Category Archives: Genetic medicine

Tulane University neuroscientist Dr. Stacy Drury will launch the Telomere Research Network to establish best practices for measuring telomere length and how it can be used as a sentinel of aging-related disease risk. Photo by Jennifer Zdon.

The National Institutes of Health awarded a $2.9 million grant to Tulane University neuroscientist Dr. Stacy Drury to lead a research network that will set methodological standards for studying a part of the chromosome that scientists increasingly recognize as an important biological marker of aging and age-related diseases.

Drury will launch theTelomere Research Network to establish best practices for measuring telomere length in population-based studies. Telomeres are the caps at the end of chromosomes that keep them from shrinking when cells replicate. Shorter telomeres are linked to higher risks for heart disease, obesity, cognitive decline, diabetes, mental illness and poor health outcomes in adulthood.

The network willdefine the extent to which telomere length can be effectively applied as a sentinel of aging-related disease risk and an indicator of environmental and psychosocial stress exposure across the life span, said Drury, the Remigio Gonzalez, MD, Professor of Child Psychiatry at Tulane University School of Medicine. We are charged with bringing together all of the international experts in the field and becoming a central focus for this research across the globe.

There has been an explosion in telomere research within the last decade. But scientists have used different measurement criteria, leading to problems replicating research results in some studies.

As it becomes clearer that it is a very powerful marker, the rigor of the science has to get better, Drury said. Because so many people are studying it in so many different ways, we don't want to dilute the impact by having lots of people using methodology that isnt the best.

The network will define the extent that telomeres can be used as a marker of environmental exposures, psychosocial stress and disease susceptibility. It will also provide a forum for researchers to share samples, research data, study protocols and discussions on best practices for the field.

The network will convene for its first meeting Dec. 5-6 in Washington, D.C. The event will be streamed online athttps://tulane.zoom.us/j/258026269.

Weatherhead Professor of Pharmacology John McLachlan is a co-investigator on the grant. Drury will be working with collaborators at the University of Groningen, University of California at San Francisco, Georgetown University, Pennsylvania State University and Rutgers University.

The NIHs National Institute on Aging and the National Institute of Environmental Health Sciences funded the initiative under grant award No.U24AG066528.

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NIH taps Tulane neuroscientist to lead effort to standardize research in genetic aging - News from Tulane

The human genome was first sequenced in 2003 by multiple research centres across the world. The breakthrough was hailed as the dawn of a new era. Genetics would swiftly transform our response to disease and lead to personalised medicine.

In the past decade there has been substantial progress in terms of studying genetic factors giving rise to disease. But much of this has been focused on European populations. Little progress has been made in examining the factors associated with disease among Africans.

Until very recently, only a few hundred whole genome sequences of individuals within Africa had been completed. Researchers largely relied on genetic data from African-Americans. These have provided many new insights. But they dont reflect the continents full genetic diversity.

Africa is known to be where humans originated. From Africa, they migrated to other parts of the world. This makes it the most genetically diverse region in the world. Diversity among other populations represents a subset of the diversity within Africa.

This genetic diversity provides unique opportunities to examine genetic factors associated with disease that cant be examined in Europeans where diversity is much lower. This highlights the need for much larger studies of genetic causes of disease within Africa.

We conducted a study to build one of the largest genome resources from within Africa. We developed a rich, diverse resource using genome wide data from 6,400 Ugandans the Uganda Genome Resource. It included whole genome sequencing of nearly 2,000 people.

The study built on the long standing research programme of the Medical Research Council Uganda and Uganda Virus Research Institute. Its aim has been to establish a clinical and genomic data resource to understand population health and disease in the region.

The team also incorporated data on 14,000 individuals from different parts of the continent. It did this in collaboration with the University of KwaZulu-Natal and the Centre of Genomics and Global Health, National Institutes of Health. This allowed us to examine genetic determinants of traits within the population.

Around a quarter of the genetic variation identified had not been discovered before. We found a higher level of genetic diversity in the Ugandan population than seen in similar studies of European populations.

Modern Uganda appears to be a complex mosaic of genetic flow from many different communities that have migrated from surrounding regions within Africa and from Europe or the Middle East. This gene flow appears to have occurred repeatedly, dating back from around 100 years ago to as long as 4,500 years ago.

Our work is an important step forward in African medical genetics research. But much more research is needed to understand how these genetic variants affect disease traits. That means looking at the functional effects of genomes on gene expression and protein levels.

In our study, we discovered ten new associations with blood traits, liver function tests and indicators of diabetes. Most of these new associations relate to genetic variants that are unique to the Ugandan population or very rare in non-Africans. These would not have been discovered even in very large studies of Europeans.

For example, we identified an association between a genetic variant that causes alpha-thalassemia, a blood disorder that leads to anaemia, and glycated haemoglobin levels, which are commonly used for diagnosis of diabetes. This genetic variant is found in 22% of Africans. It has become very common in some regions within Africa because it also protects against severe malaria. It remains very rare in other populations where malaria isnt endemic. Our findings suggest that the utility of glycated haemoglobin as a diagnostic tool for diabetes may require re-evaluation in regions where alpha-thalassemia a blood disorder that reduces the production of haemoglobin is common.

The richness of the Uganda resource also offered us other opportunities. For example, we were able to study the extent to which genetic differences influence differences in traits among Ugandans relative to previous studies in European populations. We found that heritability the extent to which genetic differences encode differences in traits or diseases may differ between Ugandans and Europeans.

We also found that height is less genetically determined in rural Ugandans relative to previous European studies. We think that this might relate to differences in the impact of environmental factors between rural Ugandan and European populations. For example, the genetic influences on height might be more limited by nutritional influences in early childhood.

Our findings highlight the usefulness of examining genetically diverse populations within Africa. They underscore how this can lead to new discoveries and help us understand the genetic encoding of traits that may be different within Africa relative to other populations.

Africa is central to our understanding of human origins, genetic diversity and disease susceptibility. There is a clear scientific and public health need to develop large-scale projects that examine disease susceptibility across diverse populations across the continent. That work should be integrated with initiatives to improve research capacity in Africa.

We now need larger and more diverse studies of genetic causes of disease across the region. These will foster the development of new treatments that will benefit people living in Africa as well as people of African descent around the world.

Future work will look at individuals from other parts of Africa. The aim will be to get a deeper understanding of genetic diversity among indigenous hunter-gatherer populations. These include the Khoe-San populations in Namibia and South Africa and the rain forest populations in central Africa. In addition, we will be expanding current studies of genetic causes of disease to 100,000 individuals across the region.

