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It hasn't been the best quarter for Myriad Genetics, Inc. (NASDAQ:MYGN) shareholders, since the share price has fallen 20% in that time. In contrast the stock is up over the last three years. However, it's unlikely many shareholders are elated with the share price gain of 47% over that time, given the rising market.

Check out our latest analysis for Myriad Genetics

While markets are a powerful pricing mechanism, share prices reflect investor sentiment, not just underlying business performance. One flawed but reasonable way to assess how sentiment around a company has changed is to compare the earnings per share (EPS) with the share price.

Over the last three years, Myriad Genetics failed to grow earnings per share, which fell 37% (annualized).

Thus, it seems unlikely that the market is focussed on EPS growth at the moment. Therefore, we think it's worth considering other metrics as well.

It could be that the revenue growth of 4.2% per year is viewed as evidence that Myriad Genetics is growing. In that case, the company may be sacrificing current earnings per share to drive growth, and maybe shareholder's faith in better days ahead will be rewarded.

You can see below how earnings and revenue have changed over time (discover the exact values by clicking on the image).

NasdaqGS:MYGN Income Statement, December 24th 2019

It's good to see that there was some significant insider buying in the last three months. That's a positive. On the other hand, we think the revenue and earnings trends are much more meaningful measures of the business. So we recommend checking out this free report showing consensus forecasts

Investors in Myriad Genetics had a tough year, with a total loss of 8.9%, against a market gain of about 40%. Even the share prices of good stocks drop sometimes, but we want to see improvements in the fundamental metrics of a business, before getting too interested. Unfortunately, last year's performance may indicate unresolved challenges, given that it was worse than the annualised loss of 6.9% over the last half decade. Generally speaking long term share price weakness can be a bad sign, though contrarian investors might want to research the stock in hope of a turnaround. If you want to research this stock further, the data on insider buying is an obvious place to start. You can click here to see who has been buying shares - and the price they paid.

Myriad Genetics is not the only stock insiders are buying. So take a peek at this free list of growing companies with insider buying.

Please note, the market returns quoted in this article reflect the market weighted average returns of stocks that currently trade on US exchanges.

If you spot an error that warrants correction, please contact the editor at editorial-team@simplywallst.com. This article by Simply Wall St is general in nature. It does not constitute a recommendation to buy or sell any stock, and does not take account of your objectives, or your financial situation. Simply Wall St has no position in the stocks mentioned.

We aim to bring you long-term focused research analysis driven by fundamental data. Note that our analysis may not factor in the latest price-sensitive company announcements or qualitative material. Thank you for reading.

Read the rest here:
Does Myriad Genetics's (NASDAQ:MYGN) Share Price Gain of 47% Match Its Business Performance? - Yahoo Finance

You've likely heard about direct-to-consumer DNA testing kits. In the past few years, at-home genetic testing has been featured in the lyrics of chart-topping songs, and has helped police solve decades-old cold cases, including identifying the Golden State Killer in California.

Even if you don't find a DNA testing kit under your own Christmas tree, there's a good chance someone you know will.

Whether you're motivated to learn about your health or where your ancestors came from, it is important to understand how these tests work - before you spit in the tube.

While exciting, there are things that these genetic testing kits cannot tell users - and important personal implications that consumers should consider.

My main area of research is around clinical genome sequencing, where we look through all of a person's DNA to help diagnose diseases. With a PhD in genetics, I often get questions from friends and family about which direct-to-consumer genetic test they should buy, or requests to discuss results. Most questions are about two types of products: ancestry and health kits.

The most popular ancestry kit is from AncestryDNA. These kits are aimed at giving users insight into where their ancestors might be from. They can also connect users with family members who have used the service and have opted into having their information shared.

Another option is Living DNA, which has a smaller dataset but provides more precise information on the UK and Ireland.

The most popular health kit is from 23andMe. Depending on the user's preference, results include information on predispositions for diseases such as diabetes and Alzheimer's, as well as on the likelihood of having certain traits such as hair colour and taste.

This company also offers ancestry analysis, as well as ancestry and trait-only kits that don't provide health information. The kit offered by the newer MyHeritage DNA also provides a combined ancestry and health option.

There are other kits out there claiming to evaluate everything from athletic potential to relationship compatibility. But gift-buyers beware: for most of these, in contrast to those above, the evidence is seriously lacking.

A direct-to-consumer DNA testing kit. (Shutterstock)

For all of these tests, customers receive a kit in the mail. The kits contain instructions for collecting a saliva sample, which you mail back to the company for analysis.

During this analysis, these popular tests do not look at the entire genome. Instead, they employ single nucleotide polymorphism (SNP) genotyping. As humans we all share 99.9 per cent of our DNA. SNPs are essentially what is left: all of the points at which we can differ from our neighbour, making us unique. SNP genotyping looks at a subset of these sites to "survey" the user's genome.

These SNPs are then compared to reference datasets of individuals with known conditions or ancestry. Most results are based on the SNPs shared with a given group.

For example, if your results say that you are 42 per cent Southeast Asian, it's because 42 per cent of your SNPs were most likely to have come from a group in the reference dataset labelled "Southeast Asian." The same goes for traits and health conditions.

Direct-to-consumer genetic tests are not a substitute for clinical assessment. The methods used differ dramatically from what is done to diagnose genetic diseases.

In a clinical setting, when suspicion of a genetic condition is high, entire genes are often analyzed. These are genes where we understand how changes in the DNA cause cellular changes that can cause the disease. Furthermore, clinical assessment includes genetic counselling that is often key to understanding results.

In contrast, findings from direct-to-consumer genetic tests are often just statistical links; there is commonly no direct disease-causing effect from the SNPs.

Users may interpret a result as positive, when the risk increase is only minimal, or entirely false. These tests can also give false reassurance because they do not sequence genes in their entirety and can miss potentially harmful variants.

These tests are exciting: they introduce new audiences to genetics and get people thinking about their health. They're also helping to build vast genetic databases from which medical research will be conducted.

But for individual users, there are important caveats to consider. Recent reports have questioned the accuracy of these tests: identical twins can receive different results. Furthermore, a lack of diversity in the reference data has caused particular concern regarding accuracy of results for ethnic minorities.

There are also concerns about the way these tests emphasize racial categories that science considers to be social constructs and biologically meaningless.

A recent paper in the British Medical Journal suggests four helpful questions for users to consider. First, users should ask themselves why they want the test. If it is to answer a medical question, then they should speak with their doctor. Users should also think about how they might feel when they receive results containing information they would rather not know.

Users should also consider issues around security and privacy. It is important to read the fine print of the service you're using, and determine whether you're comfortable sharing personal information, now and in the future.

In Canada, policies around genetics have not always kept up with the science. At present, direct-to-consumer genetic testing is unregulated. And, although Canadians have legislative protections against genetic discrimination, those laws are being challenged in the courts, and could change.

Finally, it may also be worth discussing DNA testing with relatives. We share half of our genome with our immediate family members, and smaller fractions with more distant relatives. Genetic results not only affect us, but our family.

Some users may feel they learn more about themselves. For others, results may bring people closer together - not a bad outcome for the holiday season.

At the end of the day, these genetic testing kits are for entertainment: they should not be used to assess health risk in any meaningful way.

If you have any questions related to your health or a genetic disease, discuss these with your family doctor or a suitable health-care professional.

Michael Mackley, Junior Fellow, MacEachen Institute for Public Policy and Governance; Medical Student, Dalhousie University.

This article is republished from The Conversation under a Creative Commons license. Read the original article.

Read more here:
DNA Tests Make a Fun Gift But Here's What You Need to Know Before You Unwrap - ScienceAlert

According to news articles published in early December, Veritas Genetics, a Massachusetts-based company that hoped to lower the cost of whole-genome sequencing, is suspending its U.S. operations because of a lack of investment. Articles theorize that the decreased funding was driven mainly by new CFIUS regulations and heightened CFIUS scrutiny.

Early in December 2019, Veritas announced that its adverse financing situation had forced the suspension of its U.S. business. Veritas has stated that it is assessing potential paths forward, and there are rumors that one such path is the sale of the company. Veritas will no longer sell its tests, which include genetic testing for diseases and cancers (such as the BRCA test), in the United States. Veritas will continue to operate and sell its tests outside the United States.

Veritas first launched in 2014, and since 2015 it had raised $50 million in financing. Major investors included Chinese companies, such as Lilly Asia Ventures, which invested $10 million into the company, and Simcere Pharmaceutical. However, there has been increased scrutiny in the past two years for transactions that involve Chinese investors, especially when sensitive personal information, such as genetic information, is at stake. This year, for example, CFIUS forced iCarbonX, the Chinese, majority owner of U.S. company PatientsLikeMe, to divest its stake in the U.S. company.

According to news reports, recent CFIUS activity may have scared away not only Chinese investors but also non-Chinese investors reluctant to invest in a company with Chinese ownership. Non-Chinese investors may fear that Veritass Chinese ownership will lead to increased CFIUS scrutiny of any investment into Veritas, regardless of the investors nationality. Investors may also worry that CFIUS scrutiny could delay their return on investment if their firms are forced to stall business to address CFIUSs concerns.

No doubt the proposed CFIUS regulations from September also concern foreign investors: the proposed regulations explicitly target U.S. companies that maintain or collect sensitive personal data of U.S. citizens. While most sensitive personal data only triggers the proposed regulations if the U.S. business maintains or collects such data on greater than one million individuals, companies with genetic data are considered to be covered businesses no matter how many individuals are involved. Thus, companies like Veritas will always fall under CFIUS jurisdiction if a foreign person would acquire certain rights in the company. These rights include:

Several genetic and biopharmaceutical companies expressed concern in public comments to the regulations that the proposed regulations, specifically including all genetic data in the definition of sensitive personal data, would stymie foreign investment in these companies. Several companies argued that the Department of the Treasury should revise the proposed CFIUS regulations to require that genetic data be identifiable. Companies often are in possession of anonymized genetic information, which these companies argued does not pose a risk to national security. We await publication of the final regulations and whether CFIUS will make any changes to the definition of sensitive personal data, particularly as it pertains to genetic information. It is to be seen whether U.S. companies in other industries will face similar funding obstacles as foreign investors grow more wary of CFIUS.

Original post:
Veritas, a US Genetic Sequencing Company, Suspends US Operations Due to Decreased Funding; CFIUS Thought to be Leading Cause - Lexology

It always comes back to haunt you.

