Grant will help scientists break new ground in gene editing – Newswise

Newswise AMES, Iowa A new grant will help Iowa State University researchers develop innovative gene editing technology to better understand how human genetics affect susceptibility to disease.

The four-year, $2.8 million grant from the National Institutes of Health allows Maura McGrail, an associate professor of genetics, development and cell biology and principal investigator, and her collaborators to continue their efforts to develop gene editing technologies to model human disease in zebrafish. The research aims to build new tools to determine which genes have therapeutic potential to treat human genetic diseases that affect the cardiovascular, immune and nervous systems. Zebrafish share much of their genetic makeup with humans, and the researchers hope their work will lead to more effective treatments for many of the most pressing diseases in humans.

The research team also includes Jeffrey Essner, professor of genetics, development and cell biology, and Iddo Friedberg, associate professor of veterinary microbiology and preventive medicine.

The technology that weve developed allows us to modify genes in a precise way that places gene activity under spatial and temporal control, McGrail said. One of the challenges in disease research is understanding the impact of gene loss at the cellular level. By modeling genetic disease in zebrafish, were able to reconstitute the complexity of human disease in a living system and visualize how cell processes are disrupted.

The method developed by McGrail and her colleagues combines gene editing technology with site-specific recombination enzymes. Utilizing the two in concert allows the scientists to control where and when a gene is deactivated. The new grant will also test approaches to optimize the efficiency of their method and expand on their ability to introduce more subtle gene changes frequently found in human disease genes.

Its like flipping a switch, McGrail said. We can deactivate a gene in a specific tissue, and investigate how that affects cell viability and organ function, providing insight into the process of disease pathology.

The research team also published an article in the peer-reviewed academic journal eLife, released this week, that lays the foundation for much of what they will do with the new grant. The paper describes the researchers ability to use gene editing to target integration into the genome, or introduce new DNA into the genome with great precision.

The zebrafish is a small, freshwater species, usually only a few centimeters in length, that makes an ideal model organism for genetic study because of the species transparent embryos, which allow for easy study. The zebrafish genome also shares up to 80% of the genes that cause disease in humans, Essner said.

Because of that high degree of conservation, we believe we can reach many human diseases, he said.

For instance, the researchers foresee a future in which gene editing technology could be used to treat certain kinds of cancer. McGrail said disease progression in some cancers is caused by gene deactivation, but what if doctors could reactivate those genes? Would that suppress the growth of tumors? McGrail and Essner said their research will take an important step toward answering such questions.

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Grant will help scientists break new ground in gene editing - Newswise

Singapore researches discover specific gene linked to Asian Lung Cancer – BSA bureau

New data on East Asian populations will guide researchers and clinicians to develop novel therapeutic strategies tailored to individual lung cancer patients

Singapore scientists have completed one of the largest comprehensive genome studies of Asian lung adenocarcinoma (LUAD). Findings from this landmark study, which were published in February 2020s issue of Nature Genetics, are expected to contribute to the development of personalised medicine for lung cancer treatment and prevention. The study was led by scientists from A*STARs Genome Institute of Singapore (GIS), in collaboration with the National Cancer Centre Singapore (NCCS), and the Lung Cancer Consortium Singapore (LCCS).

Worldwide, LUAD is the most common type of lung cancer, and is responsible for over one million deaths annually. It differs markedly between Asians and Europeans as Asian LUAD patients tend to be female, non-smokers, and have more mutations in an important gene known as EGFR. Past studies by GIS and NCCS have also revealed that Asian lung cancers have higher level of heterogeneity than their European counterparts.

Findings

In this study, an inter-disciplinary team of researchers built on the donated clinical samples curated by the LCCS, and sequenced and analysed the largest dataset of LUADs for East Asians (including Singaporeans who formed the majority). The study revealed that the tumour mutation landscape in Asian patients is very unique, and several new genes may be implicated in the development of lung cancers in Asians.