The data was collected by researchers from universities and research institutes from Africa and the UK, including Queen Mary University of London, the University of KwaZulu-Natal, MRC/UVRI & London School of Hygiene & Tropical Medicine Uganda Research Unit, the US National Institute of Health and the University of Cambridge.

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What we've learnt from building Africa's biggest genome library - The Conversation Africa

Washington (AFP)

In the summer, a mother in Nashville with a seemingly incurable genetic disorder finally found an end to her suffering -- by editing her genome.

Victoria Gray's recovery from sickle cell disease, which had caused her painful seizures, came in a year of breakthroughs in one of the hottest areas of medical research -- gene therapy.

"I have hoped for a cure since I was about 11," the 34-year-old told AFP in an email.

"Since I received the new cells, I have been able to enjoy more time with my family without worrying about pain or an out-of-the-blue emergency."

Over several weeks, Gray's blood was drawn so doctors could get to the cause of her illness -- stem cells from her bone marrow that were making deformed red blood cells.

The stem cells were sent to a Scottish laboratory, where their DNA was modified using Crispr/Cas9 -- pronounced "Crisper" -- a new tool informally known as molecular "scissors."

The genetically edited cells were transfused back into Gray's veins and bone marrow. A month later, she was producing normal blood cells.

Medics warn that caution is necessary but, theoretically, she has been cured.

"This is one patient. This is early results. We need to see how it works out in other patients," said her doctor, Haydar Frangoul, at the Sarah Cannon Research Institute in Nashville.

"But these results are really exciting."

In Germany, a 19-year-old woman was treated with a similar method for a different blood disease, beta thalassemia. She had previously needed 16 blood transfusions per year.

Nine months later, she is completely free of that burden.

For decades, the DNA of living organisms such as corn and salmon has been modified.

But Crispr, invented in 2012, made gene editing more widely accessible. It is much simpler than preceding technology, cheaper and easy to use in small labs.

The technique has given new impetus to the perennial debate over the wisdom of humanity manipulating life itself.

"It's all developing very quickly," said French geneticist Emmanuelle Charpentier, one of Crispr's inventors and the cofounder of Crispr Therapeutics, the biotech company conducting the clinical trials involving Gray and the German patient.

- Cures -

Crispr is the latest breakthrough in a year of great strides in gene therapy, a medical adventure started three decades ago, when the first TV telethons were raising money for children with muscular dystrophy.

Scientists practising the technique insert a normal gene into cells containing a defective gene.

It does the work the original could not -- such as making normal red blood cells, in Victoria's case, or making tumor-killing super white blood cells for a cancer patient.

Crispr goes even further: instead of adding a gene, the tool edits the genome itself.

After decades of research and clinical trials on a genetic fix to genetic disorders, 2019 saw a historic milestone: approval to bring to market the first gene therapies for a neuromuscular disease in the US and a blood disease in the European Union.

They join several other gene therapies -- bringing the total to eight -- approved in recent years to treat certain cancers and an inherited blindness.

Serge Braun, the scientific director of the French Muscular Dystrophy Association, sees 2019 as a turning point that will lead to a medical revolution.

"Twenty-five, 30 years, that's the time it had to take," he told AFP from Paris.

"It took a generation for gene therapy to become a reality. Now, it's only going to go faster."

Just outside Washington, at the National Institutes of Health (NIH), researchers are also celebrating a "breakthrough period."

"We have hit an inflection point," said Carrie Wolinetz, NIH's associate director for science policy.

These therapies are exorbitantly expensive, however, costing up to $2 million -- meaning patients face grueling negotiations with their insurance companies.

They also involve a complex regimen of procedures that are only available in wealthy countries.

Gray spent months in hospital getting blood drawn, undergoing chemotherapy, having edited stem cells reintroduced via transfusion -- and fighting a general infection.

"You cannot do this in a community hospital close to home," said her doctor.

However, the number of approved gene therapies will increase to about 40 by 2022, according to MIT researchers.

They will mostly target cancers and diseases that affect muscles, the eyes and the nervous system.

- Bioterrorism -

Another problem with Crispr is that its relative simplicity has triggered the imaginations of rogue practitioners who don't necessarily share the medical ethics of Western medicine.

Last year in China, scientist He Jiankui triggered an international scandal -- and his excommunication from the scientific community -- when he used Crispr to create what he called the first gene-edited humans.

The biophysicist said he had altered the DNA of human embryos that became twin girls Lulu and Nana.

His goal was to create a mutation that would prevent the girls from contracting HIV, even though there was no specific reason to put them through the process.

"That technology is not safe," said Kiran Musunuru, a genetics professor at the University of Pennsylvania, explaining that the Crispr "scissors" often cut next to the targeted gene, causing unexpected mutations.

"It's very easy to do if you don't care about the consequences," Musunuru added.

Despite the ethical pitfalls, restraint seems mainly to have prevailed so far.

The community is keeping a close eye on Russia, where biologist Denis Rebrikov has said he wants to use Crispr to help deaf parents have children without the disability.

There is also the temptation to genetically edit entire animal species -- malaria-causing mosquitoes in Burkina Faso or mice hosting ticks that carry Lyme disease in the US.

The researchers in charge of those projects are advancing carefully, however, fully aware of the unpredictability of chain reactions on the ecosystem.

Charpentier doesn't believe in the more dystopian scenarios predicted for gene therapy, including American "biohackers" injecting themselves with Crispr technology bought online.

"Not everyone is a biologist or scientist," she said.

And the possibility of military hijacking to create soldier-killing viruses or bacteria that would ravage enemies' crops?

Charpentier thinks that technology generally tends to be used for the better.

"I'm a bacteriologist -- we've been talking about bioterrorism for years," she said. "Nothing has ever happened."

2019 AFP

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2019: the year gene therapy came of age - FRANCE 24

Specific patterns of protein levels in our blood could be used to provide a comprehensive liquid health check that gives a snapshot of health and potentially an indication of the likelihood that we will develop certain diseases or health risk factors in the future, according to research by scientists in the U.S. and U.K. working with SomaLogic. The results of their proof-of-concept study involving more than 16,000 participants, and published in Nature Medicine, showed that while the accuracy of models based on specific protein expression patterns varied, they were all either better predictors than models based on traditional risk factors, or would constitute more convenient and less expensive alternatives to traditional testing.