Thats what Union County Sheriff Brad Whitehead says of crime in general, after his office helped detectives in Colorado arrest a suspect, at last, in a 40-year-old rape-murder case.

On January 16, 1980, Helene Pruszynski a 21-year-old radio intern was raped and murdered in a vacant field in Douglas County, Colo. Her body was found the next morning.

Finding a suspect would take much longer.

It was a combination of DNA, existing technology that was available, but then the dogged police work, 18th Judicial District Attorney (CO) George Brauchler said at a press conference almost 40 years later, upon the arrest and formal charging of James Curtis Clanton, now 62.

It was an investigation that turned up occasional suspects but just as many dead ends. Clanton, who at the time of Pruszynskis death went by the name Curtis Allen White, had been convicted of rape in Arkansas in 1975 but was paroled less than four years later. He also was arrested in Palm Beach County, Fla. on a domestic battery charge in 1998.

But despite DNA found at the crime scene, investigators couldnt connect Clanton to the crime in Colorado, at least not until some of those dead ends spawned different approaches.

RELATED: Florida man charged with murder, kidnapping in 1980 death of Colorado radio intern

In one key instance, investigators had begun to suspect a man named William White Jr., who had a criminal history. Whites DNA would prove to be an imperfect match with evidence at the Pruszyinski murder scene and he was cleared. But then detectives used a relatively new technique called genetic genealogy, which allows investigators to essentially climb "up" a family tree from an eliminated suspect to ancestors often with the help of online DNA databases to find viablesuspects among common descendants. It would turn out, White and Clanton are brothers.

Eventually, it was determined that Clanton was living in Lake Butler, Fla. and had resided there at least a decade. According to Whitehead, Clanton had no encounters with local law enforcement during those years.

In a town where Whitehead says many people grow up together and know each other, it wasnt difficult to learn that Clanton was a regular at the Full House Lounge on Fourth Avenue.

He was always a laid-back, cool guy," Tom Christakes told First Coast News at a bar. "I dont know him other than just coming here and playing pool.

Christakes added that hed been acquainted with Clanton for about five years.

I actually taught him how to bank playing pool, just a couple weeks ago,: he said. But Im, like, completely shocked.

Investigators in Douglas County, Col. asked the Union County Sheriffs Office to try getting a sample of Clantons DNA. Thats when a deputy who knew the owner of the Full House Lounge arranged a plan to retrieve a beer mug after Clanton used it. The mug was retrieved Nov. 30.

Within days, Whitehead says a DNA match was confirmed. Police arrested Clanton without incident at his home Dec. 11.

He parked his truck where he normally always does, Douglas County Sheriff Tony Spurlock said in a press conference Dec.16. Got out of his truck and was walking away from it, when he was taken in to custody.

Whitehead added, I believe once he saw us, that he felt like he knew his past had caught up with him.

Clanton was extradited to Colorado, where he was formally charged with four murder-related counts and one of kidnapping on Monday, Dec. 16. The District Attorneys office in Colorados 18th judicial district tells First Coast News its still considering whether to pursue the death penalty against Clanton.

Whatever that decision will be, District Attorney Brauchler offered a stern-yet-satisfied summation of Clantons arrest particularly the modern methods that he says solved the cold case.

There are crimes yet unsolved today that I have great optimism because of cases like this, that were going to end up solving, Brauchler told the media. And I think the public ought to feel good about that, and I think murderers ought to be scared to death of it.

In a statement on Facebook, a woman named Janet Johnson, who says Helene Pruszynski was her sister, asked that her familys privacy be respected, offering the following statement:

"I want people to know what a special person Helene was. My sister was my best friend. She was a loving daughter, sister, aunt, & friend. Helene was on track to do great things, she had a bright future ahead of her. There has not been a day that goes by that we haven't missed her. The detectives and everyone else who helped to make this day happen are my heroes. I look forward to justice being served.

More here:
'I think murderers ought to be scared to death of it...' Genetic genealogy leads to arrest of Florida man in 40-year-old cold case murder -...

This article, written byMichael Mackley, Dalhousie University, originally appeared on The Conversation and is republished here with permission:

Youve likely heard about direct-to-consumer DNA testing kits. In the past few years, at-home genetic testing has been featured in the lyrics of chart-topping songs, and has helped police solve decades-old cold cases, including identifying the Golden State Killer in California.

Even if you dont find a DNA testing kit under your own Christmas tree, theres a good chance someone you know will.

Whether youre motivated to learn about your health or where your ancestors came from, it is important to understand how these tests work before you spit in the tube.

While exciting, there are things that these genetic testing kits cannot tell users and important personal implications that consumers should consider.

Health, traits and ancestry kits

My main area of research is around clinical genome sequencing, where we look through all of a persons DNA to help diagnose diseases. With a PhD in genetics, I often get questions from friends and family about which direct-to-consumer genetic test they should buy, or requests to discuss results. Most questions are about two types of products: ancestry and health kits.

The most popular ancestry kit is from AncestryDNA. These kits are aimed at giving users insight into where their ancestors might be from. They can also connect users with family members who have used the service and have opted into having their information shared. Another option is Living DNA, which has a smaller dataset but provides more precise information on the U.K. and Ireland.

The most popular health kit is from 23andMe. Depending on the users preference, results include information on predispositions for diseases such as diabetes and Alzheimers, as well as on the likelihood of having certain traits such as hair colour and taste. This company also offers ancestry analysis, as well as ancestry and trait-only kits that dont provide health information. The kit offered by the newer MyHeritage DNA also provides a combined ancestry and health option.

There are other kits out there claiming to evaluate everything from athletic potential to relationship compatibility. But gift-buyers beware: for most of these, in contrast to those above, the evidence is seriously lacking.

How these tests work

For all of these tests, customers receive a kit in the mail. The kits contain instructions for collecting a saliva sample, which you mail back to the company for analysis.

During this analysis, these popular tests do not look at the entire genome. Instead, they employ single nucleotide polymorphism (SNP) genotyping. As humans we all share 99.9 per cent of our DNA. SNPs are essentially what is left: all of the points at which we can differ from our neighbour, making us unique. SNP genotyping looks at a subset of these sites to survey the users genome.

These SNPs are then compared to reference datasets of individuals with known conditions or ancestry. Most results are based on the SNPs shared with a given group. For example, if your results say that you are 42 per cent Southeast Asian, its because 42 per cent of your SNPs were most likely to have come from a group in the reference dataset labelled Southeast Asian. The same goes for traits and health conditions.

How they differ from clinical tests

Direct-to-consumer genetic tests are not a substitute for clinical assessment. The methods used differ dramatically from what is done to diagnose genetic diseases.

In a clinical setting, when suspicion of a genetic condition is high, entire genes are often analyzed. These are genes where we understand how changes in the DNA cause cellular changes that can cause the disease. Furthermore, clinical assessment includes genetic counselling that is often key to understanding results.

In contrast, findings from direct-to-consumer genetic tests are often just statistical links; there is commonly no direct disease-causing effect from the SNPs.

Users may interpret a result as positive, when the risk increase is only minimal, or entirely false. These tests can also give false reassurance because they do not sequence genes in their entirety and can miss potentially harmful variants.

Before you spit in a tube, stop and think

These tests are exciting: they introduce new audiences to genetics and get people thinking about their health. Theyre also helping to build vast genetic databases from which medical research will be conducted.

But for individual users, there are important caveats to consider. Recent reports have questioned the accuracy of these tests: identical twins can receive different results. Furthermore, a lack of diversity in the reference data has caused particular concern regarding accuracy of results for ethnic minorities.

There are also concerns about the way these tests emphasize racial categories that science considers to be social constructs and biologically meaningless.

A recent paper in the British Medical Journal suggests four helpful questions for users to consider. First, users should ask themselves why they want the test. If it is to answer a medical question, then they should speak with their doctor. Users should also think about how they might feel when they receive results containing information they would rather not know.

Users should also consider issues around security and privacy. It is important to read the fine print of the service youre using, and determine whether youre comfortable sharing personal information, now and in the future.

In Canada, policies around genetics have not always kept up with the science. At present, direct-to-consumer genetic testing is unregulated. And, although Canadians have legislative protections against genetic discrimination, those laws are being challenged in the courts, and could change.

Finally, it may also be worth discussing DNA testing with relatives. We share half of our genome with our immediate family members, and smaller fractions with more distant relatives. Genetic results not only affect us, but our family.

Bottom line: Its all for fun

Some users may feel they learn more about themselves. For others, results may bring people closer together not a bad outcome for the holiday season.

At the end of the day, these genetic testing kits are for entertainment: they should not be used to assess health risk in any meaningful way.

If you have any questions related to your health or a genetic disease, discuss these with your family doctor or a suitable health-care professional.

Michael Mackley, Junior Fellow, MacEachen Institute for Public Policy and Governance; Medical Student, Dalhousie University

This article is republished from The Conversation under a Creative Commons license. Read the original article.

Read the rest here:
BEYOND LOCAL: DNA tests might be a fun holiday gift, but beware of the hype - TimminsToday

BOTHELL, Wash.--(BUSINESS WIRE)--Seattle Genetics, Inc. (Nasdaq:SGEN) today announced it has completed the submission of a New Drug Application (NDA) to the U.S. Food and Drug Administration (FDA) for tucatinib. This NDA requests FDA approval of tucatinib in combination with trastuzumab and capecitabine for treatment of patients with locally advanced unresectable or metastatic HER2-positive breast cancer, including patients with brain metastases, who have received at least three prior HER2-directed agents separately or in combination, in the neoadjuvant, adjuvant or metastatic setting. The submission is based on the results of HER2CLIMB, a randomized pivotal trial comparing tucatinib added to trastuzumab and capecitabine versus trastuzumab and capecitabine alone. HER2CLIMB trial results were presented on December 11, 2019 at the 2019 San Antonio Breast Cancer Symposium and published in the New England Journal of Medicine. Tucatinib is an oral, small molecule tyrosine kinase inhibitor (TKI) that is highly selective for HER2.

Tucatinib was recently granted Breakthrough Therapy designation by the FDA in combination with trastuzumab and capecitabine, for treatment of patients with locally advanced unresectable or metastatic HER2-positive breast cancer, including patients with brain metastases, who have been treated with trastuzumab, pertuzumab, and T-DM1. This designation was based on data from the HER2CLIMB trial.

Todays submission marks another important milestone for Seattle Genetics and tucatinib, and a potential advance for patients with either locally advanced or metastatic HER2-positive breast cancer, including those with and without brain metastases, said Roger Dansey, M.D., Chief Medical Officer at Seattle Genetics. We look forward to working with the FDA on the review of this application.