One striking discovery from this study is a unique sub-group of lung tumours that appears specific to Asian lung cancers. This sub-group of lung tumours is more inflammatory in Asian patients compared to European patients, and contains high amounts of immune cells. Considering the increasing use of immunotherapy in cancer treatments, this discovery may lead to a more accurate selection of lung cancer patients who can benefit from this form of treatment.

The comprehensive analyses of the genetic and molecular features of these tumours have provided researchers and clinicians with a vista to assess the fingerprint of each lung cancer tumour. Such genomic information will deepen their understanding on how individual patients might respond differently to drug treatments, thus enabling a more precise approach to treating patients in the future. Data from this study is now publicly available via the Singapore Oncology Data Portal (OncoSG) which enables integration, visualisation, analyses, and sharing of cancer genomics datasets in Singapore.

Prof Zhai Weiwei, a principal investigator at GIS and senior author of the study, noted, This study depicted a comprehensive genomic landscape of Asian LUADs, and characterised the complex ethnic differences between Asians and Europeans.

A/Prof Daniel Tan, Senior Clinician Scientist at GIS and Senior Consultant Medical Oncologist at NCCS, said, Our study highlights how such deep genetic analysis can improve our ability to predict the behaviour of lung cancers beyond traditional clinical parameters, providing new perspectives in tailoring treatment approaches.

Prof Patrick Tan, Executive Director of GIS, said, The findings may lead to new patient stratification approaches to provide better-personalised treatment options. Novel therapies may also be developed by combining existing therapies with immunotherapy targeting Asian-specific sub-groups.

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Singapore researches discover specific gene linked to Asian Lung Cancer - BSA bureau

Genomic Medicine Market 2020 | Know the Latest COVID19 Impact Analysis And Strategies of Key Players: Ingersoll Rand, Johnson Controls, Daikin, United…

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Dyne Therapeutics Accelerates Programs in Facioscapulohumeral Muscular Dystrophy (FSHD) with Exclusive Licensing of Technologies to Target Genetic…

WALTHAM, Mass.--(BUSINESS WIRE)--Dyne Therapeutics, a biotechnology company pioneering life-transforming therapies for patients with serious muscle diseases, today announced the acceleration of its programs in facioscapulohumeral muscular dystrophy (FSHD) through the exclusive licensing of technologies to target the disease, as well as the appointment of leading researcher Jeffrey Statland, M.D., to its Scientific Advisory Board. Dr. Statland is an associate professor of neurology in the Department of Neurology at the University of Kansas Medical Center. He is also the co-principal investigator for ReSolve (Clinical Trial Readiness to Solve Barriers to Drug Development in FSHD), an ongoing observational study run by the FSHD Clinical Trial Research Network (CTRN) and supported by Dyne Therapeutics.

The intellectual property exclusively licensed by Dyne targets the gene DUX4, which is the genetic basis of FSHD, and was developed by Professor Alexandra Belayew and Dr. Frdrique Coppe at the University of Mons (UMONS) Molecular Biology Laboratory in Belgium. Dyne is advancing an FSHD program using this suite of DUX4-targeting technology in combination with its proprietary FORCETM platform.

FSHD is a rare, debilitating muscle disease for which there are no approved treatments. Dyne's proprietary FORCE platform enables targeted delivery of a therapeutic inside the muscle cells of FSHD patients, where it is expected to reduce aberrant expression of the DUX4 protein and halt the loss of muscle function that characterizes FSHD. People affected by FSHD experience muscle pain and progressive skeletal muscle loss throughout the body that significantly affects their strength, mobility and quality of life. The muscle weakness often starts in the face, making it difficult to smile, and may progress to the point where affected individuals become dependent upon the use of a wheelchair for mobility.

Dyne has made a commitment to alleviating the FSHD burden for affected individuals and families. Todays announcements represent an important step forward for Dyne as we pursue our mission of delivering life-transforming therapies for serious muscle diseases, said Joshua Brumm, president and chief executive officer of Dyne. Jeff brings comprehensive insights into FSHD, including cutting-edge research into molecular and neuroimaging biomarkers that may be useful in assessing disease progression in future clinical trials. The agreement with UMONS gives us exclusive access to intellectual property to target the genetic cause of FSHD and complements our own proprietary platform for precision delivery into muscle cells.