This proof of concept study demonstrates a new paradigm that measurement of blood proteins can accurately deliver health information that spans across numerous medical specialties and that should be actionable for patients and their healthcare providers, said Peter Ganz, MD, co-leader of this study and the Maurice Eliaser distinguished professor of medicine at UCSF and director of the Center of Excellence in Vascular Research at Zuckerberg San Francisco General Hospital and Trauma Center. I expect that in the future we will look back at this Nature Medicine proteomic study as a critical milestone in personalizing and thus improving the care of our patients. The teams published study is titled, Plasma protein patterns as comprehensive indicators of health.

Preventative medicine programs such as the U.K. National Health Services Health Check and Healthier You programs are aimed at improving individuals health and reducing the risk of developing diseases. While such strategies are inexpensive, cost-effective, and scalable, they could also be made more effective using personalized information about an individuals health and disease risk, the authors suggested. The application of big data in healthcare, assessing and analyzing detailed, large-scale datasets, makes it increasingly feasible to make predictions about health and disease outcomes and enable stratified approaches to prevention and clinical management. Protein scanning represents a potential approach to bridging the gap between the need for practicality and low cost, and the potential for personalized, systemic, and data-driven medicine.

Proteins regulate biological processes and can integrate the effects of genes with the effects of environment, age, existing diseases, and lifestyle behaviors, the authors explained. Our genomes contain about 19,000 genes that code for some 30,000 different proteins. Up to 2,200 of these proteins, including hormones, cytokines, and growth factors, are purposefully secreted into the blood, to orchestrate biological processes in health or in disease. Other proteins enter the blood through leakage from damaged or dead cells. Both secreted and leaked proteins can inform health status and disease risk.

In a proof-of-concept study based on five observational cohorts involving 16,894 participants, the researchers scanned 5,000 proteins in single blood plasma samples taken from each participant, to simultaneously capture the individualized imprints of current health status, the impact of modifiable behaviors, and incident risk of cardiometabolic diseases (diabetes, coronary heart disease, stroke, or heart failure).

To analyze the proteins in each sample the researchers used a technique that harnessed fragments of DNA known as aptamers, which bind to the target protein. In general, only specific fragments will bind to particular proteins. Using existing genetic sequencing technology, the researchers could then search for the aptamers and determine which proteins are present and in what concentrations. In total, the study carried out about 85 million protein measurements in the nearly 17,000 participants.

The researchers analyzed the results using statistical methods and machine learning techniques to develop predictive modelsfor example, that an individual whose blood contains a certain pattern of proteins is at increased risk of developing diabetes. The models covered a number of health states, including levels of liver fat, kidney function and visceral fat, alcohol consumption, physical activity, and smoking behavior, and for risk of developing type 2 diabetes and cardiovascular disease.

The accuracy of the models varied, with some showing high predictive powers, such as for percentage body fat. Other models demonstrated only modest prognostic power, such as that for cardiovascular risk, but even this was still modestly better than traditional risk factors and could also add value in overcoming the incomplete utilization of risk calculation in primary care, the team wrote. Many of the proteins measured linked to a number of health states or conditions. Leptin, for example, modulates appetite and metabolism, and was informative for predictive models of percentage body fat, visceral fat, physical activity, and fitness.

The researchers pointed out that a key feature of the study is that it used information from just one source, a single blood draw, for protein-phenotype models, the authors pointed out. This was a key objective of our health check proof of concept. The team didnt include demographic or known risk factors in their modelsunless absolutely necessary. They also didnt test whether they models could be improved by adding in other features, such as history, laboratory tests, or genetic information. It is possible that these multi-source models could improve absolute models performance, although their inclusion has potential implications for increasing costs and loss of convenience.

One difference between genome sequencing and proteomics approaches is that whereas the genome is fixed, the proteome changes over time, possibly as an individual becomes more obese, less physically active, or smokes, for example. These changes in proteins could be used to track changes in an individuals health status over a lifetime.

Proteins circulating in our blood are a manifestation of our genetic make-up as well as many other factors, such as behaviors or the presence of disease, even if not yet diagnosed, said Claudia Langenberg, M.D., from the MRC Epidemiology Unit at the University of Cambridge. This is one of the reasons why proteins are such good indicators of our current and future health state and have the potential to improve clinical prediction across different and diverse diseases.

While this study shows a proof-of-principle, the researchers acknowledged that there were limitations, and suggested that as technology improves and becomes more affordable, it is feasible that a comprehensive health evaluation using a battery of protein models derived from a single blood sample, could be offered as routine by health services. It is thus conceivable that, with further validation and the potential for expansion of the number of tests, a comprehensive, holistic health evaluation using a battery of protein models derived from a single blood sample could be performed. The next step is to test the applicability of the protein models that we have derived and validated in observational cohorts under research conditions in real-world healthcare systems.

Its remarkable that plasma protein patterns alone can faithfully represent such a wide variety of common and important health issues, and we think that this is just the tip of the iceberg, said study lead Stephen Williams, M.D., chief medical officer at SomaLogic, which is developing its SomaScan Platform and SomaSignal tests for a wide range of human diseases. We have more than a hundred tests in our SomaSignal pipeline and believe that large-scale protein scanning has the potential to become a sole information source for individualized health assessments.

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Blood Test that Measures Expression of 5,000 Proteins Shows Potential as Disease Screening Tool - Clinical OMICs News

SALT LAKE CITY, Nov. 21, 2019 (GLOBE NEWSWIRE) -- Myriad Genetics, Inc. (NASDAQ: MYGN), a leader in molecular diagnostics and precision medicine, announced that Japans Ministry of Health, Labour and Welfare (MHLW) has approved the BRACAnalysis Diagnostic System (i.e., BRACAnalysis) to help physicians determine which women with breast cancer have Hereditary Breast and Ovarian Cancer (HBOC) syndrome and qualify for additional medical management. BRACAnalysis is a genetic test that identifies germline mutations in the BRCA1/2 genes.

We are excited that the MHLW has approved the BRACAnalysis Diagnostic System for HBOC risk assessment in patients with breast cancer, said Seigo Nakamura, M.D., Ph.D., Professor and Chairman, Department of Surgery, Division of Breast Surgical Oncology and Director, Breast Center of Showa University Hospital in Tokyo and president of the Japanese Organization of Hereditary Breast and Ovarian Cancer (JOHBOC). Our goal is to use the BRACAnalysis test to identify patients with BRCA mutations and determine who will benefit from more advanced medical care.