About HER2-Positive Breast Cancer

Patients with HER2-positive breast cancer have tumors with high levels of a protein called human epidermal growth factor receptor 2 (HER2), which promotes the aggressive spread of cancer cells. An estimated 271,270 new cases of invasive breast cancer will be diagnosed in the U.S. in 2019.1 Between 15 and 20 percent of breast cancer cases worldwide are HER2-positive.2 Historically, HER2-positive breast cancer tends to be more aggressive and more likely to recur than HER2-negative breast cancer.2, 3, 4 In patients with metastatic breast cancer, the most common site of first metastasis is in bone, followed by lung, brain, and liver.5, 6 Up to 50 percent of metastatic HER2-positive breast cancer patients develop brain metastases over time.2, 7 Despite recent treatment advances, there is still a significant need for new therapies that can impact metastatic disease, especially brain metastases. There are currently no approved therapies demonstrating progression-free survival or overall survival benefit for the treatment of patients with HER2-positive metastatic breast cancer after progression on T-DM1.8, 9, 10

About HER2CLIMB

HER2CLIMB is a multinational randomized (2:1), double-blind, placebo-controlled, active comparator, pivotal clinical trial comparing tucatinib in combination with trastuzumab and capecitabine compared with trastuzumab and capecitabine alone in patients with locally advanced unresectable or metastatic HER2-positive breast cancer who were previously treated with trastuzumab, pertuzumab, and T-DM1. The primary endpoint of the trial was PFS per Response Evaluation Criteria in Solid Tumors (RECIST) v1.1 as determined by blinded independent central review (BICR) in the first 480 patients enrolled in the trial. HER2CLIMB enrolled a total of 612 patients to support the analyses of key secondary endpoints, including overall survival, PFS per BICR in patients with brain metastases at baseline, and confirmed objective response rate. Safety data were evaluated throughout the study.

About Tucatinib

Tucatinib is an investigational, orally bioavailable, potent tyrosine kinase inhibitor that is highly selective for HER2 without significant inhibition of EGFR. Inhibition of EGFR has been associated with significant toxicities, including skin rash and diarrhea. Tucatinib has shown activity as a single agent and in combination with both chemotherapy and other HER2 targeted agents such as trastuzumab.1, 2 Studies of tucatinib in these combinations have shown activity both systemically and in brain metastases. HER2 is a growth factor receptor that is overexpressed in multiple cancers, including breast, colorectal, and gastric cancers. HER2 mediates cell growth, differentiation, and survival. Tucatinib has been granted orphan drug designation by the FDA for the treatment of breast cancer patients with brain metastases.

In addition to HER2CLIMB, tucatinib is being evaluated in a randomized, double-blind, placebo-controlled, multi-center phase 3 trial of tucatinib in combination with T-DM1 compared to T-DM1 alone, in patients with unresectable locally advanced or metastatic HER2-positive breast cancer, including those with brain metastases, who have had prior treatment with a taxane and trastuzumab. The primary endpoint is progression-free survival per RECIST criteria. Secondary endpoints include overall survival, objective response rate, and duration of response. The trial is being conducted in North America and is expected to enroll approximately 460 patients. More information about the phase 3 trial, including enrolling centers, is available at http://www.clinicaltrials.gov.

Tucatinib is also being evaluated in a multi-center, open-label, single-arm phase 2 clinical trial known as MOUNTAINEER, which is evaluating tucatinib in combination with trastuzumab in patients with HER2-positive, RAS wildtype metastatic, or unresectable colorectal cancer. The primary endpoint of the trial is objective response rate by RECIST criteria. Progression-free survival, duration of response, overall survival, and safety and tolerability of the combination regimen are secondary objectives. Results for 26 patients were evaluated in an analysis and presented at the European Society for Medical Oncology (ESMO) 2019 Congress. Enrollment is ongoing. More information about the MOUNTAINEER trial, including enrolling centers, is available at http://www.clinicaltrials.gov.

About Seattle Genetics

Seattle Genetics, Inc. is a global biotechnology company that discovers, develops, and commercializes transformative medicines targeting cancer to make a meaningful difference in peoples lives. ADCETRIS (brentuximab vedotin) and PADCEV (enfortumab vedotin-ejfv) use the companys industry-leading antibody-drug conjugate (ADC) technology designed to bring a powerful medicine directly to cancer cells. ADCETRIS is approved for the treatment of several types of CD30-expressing lymphomas, and PADCEV is approved to treat adults with metastatic urothelial cancer. In addition, investigational agent tucatinib, a small molecule tyrosine kinase inhibitor, is in late-stage development for HER2-positive metastatic breast cancer, and in clinical development for metastatic colorectal cancer. The company is headquartered in Bothell, Washington, and has offices 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 FDA approval of tucatinib in combination with trastuzumab and capecitabine for treatment of patients with locally advanced unresectable or metastatic HER2-positive breast cancer, including patients with brain metastases, who have received at least three prior HER2-directed agents separately or in combination, in the neoadjuvant, adjuvant or metastatic setting; the therapeutic potential of tucatinib, including its possible efficacy, safety and therapeutic uses and anticipated development activities including ongoing and future clinical trials. 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 New Drug Application submission based on the HER2CLIMB trial may not be accepted for filing by, or ultimately approved by, the FDA in a timely manner or at all or with the requested label; the difficulty and uncertainty of pharmaceutical product development; the risk of adverse events or safety signals; and the possibility of disappointing results in ongoing or future clinical trials despite earlier promising clinical results. 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 September 30, 2019 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:

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Seattle Genetics Announces Submission of Tucatinib New Drug Application to the U.S. FDA for Patients with Locally Advanced or Metastatic HER2-Positive...

Here we are at the end of yet another year, a year that definitely went by faster than the year before or for that matter the year before that. And as ever at this time of year tis the season for casting ahead and divining what the future holds, delivering lists of top 10s and predictions of what will be hot and what will not.

In some fields, the resultant list will look very much like something delivered by the toss of a coin, but in the science and research areas it is pretty certain what will land in the top two or three subjects.

Number one has got to be climate and the impact of global warming. There is no other area that can match it for the variety and depth of research activity being applied to a whole range of climate-related subjects. And the hard news stories keep tumbling out of this endeavour, helping to show that global changes are taking place due to the alterations in climate that we as humans have set in motion.

One peer-reviewed study about the increasingly rapid loss of ice mass over Greenland was published less than a fortnight before Christmas. It showed that the biggest block of land ice in the northern hemisphere was melting away much faster than expected, seven times faster the study suggests.

Published in the journal Nature, it said the island lost 33 billion tonnes of ice on average during the last decade of the 20th century but the average annual ice loss for the most recent 10 years now stands at 254 billion tonnes of ice a year.

This is just one story and one research area, but climate-related studies arise in many fields from alteration of ocean currents to changed rainfall patterns and from species loss to poor air quality. It is also a subject area that affects us all given the potential of coastal flooding, crop losses and human migration to name but a few possible future impacts.

The impacts for humanity are also there in research into new ways to alter our genetic blueprints. The key to unlocking the potential to overcome gene-based diseases relates CRISPR CAS9, our current best technology for getting into the genome and then adding, deleting or altering individual genes.

It has the potential to reverse disease states by correcting unwanted mutations. It is being used in labs around the world as scientists seek to fully understand the method and apply it to alter genes. It is a powerful research tool, for example to create a mouse model that imitates a human disease state and then developing and testing drugs that might be used in humans. It also allows the researcher to look for any unwanted downstream effects arising from genetic alterations.

There are so many scientists using the CRISPR tools that news reports and discoveries will certainly follow. Yet most research scientists are concerned about the lack of controls or limits on what kind of genetic experiments that might be conducted on the human genome. Too little is known about unexpected problems if a number of genes are altered to eliminate a genetic disorder.

There is also the issue of genetic alteration of the germline, the genetic material that moves across to the next generation. There is currently an international block on germline alterations but that has not stopped at least one researcher who went ahead and created the worlds first two genetically modified humans. Breakthroughs will be delivered all through 2020 it is probably safe to say.

What might come third in this short list is up for grabs, and what might produce the next big scientific discovery could come from any direction. For that reason this report becomes a wish list relevant to Irish research and scientific endeavour related to our engagement with important international research bodies.

One of the most important decisions in this regard brings us closer to membership of Cern, Europes premier nuclear research body. A Dil committee studied the research and commercial potential arising from membership and called on the Government to join Cern as quickly as possible.

Cerns huge atom smasher confirmed the existence of the Higgs Boson, an international effort that involved many countries. Ireland could become more involved in this kind of research if it were a member. The Government has already taken the leap and announced our membership of the European Southern Observatory.

Our astronomers and physicists can now get access to some of the worlds largest telescopes based in Chile. The ESO is also a mill for discoveries and this membership gives us the potential to become international players in this field. And in more familiar territory, the Government has renewed its commitment to invest 100 million in the European Space Agency between now and 2024, a decision that ensures Ireland can bid for commercial contracts and researchers can participate in ESA activities. Our investment pays for itself given Irish companies can share in contracts.

All of the research areas mentioned here show how important it is to internationalise Irelands involvement in science. By doing this, we give more opportunities to promising young Irish scientists and help build a strong international reputation for research. Certainly that is not too much to ask for this Christmas.

Originally posted here:
Another year of climate change, genetics and Irish scientific ambition - The Irish Times

Biodiversity the variation in all living organisms is one of Africas richest assets. As a result, its genetic material is coveted by scientists, biotechnology companies and research institutes globally. For decades, there has been a flow of data and biosamples from the African continent to the global north. This has often been in the absence of legitimate participant consent, community engagement or data or material transfer agreements.

Biopiracy the act of directly or indirectly taking undue advantage of research participants and communities in global health research has a long and contentious history in Africa. A recent case occurred during the West African Ebola outbreak between 2014 and 2016 when thousands of biological specimens left the continent without consent. Very often there is minimal benefit sharing.

The issue has been in the news again in South Africa. Accusations have been levelled against the Wellcome Sanger Institute in the UK for allegedly attempting to commercialise data obtained from various African universities. This has reignited questions around models of consent in research, donor rights, biopiracy and genomic sovereignty.

The latest revelations show that legislation as well as academic research governance bodies have failed to adequately safeguard the rights of vulnerable participants in genomics research.

One missing piece of the puzzle is the limited empirical data on the views of people whose biosamples are taken in the name of research. This would include issues of ownership, future use, export, benefit-sharing and commercialisation.

