirus that allows it to invade cells.

Spike proteins also give the virus its distinctive appearance and account for its name. Scientists who first viewed a coronavirus through an electron microscope were reminded of the solar corona.

The candidates for a coronavirus vaccine now under development are all designed to teach the immune system to recognize these spike proteins. So far, Thielen says, that's looking like a good strategy.

"The targets for vaccine design today remain the same as we would have designed them in January," he says.

Some other well-known viruses have proved less amenable to the strategy of using the same vaccine from year to year. Influenza, for example, is constantly altering its surface proteins in ways that require annual vaccine updates for each strain that's making the rounds that year.

"Flu just really loves to change these parts," Hodcroft says. "And that's why we can end up with such different flus from season to season."

Measles represents a virus at the other extreme its genome has stayed fairly consistent over the years, at least in the ways that trigger immunity in people after infection. That means children today still get a measles vaccine that was developed in the 1960s, and it provides immunity for a lifetime.

Hodcroft says she thinks SARS-CoV-2 is likely to fall somewhere between the flu and measles when it comes to making a vaccine.

"I think in the short term we'll find something," she says. "The big question is whether this is something we'll be able to vaccinate once and then you never have to get it again, or will it be something you'll have to get every couple of years to keep your immunity up to date."

Scientists are uncertain because the coronavirus is still so new, Hodcroft says.

"We haven't really seen the full diversity of how the virus can mutate," she says. "It gathers mutations over time. We can't speed up time, so we just have to wait and see."

At the moment, though, vaccine developers have more pressing concerns than mutations. First, they'll have to demonstrate that they can produce vaccines that are both safe and effective. Then they'll have to make huge quantities.

"It's not a small feat to manufacture a vaccine for billions of people and then to get it to all of those people," Hodcroft says.

That will take months, she says, in addition to the months required to develop a vaccine in the first place.

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Coronavirus's Genetics Not Changing Much, And That Bodes Well For A Vaccine : Shots - Health News - NPR