Under the MHLW decision, physicians may use BRACAnalysis to test for BRCA mutations in women with breast cancer who meet the genetic testing guidelines defined by JOHBOC. Those patients who test positive for a deleterious BRCA mutation will be eligible to receive advanced medical management, such as prophylactic surgery or targeted therapies.

Myriads BRACAnalysis test is the gold standard for BRCA testing. The approval of BRACAnalysis for HBOC risk assessment in Japan is further validation of the quality and utility of our pioneering genetic test, said Gary A. King, executive vice president of International Operations, Myriad Genetics. We look forward to working with our commercial partners in Japan to ensure that BRACAnalysis is available to patients.

Myriad has an exclusive partnership with SRL Inc., a subsidiary of Miraca Group, to commercialize the BRACAnalysis Diagnostic System in Japan.

Todays announcement follows two prior regulatory approvals for the BRACAnalysis Diagnostic System in Japan. In February 2019, BRACAnalysis was approved as a companion diagnostic for Lynparza (olaparib) in women with ovarian cancer, and in March 2018, it was approved as a companion diagnostic for Lynparza in patients with metastatic inoperable or recurrent breast cancer.

About the BRACAnalysis Diagnostic SystemBRACAnalysis is a diagnostic system that classifies a patients clinically significant variants (DNA sequence variations) in the germline BRCA1 and BRCA2 genes. Variants are classified into one of the five categories; Deleterious, Suspected Deleterious, Variant of Uncertain Significance, Favor Polymorphism, or Polymorphism. Once the classification is completed, the results are sent to medical personnel in Japan for determining the eligibility of patients for treatment with Lynparza.

About SRLSince the establishment in 1970, SRL, Inc., a member of the Miraca Group, Japan-based leading healthcare group, has been providing comprehensive testing services as the largest commercial clinical laboratory in Japan. SRL carries out nearly 400,000,000 tests per year, covering a wide range of testing services including general/emergency testing, esoteric/research testing, companion diagnostics tests, genomic analysis, and etc. For more information, please visit https://www.srl-group.co.jp/english/.

About Myriad GeneticsMyriad Genetics Inc., is a leading precision medicine company dedicated to being a trusted advisor transforming patient lives worldwide with pioneering molecular diagnostics. Myriad discovers and commercializes molecular diagnostic tests that: determine the risk of developing disease, accurately diagnose disease, assess the risk of disease progression, and guide treatment decisions across six major medical specialties where molecular diagnostics can significantly improve patient care and lower healthcare costs. Myriad is focused on five critical success factors: building upon a solid hereditary cancer foundation, growing new product volume, expanding reimbursement coverage for new products, increasing RNA kit revenue internationally and improving profitability with Elevate 2020. For more information on how Myriad is making a difference, please visit the Company's website: http://www.myriad.com.

Myriad, the Myriad logo, BART, BRACAnalysis, Colaris, Colaris AP, myPath, myRisk, Myriad myRisk, myRisk Hereditary Cancer, myChoice, myPlan, BRACAnalysis CDx, Tumor BRACAnalysis CDx, myChoice CDx, EndoPredict, Vectra, GeneSight, riskScore, Prolaris, ForeSight and Prequel are trademarks or registered trademarks of Myriad Genetics, Inc. or its wholly owned subsidiaries in the United States and foreign countries. MYGN-F, MYGN-G.

Lynparza is a registered trademark of AstraZeneca.

Safe Harbor StatementThis press release contains forward-looking statements within the meaning of the Private Securities Litigation Reform Act of 1995, including statements relating to Japans Ministry of Health, Labour and Welfare (MHLW) marketing approval of the companys BRACAnalysis Diagnostic System to identify patients with breast cancer who would be eligible for additional medical management; the Company working with commercial partners in Japan to ensure that BRACAnalysis is available to patients; and the Company's strategic directives under the caption "About Myriad Genetics." These "forward-looking statements" are based on management's current expectations of future events and are subject to a number of risks and uncertainties that could cause actual results to differ materially and adversely from those set forth in or implied by forward-looking statements. These risks and uncertainties include, but are not limited to: the risk that sales and profit margins of our molecular diagnostic tests and pharmaceutical and clinical services may decline; risks related to our ability to transition from our existing product portfolio to our new tests, including unexpected costs and delays; risks related to decisions or changes in governmental or private insurers reimbursement levels for our tests or our ability to obtain reimbursement for our new tests at comparable levels to our existing tests; risks related to increased competition and the development of new competing tests and services; the risk that we may be unable to develop or achieve commercial success for additional molecular diagnostic tests and pharmaceutical and clinical services in a timely manner, or at all; the risk that we may not successfully develop new markets for our molecular diagnostic tests and pharmaceutical and clinical services, including our ability to successfully generate revenue outside the United States; the risk that licenses to the technology underlying our molecular diagnostic tests and pharmaceutical and clinical services and any future tests and services are terminated or cannot be maintained on satisfactory terms; risks related to delays or other problems with operating our laboratory testing facilities and our healthcare clinic; risks related to public concern over genetic testing in general or our tests in particular; risks related to regulatory requirements or enforcement in the United States and foreign countries and changes in the structure of the healthcare system or healthcare payment systems; risks related to our ability to obtain new corporate collaborations or licenses and acquire new technologies or businesses on satisfactory terms, if at all; risks related to our ability to successfully integrate and derive benefits from any technologies or businesses that we license or acquire; risks related to our projections about our business, results of operations and financial condition; risks related to the potential market opportunity for our products and services; the risk that we or our licensors may be unable to protect or that third parties will infringe the proprietary technologies underlying our tests; the risk of patent-infringement claims or challenges to the validity of our patents or other intellectual property; risks related to changes in intellectual property laws covering our molecular diagnostic tests and pharmaceutical and clinical services and patents or enforcement in the United States and foreign countries, such as the Supreme Court decision in the lawsuit brought against us by the Association for Molecular Pathology et al; risks of new, changing and competitive technologies and regulations in the United States and internationally; the risk that we may be unable to comply with financial operating covenants under our credit or lending agreements; the risk that we will be unable to pay, when due, amounts due under our credit or lending agreements; and other factors discussed under the heading "Risk Factors" contained in Item 1A of our most recent Annual Report on Form 10-K for the fiscal year ended June 30, 2019, which has been filed with the Securities and Exchange Commission, as well as any updates to those risk factors filed from time to time in our Quarterly Reports on Form 10-Q or Current Reports on Form 8-K. All information in this press release is as of the date of the release, and Myriad undertakes no duty to update this information unless required by law.