In 2011 and 2012 we surveyed participants to better understand their views. We recruited participants who had experience with research, the consent process and use of biological samples. They were engaged in studies at academic research units attached to public hospitals and private research centres.

Our findings remain relevant today as many of the issues raised by the people we spoke to have still not been addressed.

Our study was conducted over a 10 month period from September 2011 to June 2012. We sampled 200 participants in the Western Cape and Gauteng provinces in South Africa. Participants who had already consented to use of their blood for research were asked several questions including the following: how they felt about their samples being stored for future use and about them being sent abroad to foreign countries, as well as the possibility of future commercialisation.

Most participants were supportive of research. But many expressed concerns about export of their blood samples and data out of South Africa.

For their part, researchers viewed the biosamples as donations. But participants believed they had ownership rights and were keen on benefit sharing. Almost half of the participants were not in favour of broad consent delegated to a research ethics committee. Their preference was to be contacted again for consent in the future.

The legitimacy of using broad consent models for genomic research and biobanking occupies a contested space among bioethicists and researchers globally. Broad consent allows researchers to use biosamples and data indefinitely for future research.

Usually, with broad consent, future research must be approved by a Research Ethics Committee (a diverse group of experts from different research, medical, legal and ethics disciplines) and it is then not necessary to contact donors and ask for their permission to conduct research with their samples or data again.

But this type of consent is particularly contentious in resource depleted countries. This is because research participants often dont understand the complex scientific jargon used in consent documents or processes, especially where use of their samples or data in the future is concerned. This includes commercialisation.

Strong privacy protection legislation and other similar laws require specific consent. This means that individual participants need to consent to use of their data in a specific project or disease category. This makes it challenging to understand how broad consent (delegated to a research ethics committee) for unspecified future use can be legally obtained in research.

This is particularly concerning where future commercialisation may be included in broad consent models without being explicitly discussed with participants. The language used to explain commercialisation is often vague and not fully comprehensible by vulnerable populations.

South Africa also has protocols in place. For example, clear, explicit, voluntary informed consent is required for all use of data and samples belonging to research participants. If data or samples are to be transferred to other researchers in South Africa or abroad, participants ought to be aware of this and can then consent or decline. However, this is not always what happens.

In addition, if data is to be shared with another institution, a data transfer agreement or material transfer agreement must be signed prior to the transfer. This too does not always happen.

South Africa needs to up its game and reform governance around research ethics. This is particularly necessary in the context of international collaborative research. Good governance needs to incorporate transparency, fairness and honesty.

Research ethics committees and researchers need to ensure that data transfer agreements or material transfer agreements are in place prior to sharing of samples or data.

More importantly, community representatives on research ethics committees should be empowered to review consent documents to establish if appropriate language is used to explain commercialisation and data or sample sharing.

A tiered consent model gives participants choice in terms of how their data or samples could be used in the future. This happens when participants choose what they agree to in the consent document. It also allows for specific choices to be voiced on benefit sharing for participants or their respective communities.

In addition, authentic community engagement with co-creation of knowledge production and benefit sharing is essential to ensure equity in global research.

Read more from the original source:
Africa's genetic material is still being misused - The Conversation Africa

BOTHELL, Wash.--(BUSINESS WIRE)--Seattle Genetics, Inc. (Nasdaq:SGEN) today announced that the U.S. Food and Drug Administration (FDA) has granted Breakthrough Therapy designation to tucatinib, in combination with trastuzumab and capecitabine, for treatment of patients with locally advanced unresectable or metastatic HER2-positive breast cancer, including patients with brain metastases, who have been treated with trastuzumab, pertuzumab, and T-DM1. The positive topline results of the pivotal HER2CLIMB clinical trial were announced in October 2019, and additional data were presented at the 2019 San Antonio Breast Cancer Symposium (SABCS) on December 11, 2019 and were simultaneously published in the New England Journal of Medicine (NEJM). Tucatinib is an oral, small molecule tyrosine kinase inhibitor (TKI) that is highly selective for HER2.

The FDAs Breakthrough Therapy process is intended to expedite the development and review of promising drug candidates intended for serious or life-threatening conditions. Designation is based upon preliminary clinical evidence of the potential for substantial improvement over existing therapies on one or more clinically significant endpoints.

The addition of tucatinib to the commonly used combination of trastuzumab and capecitabine demonstrated superior activity compared to trastuzumab and capecitabine alone in patients with unresectable locally advanced or metastatic HER2-positive breast cancer, including those with and without brain metastases, said Roger Dansey, M.D., Chief Medical Officer at Seattle Genetics. The decision by the FDA to grant Breakthrough Therapy designation to tucatinib recognizes the urgent need for new medicines that can impact the lives of those with HER2-positive metastatic breast cancer. We intend to submit a New Drug Application to the FDA and an MAA to the EMA by the first quarter 2020, with the goal of making tucatinib available to patients in this setting as soon as possible.

This Breakthrough Therapy designation was based on data from the pivotal HER2CLIMB clinical trial, which compared tucatinib in combination with trastuzumab and capecitabine to trastuzumab and capecitabine alone in patients with locally advanced unresectable or metastatic HER2-positive breast cancer. Patients had previously received trastuzumab, pertuzumab and ado-trastuzumab emtansine (T-DM1). Patients had received a median of four prior lines of therapy overall and three in the metastatic setting. Forty-seven percent of the patients enrolled in the trial had brain metastases at the time of enrollment.

Data presented at SABCS and published in NEJM include the primary endpoint of progression-free survival (PFS) as assessed by blinded independent central review (BICR) in the first 480 patients enrolled in the trial. The primary endpoint of PFS showed that the addition of tucatinib was superior to trastuzumab and capecitabine alone, with a 46 percent reduction in the risk of disease progression or death (hazard ratio (HR)=0.54 (95% Confidence Interval (CI): 0.42, 0.71); p<0.00001). The trial met the two key secondary endpoints at interim analysis. The tucatinib arm demonstrated an improvement in overall survival, with a 34 percent reduction in the risk of death (HR=0.66 [95% CI: 0.50, 0.88]; p=0.0048), compared to the control arm. For patients with brain metastases at baseline, the tucatinib arm also demonstrated superior PFS, with a 52 percent reduction in the risk of disease progression or death, compared to the control arm (HR=0.48 [95% CI: 0.34, 0.69]; p<0.00001).

Tucatinib in combination with trastuzumab and capecitabine was generally well tolerated. The most common adverse events occurring in more than 20 percent of patients in the tucatinib arm vs. the control arm included diarrhea, palmar-plantar erythrodysaesthesia syndrome (PPE), nausea, fatigue, and vomiting. Discontinuation of tucatinib and placebo due to adverse events was 5.7 percent in the tucatinib arm and 3.0 percent in the control arm. Greater than or equal to Grade 3 diarrhea was seen in 12.9 percent of the patients in the tucatinib arm vs. 8.6 percent in the control arm. Antidiarrheal prophylaxis was not required per protocol. Antidiarrheals were used in less than half of all cycles where diarrhea was reported. In both treatment arms, when used, the duration of antidiarrheal treatment was short (median of 3 days/cycle). Greater than or equal to Grade 3 aspartate aminotransferase (AST) was seen in 4.5 percent of the patients in the tucatinib arm vs. 0.5 percent in the control arm, and alanine aminotransferase (ALT) elevation in 5.4 percent vs. 0.5 percent, respectively. Discontinuations due to liver transaminase elevations were infrequent in both arms (ALT: 1.0 vs. 0.5 percent; AST: 0.7 vs. 0.5 percent).

About HER2-Positive Breast Cancer

Patients with HER2-positive breast cancer have tumors with high levels of a protein called human epidermal growth factor receptor 2 (HER2), which promotes the aggressive spread of cancer cells. An estimated 271,270 new cases of invasive breast cancer will be diagnosed in the U.S. in 2019.1 Between 15 and 20 percent of breast cancer cases worldwide are HER2-positive.2 Historically, HER2-positive breast cancer tends to be more aggressive and more likely to recur than HER2-negative breast cancer.2, 3, 4 In patients with metastatic breast cancer, the most common site of first metastasis is in bone, followed by lung, brain, and liver.5, 6 Up to 50 percent of metastatic HER2-positive breast cancer patients develop brain metastases over time.2, 7 Despite recent treatment advances, there is still a significant need for new therapies that can impact metastatic disease, especially brain metastases. There are currently no approved therapies demonstrating progression-free survival or overall survival benefit for the treatment of patients with HER2-positive metastatic breast cancer after progression on T-DM1.8, 9, 10

About HER2CLIMB

HER2CLIMB is a multinational randomized (2:1), double-blind, placebo-controlled, active comparator, pivotal clinical trial comparing tucatinib in combination with trastuzumab and capecitabine compared with trastuzumab and capecitabine alone in patients with locally advanced unresectable or metastatic HER2-positive breast cancer who were previously treated with trastuzumab, pertuzumab and T-DM1. The primary endpoint of the trial was PFS per Response Evaluation Criteria in Solid Tumors (RECIST) v1.1 as determined by blinded independent central review (BICR) in the first 480 patients enrolled in the trial. HER2CLIMB enrolled a total of 612 patients to support the analyses of key secondary endpoints, including overall survival, PFS per BICR in patients with brain metastases at baseline and confirmed objective response rate. Safety data were evaluated throughout the study.

About Tucatinib

Tucatinib is an investigational, orally bioavailable, potent tyrosine kinase inhibitor that is highly selective for HER2 without significant inhibition of EGFR. Inhibition of EGFR has been associated with significant toxicities, including skin rash and diarrhea. Tucatinib has shown activity as a single agent and in combination with both chemotherapy and other HER2 targeted agents such as trastuzumab.1,2 Studies of tucatinib in these combinations have shown activity both systemically and in brain metastases. HER2 is a growth factor receptor that is overexpressed in multiple cancers, including breast, colorectal and gastric cancers. HER2 mediates cell growth, differentiation and survival. Tucatinib has been granted orphan drug designation by the FDA for the treatment of breast cancer patients with brain metastases.

In addition to HER2CLIMB, tucatinib is being evaluated in a randomized, double-blind, placebo-controlled, multi-center phase 3 trial of tucatinib in combination with T-DM1 compared to T-DM1 alone, in patients with unresectable locally advanced or metastatic HER2-positive breast cancer, including those with brain metastases, who have had prior treatment with a taxane and trastuzumab. The primary endpoint is progression-free survival per RECIST criteria. Secondary endpoints include overall survival, objective response rate and duration of response. The trial is being conducted in North America and is expected to enroll approximately 460 patients. More information about the phase 3 trial, including enrolling centers, is available at http://www.clinicaltrials.gov.

Tucatinib is also being evaluated in a multi-center, open-label, single-arm phase 2 clinical trial known as MOUNTAINEER, which is evaluating tucatinib in combination with trastuzumab in patients with HER2-positive, RAS wildtype metastatic or unresectable colorectal cancer. The primary endpoint of the trial is objective response rate by RECIST criteria. Progression-free survival, duration of response, overall survival and safety and tolerability of the combination regimen are secondary objectives. Results for 26 patients were evaluated in an analysis and presented at the European Society for Medical Oncology (ESMO) 2019 Congress. Enrollment is ongoing. More information about the MOUNTAINEER trial, including enrolling centers, is available at http://www.clinicaltrials.gov.

About Seattle Genetics

Seattle Genetics, Inc. is an emerging multi-product, global biotechnology company that develops and commercializes transformative therapies targeting cancer to make a meaningful difference in peoples lives. ADCETRIS (brentuximab vedotin) utilizes the companys industry-leading antibody-drug conjugate (ADC) technology and is currently approved for the treatment of multiple CD30-expressing lymphomas. Beyond ADCETRIS, the company has a late-stage pipeline including enfortumab vedotin for metastatic urothelial cancer, currently being reviewed for approval by the FDA, and tisotumab vedotin in clinical trials for metastatic cervical cancer, which utilize our proprietary ADC technology. In addition, tucatinib, a small molecule tyrosine kinase inhibitor, is in late-stage development for HER2-positive metastatic breast cancer and in clinical development for metastatic colorectal cancer. We are also leveraging our expertise in empowered antibodies to build a portfolio of proprietary immuno-oncology agents in clinical trials targeting hematologic malignancies and solid tumors. The company is headquartered in Bothell, Washington, and has a European office in Switzerland. 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 therapeutic potential of tucatinib, including its possible efficacy, safety and therapeutic uses; anticipated development activities including ongoing and future clinical trials; and intended regulatory actions, including the plan to submit an NDA to the FDA and a MAA to the EMA by the first quarter of 2020. 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 difficulty and uncertainty of pharmaceutical product development, the risk of adverse events or safety signals, the possibility of disappointing results in ongoing or future clinical trials despite earlier promising clinical results, the possibility of delays in the submission of an NDA to the FDA and a MAA to the EMA, the possibility that data from the HER2CLIMB trial may not be sufficient to support approval of tucatinib, the possibility of adverse regulatory action. 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 September 30, 2019 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. American Cancer Society, Cancer Facts and Figures 2018-2019.

2. Loibl S, Gianni L (2017). HER2-positive breast cancer. The Lancet 389(10087): 2415-29.

3. Slamon D, Clark G, Wong S, et al. (1987). Human breast cancer: correlation of relapse and survival with amplification of the HER-2/neu oncogene. Science 235(4785): 177-82.

4. American Cancer Society (ACS) (2018). Breast cancer HER2 status. Accessed: December 10, 2018.

5. Kennecke H, Yerushalmi R, Woods R, et al. (2010). Metastatic Behavior of Breast Cancer Subtypes. Journal of Clinical Oncology 28(20): 3271-7.

6. Berman AT, Thukral AD, Hwang W-T, et al. (2013). Incidence and Patterns of Distant Metastases for Patients With Early-Stage Breast Cancer After Breast Conservation Treatment. Clinical Breast Cancer 13(2): 88-94.

7. Duchnowska R, Loibl S, Jassem J (2018). Tyrosine kinase inhibitors for brain metastases in HER2-positive breast cancer. Cancer Treatment Reviews 67: 71-7.

8. Verma S, Miles D, Gianni L, et al. (2012). Trastuzumab Emtansine for HER2-Positive Advanced Breast Cancer. New England Journal of Medicine 367(19): 1783-91.

9. Geyer CE, Forster J, Lindquist D, et al. (2006). Lapatinib plus Capecitabine for HER2-Positive Advanced Breast Cancer. New England Journal of Medicine 355(26): 2733-43.

10. Blackwell KL, Burstein HJ, Storniolo AM, et al. (2012). Overall Survival Benefit With Lapatinib in Combination With Trastuzumab for Patients With Human Epidermal Growth Factor Receptor 2Positive Metastatic Breast Cancer: Final Results From the EGF104900 Study. Journal of Clinical Oncology 30(21): 2585-92.

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Seattle Genetics Announces U.S. FDA Grants Breakthrough Therapy Designation for Tucatinib in Locally Advanced or Metastatic HER2-Positive Breast...

Diversity starts at the gene level

Natural killer (NK) cells are immune cells with potent antiviral and antitumor activities. These cells express several germline-encoded inhibitory receptors (KIRs) that prevent NK cells from killing healthy cells but enable the targeting of infected and transformed cells. Using various imaging techniques and functional assays, Kennedy et al. investigated the effects of genetic diversity in KIR-encoding genes on receptor organization and activity. They found that KIRs encoded by distinct genes were present at varying abundances and in clusters of varying sizes, which led to differences in downstream signaling that affected NK cell function. Together, these data suggest that genetic diversity in KIR-encoding genes affects receptor organization, signaling, and functional outcomes.

Genetic diversity in human natural killer (NK) cell receptors is linked to resistance and susceptibility to many diseases. Here, we tested the effect of this diversity on the nanoscale organization of killer cell immunoglobulin-like receptors (KIRs). Using superresolution microscopy, we found that inhibitory KIRs encoded by different genes and alleles were organized differently at the surface of primary human NK cells. KIRs that were found at low abundance assembled into smaller clusters than those formed by KIRs that were more highly abundant, and at low abundance, there was a greater proportion of KIRs in clusters. Upon receptor triggering, a structured interface called the immune synapse assembles, which facilitates signal integration and controls NK cell responses. Here, triggering of low-abundance receptors resulted in less phosphorylation of the downstream phosphatase SHP-1 but more phosphorylation of the adaptor protein Crk than did triggering of high-abundance receptors. In cells with greater KIR abundance, SHP-1 dephosphorylated Crk, which potentiated NK cell spreading during activation. Thus, genetic variation modulates both the abundance and nanoscale organization of inhibitory KIRs. That is, as well as the number of receptors at the cell surface varying with genotype, the way in which these receptors are organized in the membrane also varies. Essentially, a change in the average surface abundance of a protein at the cell surface is a coarse descriptor entwined with changes in local nanoscale clustering. Together, our data indicate that genetic diversity in inhibitory KIRs affects membrane-proximal signaling and, unexpectedly, the formation of activating immune synapses.

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Genetic diversity affects the nanoscale membrane organization and signaling of natural killer cell receptors - Science

Over the past few years most Americans have been more and more curious about their family trees thanks to kits like 23 and Me and Ancestry.com. But did you know your DNA could be used to solve cold cases, convict people whove committed violent crimes, and even exonerate the wrongfully accused?One local genealogist explains why this seeming harmless gift could unlock a world of answered questions for law enforcement.Closure, is the driving force behind genetic genealogists Shera LaPoint.To be able to give that gift to some one has changed my life. Its the most rewarding thing Ive ever done.

Throughout the years she has closed dozens of cold cases thanks familial DNA but the popularity of DNA testing groups like 23 and Me, have a lesser known option that can be beneficial to law enforcement.

As a tester you have a right to decide what information you want to put out there and who its shared with.

Users can also opt into sharing their DNA with officers helping them in several ways, thanks to new technology.

By uploading your DNA you never know who you will be actually helping. We can take these criminals off the streets, we can exonerate innocent people, we can identify John and Jane Does, and also the fallen military who are unnamed, said LaPoint.They can use my DNA or someone I manage that has agreed to opt in, to help capture a dangerous individuals, then I really dont have a problem, says Mark Richard.

Mark Richard, supports opting into sharing DNA with law enforcement because he says it can close dark chapters in peoples lives.

Richard adds, sometimes these are unsolved crimes where families can not get closure. People dont know what happened from an incident you know someone got murdered or raped and people never know who did it. Then these cases go cold because they didnt have the DNA back then so this is giving families an opportunity for closure.Then you give a DNA kit as a Christmas gift, think about going the extra mile and giving a little bit extra by uploading your DNA. Opting into law enforcement use, and lets make a difference in this world, said LaPoint.Aside from working on cold cases, Shera also uses genetic geology to connect adoptees with their parents . For more information about Shera and all her works, click here.

The rest is here:
Genetic Genealogy Helping Law Enforcement Close Cold Cases and More - News15 | Lafayette, LA - FOX 15

1. Apple is offering free genetic tests to all its Silicon Valley employees  CNBC
2. Apple to offer free genetic testing for employees, report says  Business Insider
3. Apple partners with Color to provide free genetics tests to employees  Becker's Hospital Review
4. Apple Offers Free Genetic Testing to Cupertino Employees  MacRumors
5. Apple's AC Wellness offering free genetic testing to employees  AppleInsider
6. View full coverage on Google News

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Apple is offering free genetic tests to all its Silicon Valley employees - CNBC

In a new study, a high genetic risk score (GRS) was associated with an increased risk of organ damage, renal (kidney) dysfunction and mortality in people with lupus. Organ damage, cardiovascular disease, proliferative nephritis (kidney lesions), end-stage renal disease (ESRD) and presence of antiphospholipid antibodies were successfully predicted by a high GRS in people with lupus. GRSs have been applied in several fields of medicine and may be a potential tool for prediction of disease severity in lupus.

Clinical data from 1,001 people with lupus were analyzed. Their health outcomes and cumulative genetic risk were compiled and compared against the GRSs of 5,524 people with lupus and 9,859 healthy people. Lupus was more prevalent in the high-, compared with the low-GRS group Patients in the high GRS group had a 6-year earlier average disease onset, displayed higher prevalence of damage accrual, ERSD, proliferative nephritis, certain types of autoantibodies and positive lupus anticoagulant test, compared with patients in the low-GRS group. Survival analysis showed earlier onset of the first organ damage, first cardiovascular event, nephritis, ESRD and decreased overall survival in people with high GRSs compared to those with low scores.

Genetic profiling may be useful for predicting outcomes in people with lupus and aid in the clinical decision process. Understanding the genetic contribution to permanent organ damage is important for understanding how lupus develops. Learn more about the genetics of lupus.