Media Contact: Ron Rogers(801) 584-3065rrogers@myriad.com

Investor Contact:Scott Gleason(801) 584-1143sgleason@myriad.com

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Myriad Genetics Announces Regulatory Approval of the BRACAnalysis Diagnostic System in Japan for Breast Cancer Patients - BioSpace

Her genetic makeup indicated that she would almost certainly get Alzheimers disease by the age of 50. But one woman escaped that fate. She lived into her 70s before experiencing any issues with thinking skills, and even then avoided the worst of the condition.

Could this womans rare genetic mutation shift our understanding of Alzheimers disease?

Thats the theory from scientists who studied the case of a Colombian woman with a unique quirk of DNA that kept dementia at bay for decades. She was seemingly protected from the effects of Alzheimer's though her brain had already developed a key characteristic of the disease. In a study published earlier this month in the journal Nature Medicine, the researchers note that the findings could shed light on new ways of treating and possibly preventing the degenerative brain disease.

For most people, the causes of Alzheimers are largely unknown and not dictated by genetic predisposition. But the woman, who was not named in the study, was part of a group of Colombian families with a high genetic likelihood of developing early-onset Alzheimers. These 1,200 individuals, most from the town of Yarumal, tend to experience problems with memory and thinking skills at an unusually early age, typically in their 40s.

Yet it wasnt until her 70s that the woman developed any mental problems at all. Later in life she was diagnosed with whats called mild cognitive impairment, where her thinking skills had dulled, but not to the point of a dementia diagnosis. In other words, no Alzheimer's.

Tests on the womans brain showed high levels of amyloid beta, a sticky protein that accumulates into the plaques that have become a hallmark of the disease. But she didnt present any of the symptoms associated with Alzheimers, such as memory loss and behavioral issues. Nor did she show other neurological signs of the disease, like tangles of tau, a protein that accumulates in the brains of Alzheimers patients. She also suffered little neurodegeneration, the death of the brains nerve cells.

So, what kept her healthy for all those years?

In addition to the mutation that causes early-onset Alzheimers, the researchers found another rare mutation, in a gene called APOE. Usually, the gene is known for making molecules that carry cholesterol and other fats through the bloodstream.

Dubbed the Christchurch mutation, after the New Zealand town where it was discovered in 1987, the rare gene may have helped to counteract the negative effects of Alzheimers, staving off the onset of dementia.

And while the study authors note that the groundbreaking case provides new possibilities for treating Alzheimers disease, further research and a larger sample size are needed to establish a link between the Christchurch mutation and protection from the disease.

It has to be hoped that this spurs research into [additional] therapies, saidJohn Hardy, a neuroscientist at University College London who was not involved in the research, in a prepared statement. It is, however, a single case report and it is prudent to be cautious about over-interpreting a single patients data.

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Alzheimer's Plagued Her Family. But a Rare Genetic Mutation Spared This Woman's Mind - Discover Magazine

During the process ofin vitrofertilization (IVF), it is not unusual for embryos to undergo preimplantation genetic diagnosis (PGD) identify specific inherited disease-causing mutations for single-gene disorders, like cystic fibrosis. Recently, new developments in genetics have given the ability to assign individuals "polygenic scores," which can somewhat explain the variability seen in complex human traits. This concept, applied to IVF embryos, has raised the prospect of "designer babies." However, there has been no research published to indicate the potential success of polygenic embryo selection.

"The notion that you could accurately choose your child's height or select for a higher IQ, like in the movie 'Gattaca,' has never been tested," said Dr. Lencz, professor in the Institute of Behavioral Science at the Feinstein Institutes and co-corresponding author of the Cell paper. "Through our research, we can confidently say that trait predictions for embryos based on polygenic scores are not very accurate."

Dr. Lencz and the team analyzed embryo selection for height and IQ in the context of a hypothetical IVF cycle. Investigators used three sources of data to evaluate the efficacy of trait selection, including a mathematically-derived genetic model, simulated embryo genomes, and a real dataset of nuclear families with large numbers of offspring (10 on average) who are now fully-grown adults with available genetic and trait (height) data.

The results concluded that screening for such traits using polygenic scores would leave a large margin for error. For example, children with the highest polygenic score for height were only the tallest in a quarter of families analyzed.

"Dr. Lencz's study adds important data highlighting the unreliability of trait selection by current methods of embryo genetic screening," saidKevin J. Tracey, MD,president and CEO of the Feinstein Institutes.

The ethical and legal debate surrounding polygenic embryo selection is already underway, but, until now, without a solid scientific foundation. The research team hopes that this work will promote an open and evidence-based discussion of these aspects among the public and policymakers.

Previously, an overview of this research was presented at the American Society for Human Genetics Annual Meeting in October by Dr. Lencz's co-lead, Dr. Shai Carmi of the Hebrew University of Jerusalem.

About the Feinstein Institutes The Feinstein Institutes for Medical Researchis the research arm of Northwell Health, the largest health care provider and private employer in New York. Home to 50 research labs, 2,500 clinical research studies and 4,000 researchers and staff, the Feinstein Institutes is raising the standard of medical innovation through its five institutes of behavioral science, bioelectronic medicine, cancer, health innovations and outcomes, and molecular medicine. We're making breakthroughs in genetics, oncology, brain research, mental health, autoimmunity, and bioelectronic medicine a new field of science that has the potential to revolutionize medicine. For more information about how we're producing knowledge to cure disease, visit feinstein.northwell.edu.

SOURCE The Feinstein Institutes for Medical Research

http://www.feinstein.northwell.edu

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New research casts doubt on near reality of 'designer babies' - PRNewswire

Matthew Breen, a professor of genomics at NCState, says his 25-year career has roots in childhood heartbreak.

When I was young, my family had two dogs die from cancer and there was very little we could do to help them, says Breen. There were great strides being made with human cancer research, so why were we unable to help our animal companions more?

We are committed to making that change happen at NCState, he adds.

Today, the internationally recognized researcher specializes in molecular cytogenetics: the study of the structure and function of cells and chromosomes. His work in the College of Veterinary Medicine is helping our pets live longer, healthier lives and unlocking new insights about human cancers along the way.

Since joining NCStates faculty in 2002, Breen has focused on exploring the genetics and genomics of animal diseases, including how they initiate and respond to treatment.

He was a member of the team that sequenced the canine genome 14 years ago. The project sparked a new area of focus in his field: comparing the canine and human genomes to accelerate discoveries for both.

Humans and their furry friends actually share a very similar genetic makeup. And they share certain types of cancers, too. Many cancers diagnosed in humans and dogs have a similar pathology and clinical presentation, says Breen.

But when it comes to canines, its often easier to pinpoint the genetic abnormalities that lead to those cancers. This is especially the case for purebreds. Dogs of the same breed have less genetic variation among them than humans or mixed-breed dogs, making them an ideal genetic model.

Now, Breens lab works extensively in the area and hes become a pioneer in comparative oncology.

By working with human and animal cancers side by side, we are able to find shared features that may help identify the drivers of these cancers and provide opportunities to highlight targets for new therapies, says Breen.

Take, for example, Breens work with the BRAF gene.

Six years ago, his team discovered that a single mutation in the gene was found in 85% of dogs with transitional cell carcinoma (TCC) also called urothelial carcinoma (UC) which is the most common form of bladder cancer in canines. More than 80,000 dogs in the United States will be affected this year alone.

This particular BRAF mutation was already known to exist in some human cancers, but Breens discovery helped unlock its significance for both species. It also revealed an opportunity to create a much-needed tool to aid diagnosis.

By working with human and animal cancers side by side, we are able to find shared features.

In most cases, canine bladder cancer isnt diagnosed until it has reached an advanced stage. Thats because the cancer shares many clinical signs with other, more common urinary tract conditions.

Treatments for the common alternatives may alleviate symptoms temporarily, but they mask the larger problem and buy the cancer more time to progress. In fact, upon diagnosis, more than half of canine bladder cancer cases have already spread.

Identifying the BRAF mutation as a genetic signature of canine bladder cancer was a powerful insight. From there, Breens team began developing a molecular diagnostics test that could identify the mutation and detect the cancer earlier than ever.

That molecular test called CADET BRAF was developed in Breens research laboratory in 2014. Using a urine sample, the system detects cells that possess the BRAF mutation and can monitor changes in the number of mutated cells being shed during treatment of canine TCC and UC.

CADET BRAF represents the worlds first liquid biopsy for the detection of cancer in veterinary medicine, says Breen.

It offers several improvements over current alternatives. Requiring only a simple free-catch urine sample, CADET BRAF is the only non-invasive approach. Other methods often involve costly procedures, such as sedation or anesthesia, that carry additional risks.

The test can also detect bladder cancer in the early stages of the disease, potentially leading to improved outcomes.

CADET BRAF represents the worlds first liquid biopsy for the detection of cancer in veterinary medicine.

We can detect the cancer in dogs that have already presented with clinical signs and avoid repeated attempts to treat solely the signs, says Breen. That allows more time for the veterinarian and owner to develop a plan to treat the root cause. In addition, we have been able to detect the presence of very early disease, several months before the dog has any clinical signs.

Now we have to determine how to manage these preclinical patients, and that is part of ongoing work by our team at NCStates College of Veterinary Medicine, he adds.

The test is also dependable. After rigorous validation of thousands of dogs, Breen says hes found that the presence of the BRAF mutation in canine urine is a highly reliable indicator of the presence of TCC/UC. Weve shown the BRAF mutation isnt found in the urine of healthy dogs or dogs that have other common conditions such as bladder polyps, inflammation or chronic cystitis, he says.

In the two years following the development of CADET BRAF, Breen focused on developing a strong proof of concept. Teaming up with the American Kennel Club, he recruited urine samples from hundreds of dogs to show that the approach could work with real patients.

His next step was commercialization. Breens startup, Sentinel Biomedical, was formed in 2015. Located right on NCStates campus, the company works to develop and scale diagnostic tests for the health care industry.

Since its formation, theyve developed another product called CADET BRAF-PLUS. The test is designed for dogs who dont have the BRAF mutation but do show clinical signs of TCC/UC. It can detect over two-thirds of bladder cancer cases not identified by CADET BRAF, increasing the overall detection sensitivity of the tests to over 95%.

Headquartered right on NCStates campus, Sentinel Biomedical seeks to improve diagnosis and treatment for dogs and their owners.

Find out more

Whats next for Sentinel Biomedical? It recently announced a joint venture with Antech Diagnostics, part of MARS. Together theyve formed Antech Molecular Innovations, also based on NCStates Centennial Campus, and work to broaden access to CADET BRAF and CADET BRAF-PLUS.

With the distribution channels of one of the worlds largest animal health providers, we are providing veterinarians with easy access to the tests we develop and enhancing our ability to become a global leader in innovation for veterinary molecular diagnostics, says Breen. And because our work is translational, we also have greater potential to translate our findings to humans.

This will bring the innovations developed at NCState to a whole new level.

Today, the National Cancer Institute spends $6 billion on cancer research annually, and its estimated that less than 0.5% is directed toward veterinary oncology. But Breen sees his innovations and those of his colleagues across the nation as promising steps in the right direction.

Currently, hes involved in a clinical study in the College of Veterinary Medicine that will evaluate the timeline between when a BRAF mutation is detected in a dogs urine and when that dog begins to show clinical signs of TCC/UC. Breen hopes this knowledge will lead to earlier intervention, improved quality of life and increased survival rates.

This will bring the innovations developed at NCState to a whole new level.

Recent collaborations with colleagues at Duke Cancer Institute are also exploring the genetic and environmental factors shared between canine and human bladder cancers. A study proposed by this multidisciplinary team was awarded funding from the V Foundation for Cancer Research in 2019. Such comparative oncology studies, Breen says, have the potential to realize the true value that dogs can bring to our fight against cancer.

Through Antech Molecular Innovations, Sentinel Biomedical has begun pursuing more projects to provide rapid, accessible molecular diagnostics for a variety of cancers that impact our pets and ourselves.

For now, Breen is excited to see his work take on a wider reach. These cancer detection tests will help a new generation of canine companions and their human friends (maybe even kids who are experiencing what Breen did as a child). Whats more, the increased volumes of data theyll collect may unlock insights that lead to the development of new treatment opportunities for cancers in both species.

Although we may not be able to help all dogs with cancer today, we are driven to learn from their cancers to help the dogs of tomorrow, and the families who care for them, says Breen.