Read the study

Continue reading here:
Genetic Risk Scores May Predict Severity and Outcomes in People with Lupus - Lupus Foundation of America

Jens Carlsson of the UCD School of Biology is co-founder of the Area 52 research group that aims to solve a variety of genetic questions.

After completing his PhD in 2001, followed by a stint at the Danish Institute for Freshwater Research in Silkeborg, assistant professor Jens Carlsson travelled to the US in 2002 to work as a postdoc at the Virginia Institute for Marine Science.

In 2007, he was appointed a visiting associate professor at Duke University, North Carolina, to research the population structure of striped sea bass.

In 2009, he travelled to Ireland to work at University College Cork as a senior research fellow, which included work on deep sea vessels. Then, in 2012, he made the move to University College Dublin and established his research group, Area 52.

Too many people have been watching the CSI TV series and have strange ideas of how a modern genetics laboratory works JENS CARLSSON

I think I have had an interest in fish since I was introduced to fishing as a kid. While completing my BSc project, I was fascinated by the questions you could ask and answer using scientific approaches.

The freedom that academic research has for coming up with projects and then sourcing funding, to actually examine these questions, was probably the reason why I stayed on in science.

The research group Area 52 quickly developed when I started working in UCD. It is now a rather diverse group and we take on research questions from a wide range of disciplines from viral diseases in fish to identification of human remains.

It is the use of genetic methods that allows us to work with these very diverse questions and, so far, all organisms have DNA or RNA so there are a huge variety of questions that we can address.

This also means that we collaborate with a large number of colleagues. While we have the genetic expertise, we also need to work with people who understand the biology and ecology of the organisms.

When Area 52 started, it was only myself and my wife and lab manager in the lab group. But now it has grown significantly and consists of undergraduates, summer interns, visiting students, MSc students, PhD candidates, postdocs, research fellows and research scientists.

I believe that genetics has the capacity to answer questions that no other research field can do.

For example, when you look at marine fish, there are no clear barriers preventing different populations from mixing. However, this does not mean that the fish all belong to the same biological unit or population.

While fish from multiple biological units can mix at feeding areas, they often return to specific spawning sites with each spawning site representing a single biological unit.

Multiple species have been shown using genetics separated into different populations to represent different biological units. This has profound implications for the management of fisheries species, as the level where management needs to take place is natural biological units and this might differ depending on the time of the year.

You might have multiple populations mixing at feeding grounds and it is very difficult to say which fish came from which population when being caught in commercial fisheries as they tend to look the same. However, by using genetic tools we are able to say which individual belongs to which population.

Furthermore, Area 52 has a strong focus on developing non-invasive sampling methods for studies of terrestrial mammals such as elephants, zebras and giraffes primarily in Kenya.

It is often very difficult and invasive to collect genetic material for these animals. We focus on using scat samples that are completely non-invasive. The animal does its business and we collect the scat and use that as source of genetic material.

Area 52 often works with method development and these methods can obviously be used in the commercial world. For example, the management of fisheries species and the integrity of supply chains.

However, the main focus of the lab is in deploying the methods we develop in conservation and environmental monitoring of water ecosystems.

It is always difficult to find time to do the research. You are teaching, mentoring, doing research and administration. At the same time, you need to secure funding for your research and that is difficult.

This is not only because of the lack of time, but also because of the strong competition among researchers for the very limited funding. This means that you can spend significant time on writing a grant application and then it is not funded. I wish the success rate of grants would be higher.

Too many people have been watching the CSI TV series and have strange ideas of how a modern genetics laboratory works.

The big question is climate change and how that will affect distribution and survival of species. This is a very important question requiring collaboration among a large number of researchers from many different fields of science.

Are you a researcher with an interesting project to share? Let us know by emailing editorial@siliconrepublic.com with the subject line Science Uncovered.

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Fishy genetics: A behind-the-scenes look at UCD's Area 52 - Siliconrepublic.com

This week, GEDmatch, a genetic genealogy company that gained notoriety for giving law enforcement access to its customers DNA data, quietly informed its users it is now operated by Verogen, Inc., a company expressly formed two years ago to market next-generation [DNA] sequencing technology to crime labs.

What this means for GEDmatchs 1.3 million users and for the 60% of white Americans who share DNA with those users remains to be seen.

GEDmatch allows users to upload an electronic file containing their raw genotyped DNA data so that they can compare it to other users data to find biological family relationships. It estimates how close or distant those relationships may be (e.g., a direct connection, like a parent, or a distant connection, like a third cousin), and it enables users to determine where, along each chromosome, their DNA may be similar to another user. It also predicts characteristics like ethnicity.

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An estimated 30 million people have used genetic genealogy databases like GEDmatch to identify biological relatives and build a family tree, and law enforcement officers have been capitalizing on all that freely available data in criminal investigations. Estimates are that genetic genealogy sites were used in around 200 cases just last year. For many of those cases, officers never sought a warrant or any legal process at all.

Earlier this year, after public outcry, GEDmatch changed its previous position allowing for warrantless law enforcement searches, opted out all its users from those searches, and required all users to expressly opt in if they wanted to allow access to their genetic data. Only a small percentage did. But opting out has not prevented law enforcement from accessing consumers genetic data, as long as they can get a warrant, which one Orlando, Florida officer did last summer.

Law enforcement has argued that people using genetic genealogy services have no expectation of privacy in their genetic data because users have willingly shared their data with the genetics company and with other users and have consented to a companys terms of service. But the Supreme Court rejected a similar argument in Carpenter v. United States.

In Carpenter, the Court ruled that even though our cell phone location data is shared with or stored by a phone company, we still have a reasonable expectation of privacy in it because of all the sensitive and private information it can reveal about our lives. Similarly, genetic data can reveal a whole host of extremely private and sensitive information about people, from their likelihood to inherit specific diseases to where their ancestors are from to whether they have a sister or brother they never knew about. Researchers have even theorized at one time or another that DNA may predict race, intelligence, criminality, sexual orientation, and political ideology. Even if later disproved, officials may rely on outdated research like this to make judgements about and discriminate against people. Because genetic data is so sensitive, we have an expectation of privacy in it, even if other people can access it.

However, whether individual users of genetic genealogy databases have consented to law enforcement searches is somewhat beside the point. In all cases that we know of so far, law enforcement isnt looking for the person who uploaded their DNA to a consumer site, they are looking for that persons distant relatives people who never could have consented to this kind of use of their genetic data because they dont have any control over the DNA they happen to share with the sites users.

That means these searches are nothing more than fishing expeditions through millions of innocent peoples DNA. They are not targeted at finding specific users or based on individualized suspicion a fact the police admit because they dont know who their suspect is. They are supported only by the hope that a crime scene sample might somehow be genetically linked to DNA submitted to a genetic genealogy database by a distant relative, which might give officers a lead in a case. Theres a real question whether a warrant that allows this kind of search could ever meet the particularity requirements of the Fourth Amendment.

These are also dragnet searches, conducted under general warrants, and no different from officers searching every house in a town with a population of 1.3 million on the off chance that one of those houses could contain evidence useful to finding the perpetrator of a crime. With or without a warrant, the Fourth Amendment prohibits searches like this in the physical world, and it should prohibit genetic dragnets like this one as well.

We need to think long and hard as a society about whether law enforcement should be allowed to access genetic genealogy databases at all even with a warrant. These searches impact millions of Americans. Although GEDmatch likely only encompasses about 0.5% of the U.S. adult population, research shows 60% of white Americans can already be identified from its 1.3 million users. This same research shows that once GEDmatchs users encompass just 2% of the U.S. population, 90% of white Americans will be identifiable.

Although many authorities once argued these kinds of searches would only be used as a way to solve cold cases involving the most terrible and serious crimes, that is changing; this year, police used genetic genealogy to implicate a teenager for a sexual assault. Next year it could be used to identify political or environmental protestors. Unlike established criminal DNA databases like the FBIs CODIS database, there are currently few rules governing how and when genetic genealogy searching may be used.

We should worry about these searches for another reason: they can implicate people for crimes they didnt commit. Although police used genetic searching to finally identify the man they believe is the Golden State Killer, an earlier search in the same case identified a different person. In 2015, a similar search in a different case led police to suspect an innocent man. Even without genetic genealogy searches, DNA matches may lead officers to suspect and jail the wrong person, as happened in a California case in 2012. That can happen because we shed DNA constantly and because our DNA may be transferred from one location to another, possibly ending up at the scene of a crime, even if we were never there.

All of this is made even more concerning by the recent acquisition of GEDmatch by a company whose main purpose is to help the police solve crimes. The ability to research family history and disease risk shouldnt carry the threat that our data will be accessible to police or others and used in ways we never could have foreseen. Genetic genealogy searches by law enforcement invade our privacy in unique ways they allow law enforcement to access information about us that we may not even know ourselves, that we have no ability to hide, and that could reveal more about us in the future than scientists know now. These searches should never be allowed even with a warrant.

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Genetic Testing Company Acquired by Company With Ties to FBI and Law Enforcement - Truthout

The deal will grant 1933 Industries license to the DNA brand for the production and sale of hemp-derived CBD products

1933 Industries Inc () (OTCMKTS:TGIFF) announced Thursday that it has signed a second licensing agreement with OG DNA Genetics, a globally recognized leading cannabis brand.

The agreement will grant 1933 Industries the license to the DNA brand for the production and sale of hemp-derived CBD products signaling DNAs first entry into the cannabidiol market. DNA will leverage 1933s vast distribution network of over 800 retail outlets throughout the US.

In 2018, the Farm Bill was passed through legislation federally legalizing the cultivation of hemp and permitting the sale of hemp-derived CBD products. This gives DNA the ability to expand itsreach into the rapidly developing CBD market and provide the highest-quality products to all 50 states and globally.

We are excited to expand our partnership with 1933, one of the leaders in the CBD wellness space, said Don Morris, co-founder of DNA Genetics. It feels good to build on an already strong relationship with a like-minded company committed to putting out the best quality products.

Chris Rebentisch, CEO of 1933 Industries, said DNA has the best quality products in the market.

Its fitting that we would work together to help bring the legacy brand into the CBD wellness space. We have an amazing lineup of products and are excited to leverage DNAs global reach through this agreement, Rebentisch said.

For more than 15 years, genetics developed by DNA have won more than 200 awards in all categories at the most prestigious cannabis events around the world, making DNA the global standard in breeding and growing truly best-in-class strains.

These awards include the High Times Top 10 Strain of the Year,which was inducted into The High Times seedbank hall of fame in 2009, the High Times 100 list of the most influential people in the industry and the High Times Trailer Blazers Award, for contributions made towards uniting the fields of entrepreneurship, politics and medicine.

1933 Industries, based in Chilliwack, British Columbia, owns licensed medical and adult-use cannabis cultivation and production assets, proprietary hemp-based, CBD-infused branded products, CBD extraction services and a specialized cannabis advisory firm.

Shares recently traded up 2.6% to C$0.20 in Canada.

--ADDS share price--

Contact the author: [emailprotected]

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1933 Industries signs second licensing deal with OG DNA Genetics - Proactive Investors USA & Canada

Every minute of every day our bodies are bombarded with millions of different molecules that we breathe, eat and touch including bacteria, viruses, chemicals and seemingly harmless compounds like food and pollen.

For every one of these encounters, our immune system has to decide if the substance is a threat or not, if it is foreign or self and how the body should respond to stay healthy. To do this, we rely on two immune systems working in tandem.

Scientists have discovered a new human autoinflammatory disease that results from a mutation in an important gene in one of these systems.

The syndrome, now known as CRIA (cleavage-resistant RIPK1-induced autoinflammatory) syndrome causes recurring episodes of debilitating and distressing fever and inflammation.

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Our bodys first line of defence is the innate immune system that is effectively a hard wired and fast response, explains Dr Najoua Lalaoui from the Walter and Eliza Hall Institute of Medical Research (WEHI) and the Department of Medical Biology at the University of Melbourne.

This system works in the skin and mucous membranes like the mouth, making sure that any invaders like bacteria are detected and destroyed quickly, she says.

If pathogens do enter the body, the innate immune cells move to the site of infection and physically devour invaders and activate chemical messengers to alert the body.

This can lead to an inflammatory reaction where blood circulation is increased, the affected area becomes swollen and hot, and the person may experience fever. When these chemical messengers are over-active it can result in conditions like colitis, arthritis and psoriasis.

Supporting this system is the adaptive immunity system that involves antibodies that recognise and then train the body to respond to threats. This is our memory immunity and the basis of how vaccinations work.

Scientists from the WEHI, with colleagues at the National Institutes of Health (NIH) in the United States, have been working to understand why patients from three families suffered from a history of painful swollen lymph nodes, fever and inflammation.

The families had a range of other inflammatory symptoms which began in childhood and continued into their adult years.

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This type of repeated fever often indicates an issue with the innate immune system and the same disease in an extended family can indicate genetic changes that are passed from parents to their children, explains Dr Lalaoui.

Previous tests didnt identify any known cause.

But by sequencing the patients genomes, the NIH team identified a mutation in DNA that codes for a molecule known as RIPK that they suspected might cause the disease.

RIPK is a critical regulator of inflammation and the cell death pathway responsible for cleaning up damaged cells or those infected by pathogens.

Professor John Silke from the Walter and Eliza Hall Institute and his team have been studying RIPK1 for more than 10 years. His team had previously shown that damaging the RIPK1 gene could lead to uncontrolled inflammation and cell death.

RIPK1 is a potent controller of cell death, which means cells have had to develop many ways of regulating its activity, Professor Silke says.

In this paper, we showed that one way that the cell regulates its activity is by cleaving RIPK1 into two pieces to disarm the molecule and halt its role in driving inflammation.

In this condition (CRIA), the mutations are preventing the molecule from being cleaved into two pieces, resulting in autoinflammatory disease. This helped confirm that the mutations identified by the NIH researchers were indeed causing the disease, he says.

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He explains that mutations in RIPK1 can drive both too much inflammation as in autoinflammatory and autoimmune diseases and too little inflammation, resulting in immunodeficiency.

There is still a lot to learn about the varied roles of RIPK1 in cell death, and how we can effectively target RIPK1 to treat disease.

In CRIA syndrome, the mutation in RIPK1 overcomes all of the normal checks and balances that exist, resulting in uncontrolled cell death and inflammation, says Dr Steven Boyden from the National Human Genome Research Institute at the NIH.

Dr Boyden says the first clue that the disease was linked to cell death was when they delved into the patients exomes the part of the genome that encodes all of the proteins in the body.

The team sequenced the entire exome of each patient and discovered unique mutations in the exact same amino acid of RIPK1 in each of the three families.

It is remarkable, like lightning striking three times in the same place. Each of the three mutations has the same result it blocks cleavage of RIPK1 which shows how important RIPK1 cleavage is in maintaining the normal function of the cell, says Dr Boyden.

Dr Lalaoui said the WEHI researchers then confirmed the link between the RIPK1 mutations and CRIA syndrome in laboratory models.

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We showed that mice with mutations in the same location in RIPK1 as in the CRIA syndrome patients, had a similar exacerbation of inflammation, she says.

Dr Dan Kastner from NIH widely regarded as the father of autoinflammatory disease says colleagues had treated CRIA syndrome patients with a number of anti-inflammatory medications, including high doses of corticosteroids and biologics, compounds that block specific parts of the immune system.

And although some of the patients markedly improved, others responded less well or had significant side effects.

Understanding the molecular mechanism by which CRIA syndrome causes inflammation provides an opportunity to get right to the root of the problem, Dr Kastner says.

Dr Kastner noted that RIPK1 inhibitors, which are already available on a research basis, may provide a focused, precision medicine approach to treating patients.

RIPK1 inhibitors may be just what the doctor ordered for these patients. The discovery of CRIA syndrome also suggests a possible role for RIPK1 in a broad spectrum of human illnesses, such as colitis, arthritis and psoriasis.

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The genetic mutation behind a new autoinflammatory disease - Pursuit

A genetic variant found in about 3% of people of African ancestry is a more significant cause of heart failure than previously believed, according to a multi-institution study led by researchers at Penn Medicine. The researchers also found that this type of heart failure is underdiagnosed. According to their study, 44% of TTR V122Ivariant carriers older than age 50 had heart failure, but only 11% of these individuals had been diagnosed with hATTR-CM. The average time to diagnosis was three years, indicating both high rates of underdiagnoses and prolonged time to appropriate diagnosis

This study suggests that workup for amyloid cardiomyopathy and genetic testing of TTR should be considered, when appropriate, to identify patients at risk for the disease and intervene before they develop more severe symptoms or heart failure, said the studys lead author Scott Damrauer, M.D., an assistant professor of Surgery at Penn Medicine and a vascular surgeon at the Corporal Michael J. Crescenz VA Medical Center. (Penn Medicine consists of the Raymond and Ruth Perelman School of Medicine at the University of Pennsylvania and the University of Pennsylvania Health System.)

In this study, researchers from Penn Medicine and the Icahn School of Medicine at Mount Sinai used a genome-first approach, performing DNA sequencing of 9,694 individuals of African and Latino ancestry enrolled in either the Penn Medicine BioBank (PMBB) or the Icahn School of Medicine at Mount Sinai BioMe biobank (BioMe). Researchers identified TTR V122I carriers and then examined longitudinal electronic health record-linked genetic data to determine which of the carriers had evidence of heart failure.

The findings, which were published today in JAMA, are particularly important given the US Food and Drug Administrations (FDA) approval of the first therapy (tafamidis) for ATTR-CM in May 2019. Prior to tafamidiss approval, treatment was largely limited to supportive care for heart failure symptoms and, in rare cases, heart transplant.

Our findings suggest that hATTR-CM is a more common cause of heart failure than its perceived to be, and that physicians are not sufficiently considering the diagnosis in certain patients who present with heart failure, said the studys corresponding author Daniel J. Rader, M.D., chair of the Department of Genetics at Penn Medicine. With the recent advances in treatment, its critical to identify patients at risk for the disease and, when appropriate, perform the necessary testing to produce an earlier diagnosis and make the effective therapy available.

hATTR-CM, also known as cardiac amyloidosis, typically manifests in older patients and is caused by the buildup of abnormal deposits of a specific transthyretin protein known as amyloid in the walls of the heart. The heart walls become stiff, resulting in the inability of the left ventricle to properly relax and adequately pump blood out of the heart. However, this type of heart failurewhich presents similar to hypertensive heart disease is common, and the diagnosis of hATTR-CM is often not considered.

Tafamidis meglumine is a non-NSAID benzoxazole derivative that binds to TTR with high affinity and selectivity. TTR acts by transporting the retinol-binding protein-vitamin A complex. It is also a minor transporter of thyroxine in blood. Its tetrameric structure can become amyloidogenic by undergoing rate-limiting dissociation and monomer misfolding.

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Penn Team Finds Genetic Variant Largely Found in Patients of African Descent that Increases Heart Failure Risk - Clinical OMICs News

Our lives have been transformed by the information age. But what's coming next is likely to be more profound, call it the genetic information age. We have mapped the human genome and in just the last few years we have learned to read and write DNA like software. And you're about to see a few breakthroughs-in-waiting that would transform human health. For a preview of this revolution in evolution we met George Church, a world leading geneticist, whose own DNA harbors many eccentricities and a few genes for genius.

We found George Church in here.

Cory Smith: Most of these are frozen George. Little bits of George that we have edited all in different tubes.

Church threw himself into his work, literally. His DNA is in many of the experiments in his lab at Harvard Medical School. The fully assembled George Church is 6'5" and 65. He helped pioneer mapping the human genome and editing DNA. Today, his lab is working to make humans immune to all viruses, eliminate genetic diseases, and reverse the effects of time.

Scott Pelley: One of the things your lab is working on is reversing aging.

George Church: That's right.

Scott Pelley: How is that possible?

George Church: Reversing aging is one of these things that is easy to dismiss to say either we don't need it or is impossible or both.

Scott Pelley: Oh, we need it.

George Church: Okay. We need it. That's good. We can agree on that. Well, aging reversal is something that's been proven about eight different ways in animals where you can get, you know, faster reaction times or, you know, cognitive or repair of damaged tissues.

Scott Pelley: Proven eight different ways. Why isn't this available?

George Church: It is available to mice.

In lucky mice, Church's lab added multiple genes that improved heart and kidney function and levels of blood sugar. Now he's trying it in spaniels.

Scott Pelley: So is this gene editing to achieve age reversal?

George Church: This is adding genes. So, it's not really editing genes. It's, the gene function is going down, and so we're boosting it back up by putting in extra copies of the genes.

Scott Pelley: What's the time horizon on age reversal in humans?

George Church: That's in clinical trials right now in dogs. And so, that veterinary product might be a couple years away and then that takes another ten years to get through the human clinical trials.