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Sniffing Out Cancer in Canines And Humans, Too - NC State News

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Describing the structure of cilia opens doors to understanding range of diseases

Cilia contain structures called ciliary doublet microtubules. Pictured is a cross section of one of these structures. A new study from Washington University School of Medicine in St. Louis and Harvard Medical School has described the most detailed picture yet of these vital cellular structures. The microtubule is shown in gray, and the newly identified proteins decorating the microtubule are depicted in various colors.

Cilia, or flagella whiplike appendages on cells perform diverse tasks required to keep the body healthy. When cilia malfunction, the consequences can be devastating, causing a range of problems, from blindness, to lung and kidney diseases, to congenital heart defects. Now, scientists have revealed the first detailed look at the inner structure of cilia.

The newly revealed structure offers a starting point to begin exploring how cilia are assembled during development, how they are maintained over a cells life span, and how they might become dysfunctional if some of the cogs in these complex molecular machines are mutated or missing. The structure of these microscopic molecular machines common to cells in organisms from algae to people potentially will answer questions about human health and disease.

The research, by investigators at Washington University School of Medicine in St. Louis and Harvard Medical School, was published recently in the journal Cell.

This new study is exciting because it fills in a lot of missing information about the structure of cilia, said senior author Rui Zhang, PhD, an assistant professor of biochemistry and molecular biophysics at Washington University. When cilia dont work properly, bad things happen. We need to know details of the structure in order to develop treatments for diseases, or strategies to prevent the developmental defects that can occur in the early embryo if the cilia are not functioning as they should.

In the respiratory tract, cilia move mucus and protect against viral and bacterial illnesses. In the reproductive tract, they propel sperm to fertilize an egg. Cilia also perform vital tasks in the brain, the kidney, the pancreas and in bone growth. And in the earliest stages of development, the rotational motion of specialized cilia in the embryo defines the bodys left-right asymmetry and where organs are placed. Without properly functioning cilia, the heart may not end up on the left side, where it should be, and it may not function properly.

Cilia are implicated in multiple human disorders, including polycystic kidney disease, which affects some 600,000 Americans and requires dialysis; primary ciliary dyskinesia, which causes chronic lung disease, misplaced organs and infertility; Bardet-Biedl syndrome, which causes patients to become blind in childhood and leads to diabetes, kidney disease and extreme obesity; and many congenital heart defects, which occur when left-right asymmetry goes awry and require complex surgeries to repair.

In the new study, the researchers used a technique called single particle cryo-electron microscopy to get a first look at 33 specific proteins arranged inside cilia within structures called ciliary microtubule doublets in a strict repeating pattern.

Before this work, everyone assumed these proteins inside cilia just stabilize the structure, which is true for a subset of the proteins, especially when you consider the forces produced by the continuous beating of the cilia, Zhang said. But based on how they are arranged inside this structure, we believe these proteins are doing many more things.

Since many of the proteins protrude through the cilia, Zhang and his colleagues speculate that they may allow for communication between the inside and the outside of the ciliary microtubule doublets; govern the function of enzymes that make important biochemical reactions possible; and sense changes in the calcium concentration of the environment, which plays a role in triggering the cilia to beat.

Among the proteins identified, five are associated with diseases that have been studied in mice and people, said co-author Susan K. Dutcher, PhD, a professor of genetics at Washington University. But until now, no one knew that these proteins were found inside cilia. We are just beginning to understand their roles in normal and disease states.

The researchers studied cilia in a type of algae calledChlamydomonas reinhardtii, which are single-celled organisms that have cilia structurally and biochemically similar to those of more complex organisms, including people. One question Dutcher is interested in answering is how the proteins making up cilia structure govern the type of motion that the cilia perform. The cilia of single-celled C. reinhardtii are capable of more than one type of motion.

In some situations, the cilia are doing what you might consider a breast stroke, Dutcher said. In others, the motion is more of an S-shaped wave. The cilia of many cells in mammals can only produce one of these motions. But the single-celled C. reinhardtii, perhaps to help it adapt to its environment, can switch between them. Thats why were studying algae at a medical school the genetic problems we can study in the cilia of these organisms are similar to the ones that can occur in people, often with devastating consequences.

Zhang, Dutcher and their colleagues have plans to use the latest techniques of cryo-electron microscopy to study the Chlamydomonas mutants of each of the 33 proteins inside cilia to seek answers to many questions that have arisen from this new and detailed knowledge of the structure.

This work was supported by the National Institute of General Medical Sciences (NIGMS) of the National Institutes of Health (NIH), grant number R01GM032843; the International Retinal Research Foundation; the E. Matilda Ziegler Foundation for the Blind; the Smith Family Foundation; and the Pew Charitable Trusts.

Ma M, Stoyanova M, Rademacher G, Dutcher SK, Brown A, Zhang R. Structure of the decorated ciliary doublet microtubule. Cell. Oct. 31, 2019.

Washington University School of Medicines 1,500 faculty physicians also are the medical staff of Barnes-Jewish and St. Louis Childrens hospitals. The School of Medicine is a leader in medical research, teaching and patient care, ranking among the top 10 medical schools in the nation by U.S. News & World Report. Through its affiliations with Barnes-Jewish and St. Louis Childrens hospitals, the School of Medicine is linked to BJC HealthCare.

Original post:
Scientists unravel mysteries of cells' whiplike extensions - Washington University School of Medicine in St. Louis

At the start of this decade, the federal government called out consumer DNA testing as a burgeoning scam industry. Little did we know how it would explode in popularity.

In 2010, the U.S. Government Accountability Office (GAO) published an investigative report that bashed consumer DNA test companies for misleading the public. It accused them of deceptively claiming their products could predict the odds of developing more than a dozen medical conditions; some even went as far to offer equally dubious dietary supplements. The report had followed a similar lambasting of the industry by the GAO in 2006.

Also in 2010, the FDA publicly warned 23andMe and other companies that genetic health tests were considered medical devices and needed to be cleared by the FDA before they could be sold to the public. Three years later, following a lack of response from 23andMe, the agency took the harsh step of temporarily banning 23andMe from selling its health-related tests at all.

Despite these hurdles, the DNA testing industry has nonetheless exploded. According to a report by MIT Technology Review this February, more than 26 million people have had their DNA tested by the biggest names in the industry, with AncestryDNA, 23andMe, and MyHeritage being the top three.

Consumer DNA testing is undoubtedly now mainstreambut its not much less scammy than it was when the decade started.

The industry has existed since the late 1990s. But in 2007, the new kid on the block, 23andMe, became the first company to offer a particular kind of at-home DNA test that was cheap, easy to use, and promised to track back your origins further back than ever before.

23andMes testsand eventually those of its competitorssearch for and analyze the most common genetic variations, called single nucleotide polymorphisms (SNPs), in our autosomal DNA, the 22 of 23 pairs of chromosomes not used to determine sex. For as little as $99 and a spit sample, these SNP-based tests are advertised to determine a persons ancestry or genetic health risks. But much of this realm of consumer DNA testing, as the GAO report showed, can uncharitably be described as complete bullshit.

The crux of the problem is that our genetics are only a piece of the puzzle that influences our health. Sure, you can sometimes point to a specific gene mutation that always makes someone sick in a specific way if they carry it. But much more often, its a complex, barely understood mix of gene variants that predispose us to develop cancer or heart diseaseand that risk can be amplified or muted by our environment (including the crucial months we spend in the womb).

In the earliest days, companies didnt much care for this complexity, using weak evidence to make sweeping health claims about which genes ought to make you more of a fish eater or develop diabetes.

Following the FDAs ban in 2013, 23andMe spent the next two years devising genetic health tests that wouldnt overpromise. In 2015, it was allowed to sell tests that told people if they carried a recessive mutation for genetic conditions like Bloom syndrome and sickle-cell disease. A positive test meant their children would have a 25 percent chance of having the condition if both parents were carriers. Two years later, it became the first company with FDA-approved tests that were allowed to tell people about their risk of developing one of 10 diseases or conditions, such as late-onset Alzheimers or celiac disease.

23andMes return to the health side of things wasnt the only fuse that lit a fire under the consumer DNA industrythe tens of millions in annual advertising now being spent by companies like MyAncestry certainly helped, too. But regardless, the FDAs approval of these tests signaled a new opening in the industry. And unsurprisingly, the industry as a whole has ballooned, as has the glut of scammy services on offer.

Many of these companies now steer clear of making blanket health claims, but it doesnt make them any less laughable. Your DNA results can apparently tell you whether youve found your romantic match, how to be good at soccer, and, like a decade ago, how to find the perfect diet and avoid bloating. Just dont pay attention to the studies showing that theres no consistent link between genes seemingly tied to our nutrition and any actual diet-related conditions.

Its not only the tests vaguely connected to our health that are the problem. As Gizmodo once illustrated, even relying on these DNA tests to figure out your ancestry is a dicey proposition. At best, youre roughly estimating where your recent ancestors lived, but that estimate can vary widely depending on which company does the testing, thanks to the different algorithms they use. And the farther away your lineage is from Europe, the less accurate these tests will be for you, thanks to the fact that the algorithmsas well as the research linking genes to our healthare largely based on the DNA of white Americans and Europeans.

Health and ancestry aside, sharing your DNA with the outside world can have unintended consequences. Law enforcement agencies are now using genealogy databases to solve criminal cases, by connecting anonymous crime scene DNA to DNA submitted to these family tree companies, working backward through distant relatives to identify their suspect. And while some people may be fine with this genetic sleuthing, there are no clear rules on how this data can be used by law enforcementtheres merely the promise by private companies that they will share responsibly. This November, police in Florida obtained a warrant to search through a third-party genealogy database, months after the service had enforced a new opt-in policy meant to let users decide if they wanted their data to be searchable by police in these cases.

At a certain point, it wont even matter whether youve decided to share your DNA. A study last October estimated that once enough peoples DNA is in a databasea scant 2 to 3 percent of any given populationanyone could conceivably track the identity of every person in that population using the same techniques genetic detectives are using now. And researchers have already demonstrated how less scrupulous forces, including hackers, could actively manipulate these databases.

None of this is meant to diminish the real potential of genetics as a field of research and medicine, nor the progress that has been made over the past decade.

Companies like 23andMe rely on detecting thousands of genetic markers still only a tiny slice of our DNA. But the technology that allows a persons entire genome to be sequenced has vastly improved, scaling down its costs and upkeep over the past decade. These techniques can scan a persons whole genome as well as the smaller part of the genome that codes for the proteins our bodys cells make, called the exome.

In 2010, for instance, the company Illumina initially offered its whole genome sequencing at $50,000 a person; this year, Veritas dropped the price of its service to only $600 and says it may soon charge as little as $100.

These innovations have led to large-scale research projects that collect genetic data from hundreds of thousands of people at once. Scientists can scour through these large datasets to find new links between our genes, traits, and medical conditions. This research has helped us better understand longstanding questions about our biology and health. Someday soon, genetic sequencing may also help us optimize the existing medical treatments people get, particularly for conditions like cancer.

Right now, though, its still up in the air how useful this info dump really is to the average person looking to stay healthy.

In March, 23andMe debuted (or more accurately, reintroduced) a service that tells people about their genetic risk of type 2 diabetes. Unlike the tests approved by the FDA, it relies on whats known as a polygenic risk score. This adds up the very small contribution of many genetic markers to a particular condition, which combined might be enough to nudge your overall risk upwards.

The trouble is that these markers have little to do with why you get type 2 diabetesyour age or weight play a much bigger role. And even if the test does consider you genetically unlucky (an average risk difference of 5 percent from a typical person), the advice youll get is the same that anyone hoping for a long, healthy life would get: eat more vegetables and exercise more. This test, as well as many of those offered by the hundreds of big and small DNA testing companies on the market, illustrates the uncertainty of personalized consumer genetics.

The bet that companies like 23andMe are making is that they can untangle this mess and translate their results back to people in a way that wont cross the line into deceptive marketing while still convincing their customers they truly matter. Other companies have teamed up with outside labs and doctors to look over customers genes and have hired genetic counselors to go over their results, which might place them on safer legal and medical ground. But it still raises the question of whether people will benefit from the information they get. And because our knowledge of the relationship between genes and health is constantly changing, its very much possible the DNA test you take in 2020 will tell you a totally different story by 2030.

Given how popular at-home DNA testing has become, theres really no sealing the genie back in the bottle. So if you want to get your genetic horoscope read this holiday, dont let me stop you. But its a big decision you should sleep on. After all, once your DNA is out there, theres no going back.

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Consumer DNA Testing May Be the Biggest Health Scam of the Decade - Gizmodo