Human trials of a personal kind made George Church an unlikely candidate to alter human evolution. Growing up in Florida, Church was dyslexic, with attention deficit, and frequently knocked out by narcolepsy.

Scott Pelley: What was it that made you imagine that you could be a scientist?

George Church: The thing that got me hooked was probably the New York World's Fair in 1964. I thought this is the way we should all be living. When I went back to Florida, I said, "I've been robbed," you know? "Where is it all?" So, I said, "Well, if they're not going to provide it, then I'm gonna provide it for myself."

With work and repetition, he beat his disabilities and developed a genius for crystallography, a daunting technique that renders 3D images of molecules through X-rays and math. But in graduate school at Duke, at the age of 20, his mania for the basic structures of life didn't leave time for the basic structure of life.

Scott Pelley: You were homeless for a time.

George Church: Yeah. Briefly.

Scott Pelley: Six months.

George Church: Six months.

Scott Pelley: And where were you sleeping when you were homeless?

George Church: Well, yeah. I wasn't sleeping that much. I was mostly working. I'm narcoleptic. So, I fall asleep sitting up anyway.

His devotion to crystallography was his undoing at Duke.

George Church: I was extremely excited about the research I was doing. And so, I would put in 100-plus hours a week on research and then pretty much didn't do anything else.

Scott Pelley: Not go to class.

George Church: I wouldn't go to class. Yeah.

Duke kicked him out with this letter wishing him well in a field other than biology. But, it turned out, Harvard needed a crystallographer. George Church has been here nearly 40 years. He employs around 100 scientists, about half-and-half men and women.

Scott Pelley: Who do you hire?

George Church: I hire people that are self-selecting, they see our beacon from a distance away. There are a lot of people that are a little, you know, might be considered a little odd. "Neuroatypicals," some of us are called.

Scott Pelley: "Neuroatypical?"

George Church: Right.

Scott Pelley: Unusual brains?

George Church: Right, yeah.

Parastoo Khoshakhlagh: One thing about George that is very significant is that he sees what you can't even see in yourself.

Parastoo Khoshakhlagh and Alex Ng are among the "neuroatypicals." They're engineering human organ tissue.

Cory Smith: I think he tries to promote no fear of failure. The only fear is not to try at all.

Cory Smith's project sped up DNA editing from altering three genes at a time to 13,000 at a time. Eriona Hysolli went to Siberia with Church to extract DNA from the bones of wooly mammoths. She's editing the genes into elephant DNA to bring the mammoth back from extinction.

Eriona Hysolli: We are laying the foundations, perhaps, of de-extinction projects to come.

Scott Pelley: De-extinction.

Eriona Hysolli: Yes.

Scott Pelley: I'm not sure that's a word in the dictionary yet.

Eriona Hysolli: Well, if it isn't, it should be.

Scott Pelley: You know there are people watching this interview who think that is playing God.

George Church: Well, it's playing engineer. I mean, humans have been playing engineer since the dawn of time.

Scott Pelley: The point is, some people believe that you're mucking about in things that shouldn't be disturbed.

George Church: I completely agree that we need to be very cautious. And the more powerful, or the more rapidly-moving the technology, the more cautious we need to be, the bigger the conversation involving lots of different disciplines, religion, ethics, government, art, and so forth. And to see what it's unintended consequences might be.

Church anticipates consequences with a full time ethicist in the lab and he spends a good deal of time thinking about genetic equity. Believing that genetic technology must be available to all, not just those who can afford it.

We saw one of those technologies in the hands of Alex Ng and Parastoo Khoshakhlagh. They showed us what they call "mini-brains," tiny dots with millions of cells each. They've proven that cells from a patient can be grown into any organ tissue, in a matter of days, so drugs can be tested on that patient's unique genome.

Scott Pelley: You said that you got these cells from George's skin? How does that work?

Alex Ng: We have a way to reprogram essentially, skin cells, back into a stem cell state. And we have technologies where now we can differentiate them into tissue such as brain tissue.

Scott Pelley: So you went from George's skin cells, turned those into stem cells, and turned those into brain cells.

Alex Ng: Exactly. Exactly.

Scott Pelley: Simple as that.

Organs grown from a patient's own cells would eliminate the problem of rejection. Their goal is to prove the concept by growing full sized organs from Church's DNA.

George Church: It's considered more ethical for students to do experiments on their boss than vice versa and it's good to do it on me rather than some stranger because I'm as up to speed as you can be on the on the risks and the benefits. I'm properly consented. And I'm unlikely to change my mind.

Alex Ng: We have a joke in the lab, I mean, at some point, soon probably, we're going to have more of his cells outside of his body than he has himself.

Church's DNA is also used in experiments designed to make humans immune to all viruses.

George Church: We have a strategy by which we can make any cell or any organism resistant to all viruses by changing the genetic code. So if you change that code enough you now get something that is resistant to all viruses including viruses you never characterized before.

Scott Pelley: Because the viruses don't recognize it anymore?

George Church: They expect a certain code provided by the host that they replicate in. the virus would have to change so many parts of its DNA or RNA so that it can't change them all at once. So, it's not only dead. But it can't mutate to a new place where it could survive in a new host.

Yes, he's talking about the cure for the common cold and the end of waiting for organ transplants. It's long been known that pig organs could function in humans. Pig heart valves are routinely transplanted already. But pig viruses have kept surgeons from transplanting whole organs. Church's lab altered pig DNA and knocked out 62 pig viruses.

Scott Pelley: What organs might be transplanted from a pig to a human?

George Church: Heart, lung, kidney, liver, intestines, various parts of the eye, skin. All these things.

Scott Pelley: What's the time horizon on transplanting pig organs into human beings?

George Church: you know, two to five years to get into clinical trials. And then again it could take ten years to get through the clinical trials.

Church is a role model for the next generation. He has co-founded more than 35 startups. Recently, investors put $100 million into the pig organ work. Another Church startup is a dating app that compares DNA and screens out matches that would result in a child with an inherited disease.

George Church: You wouldn't find out who you're not compatible with. You'll just find out who you are compatible with.

Scott Pelley: You're suggesting that if everyone has their genome sequenced and the correct matches are made, that all of these diseases could be eliminated?

George Church: Right. It's 7,000 diseases. It's about 5% of the population. It's about a trillion dollars a year, worldwide.

Church sees one of his own genetic differences as an advantage. Narcolepsy lulls him several times a day. But he wakes, still in the conversation, often, discovering inspiration in his twilight zone.

Scott Pelley: If somebody had sequenced your genome some years ago, you might not have made the grade in some way.

George Church: I mean, that's true. I would hope that society sees the benefit of diversity not just ancestral diversity, but in our abilities. There's no perfect person.

Despite imperfection, Church has co-authored 527 scientific papers and holds more than 50 patents. Proof that great minds do not think alike.

The best science can tell, it was about 4 billion years ago that self-replicating molecules set off the spark of biology. Now, humans hold the tools of evolution, but George Church remains in awe of the original mystery: how chemistry became life.

Scott Pelley: Is the most amazing thing about life, then, that it happened at all?

George Church: It is amazing in our current state of ignorance. We don't even know if it ever happened ever in the rest of the universe. it's awe-inspiring to know that it either happened billions of times, or it never happened. Both of those are mind boggling. It's amazing that you can have such complex structures that make copies of themselves. But it's very hard to do that with machines that we've built. So, we're engineers. But we're rather poor engineers compared to the pseudo engineering that is biological evolution.

Produced by Henry Schuster. Associate producer, Rachael Morehouse. Broadcast associate, Ian Flickinger.

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Harvard geneticist George Church's goal: to protect humans from viruses, genetic diseases, and aging - 60 Minutes - CBS News

For marginalized people, the tech worlds constant barrage of innovations is getting exhausting. It seems like every week, science and tech pioneers are revealing new projects that pose a clear threat to anyone not white, cisgender, or malewhether its porn deepfakes or algorithms that judge womens boobs.

Enter Harvard Medical School, where researchers are creating a new dating app that matches people based on their DNA. The goal is to create a system that screens out matches that would result in a child with an inherited disease, according to a report aired Sunday night on 60 Minutes.

In other words, its a dating app for eugenicsthe disturbing ideological practice of systematically discriminating against people based on genetic qualities judged to be undesirable or inferior.

The app is being developed by a team of geneticists led by George Church, who, in the same interview, defended accepting money for his lab donated by convicted pedophile Jeffrey Epstein. Churchs lab is most famous for its work on the gene-editing technology CRISPR/Cas9, and its researchers are looking at ways to make humans immune to viruses, reverse the effects of aging, and de-extinct animals. Its 7,000 diseases, its about 5 percent of the population, [and] about $1 trillion a year worldwide in medical expenses, Church told 60 Minutes.

But for anyone not white, cis, able-bodied, or male, its obvious where all this is going.

Eugenics has long been a fascination of Nazis and white supremacists, who dream of creating a white and genetically pure master race. Dystopian sci-fi tales like Gattaca have also warned of the horrifying dangers of organizing society based on the perceived desirability (or undesirability) of peoples genetic code.

For people who exist outside mainstream gender norms, these dangers are very real. Last week, Newsweek reported on a team of researchers at the University of Michigan who are attempting to identify regions of the brain associated with gender dysphoriathe discomfort which occurs when a persons gender does not match the sex they were assigned at birth.

Many, but not all transgender people experience gender dysphoria, and it has been used to establish a system of medical gatekeeping that pathologizes trans people and controls access to treatments like hormone replacement therapy and gender-affirming surgeries. But even if scientists identified some hypothetical trait that causes people to be trans, choosing to edit out those traits would be an attempt to effectively erase trans people from existence.

Meanwhile, research into trans medical treatments remains severely underfunded. The federal government is also trying to make it legal for medical providers to refuse to treat trans patientswhether for gender dysphoria or a broken arm.

In other words, these cis researchers, funders, and policymakers seem more interested in curing or erasing trans people than finding better and cheaper ways of treating themor anyone else labeled as falling outside the norm of biologic desirability. Churchs lab, for example, recently received over $100 million for its work on gene-editing.

Church says he is being careful, and claims his lab has appointed a full-time ethicist on its staff to work toward the goal of genetic equitywhere all people have access to genetic technology, regardless of race or economic status.

But for marginalized people suffering under deeply unequal and discriminatory systems of power, that mission seems dangerously naive. If the people who risk being most harmed by these innovations arent intimately involved in their development, maybe its better toyou knownot make them at all?

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A Genetic Dating App Is a Horrifying Thing That Shouldnt Exist - Free