There is a critical need for therapies to treat FSHD, which takes a debilitating physical and emotional toll on affected individuals and families, said Dr. Statland. The Dyne team is advancing FSHD research with their support of the ReSolve study and I believe their FORCE platform holds great potential. I am delighted to join Dynes Scientific Advisory Board.

Dr. Statland is an associate professor of neurology at the University of Kansas Medical Center, with both clinical and research training in neuromuscular diseases. His primary research interest is in FSHD. In addition to co-leading the ReSolve Natural History Study, Dr. Statland, with his collaborators at the University of Rochester Medical Center, is developing a disease-specific patient-reported health inventory and molecular and neuroimaging biomarkers of disease activity for future FSHD clinical trials. Dr. Statland holds a B.A. from Sarah Lawrence College, an MFA from Emerson College and an M.D. from the University of Kansas School of Medicine. He completed residency training in the Department of Neurology at the University of Kansas Medical Center and also conducted a fellowship in experimental therapeutics of neurologic disorders in the Department of Neurology at the University of Rochester Medical Center. He is board certified by the American Board of Psychiatry and Neurology.

About Dyne Therapeutics

Dyne Therapeutics is pioneering life-transforming therapies for patients with serious muscle diseases. The companys FORCETM platform delivers oligonucleotides and other molecules to skeletal, cardiac and smooth muscle with unprecedented precision to restore muscle health. Dyne is advancing treatments for myotonic dystrophy type 1 (DM1), Duchenne muscular dystrophy (DMD) and facioscapulohumeral muscular dystrophy (FSHD). Dyne was founded by Atlas Venture and is headquartered in Waltham, Mass. For more information, please visit http://www.dyne-tx.com, and follow us on Twitter, LinkedIn and Facebook.

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Dyne Therapeutics Accelerates Programs in Facioscapulohumeral Muscular Dystrophy (FSHD) with Exclusive Licensing of Technologies to Target Genetic...

New Stem Cell-Based Topical Solution Helps Bald People Regrow Hair – SciTechDaily

A clinical trial showed the ability of a stem cell-based topical solution to regrow hair in people with male/female pattern baldness.

The results of a clinical trial released today (May 18, 2020) in STEM CELLS Translational Medicinedemonstrate how a topical solution made up of stem cells leads to the regrowth of hair for people with a common type of baldness.

Androgenetic alopecia (AGA) commonly known as male-pattern baldness (female-pattern baldness in women) is a condition caused by genetic, hormonal and environmental factors. It affects an estimated 50 percent of all men and almost as many women older than 50. While it is not a life-threatening condition, AGA can lower a persons self-esteem and psychological well-being. There are a few FDA-approved medications to treat hair loss, but the most effective can have side effects such as loss of libido and erectile dysfunction. Therefore, the search continues for a safer, effective treatment.

Adipose tissue-derived stem cells (ADSCs) secrete several growth hormones that help cells develop and proliferate. According to laboratory and experimental studies, growth factors such as hepatocyte growth factor (HGF), vascular endothelial growth factor (VEGF), insulin-like growth factor (IGF) and platelet-derived growth factor (PDGF) increase the size of the hair follicle during hair development.

A more enriched adipose-derived stem cells-constituent extract (ADSC-CE) with stem cell proteins is obtained by disruption of the ADSC membrane using a low frequency of ultrasound wave. Credit: AlphaMed Press

Recent studies have shown that ADSCs promote hair growth in both men and women with alopecia. However, no randomized, placebo-controlled trial in humans has explored the effects and safety of adipose-derived stem cell constituent extract (ADSC-CE) in AGA. We aimed to assess the efficacy and tolerability of ADSC-CE in middle-aged patients with AGA in our study, hypothesizing that it is an effective and safe treatment agent, said Sang Yeoup Lee, M.D., Ph.D., of the Family Medicine Clinic and Research Institute of Convergence of Biomedical Science and Technology, Pusan National University Yangsan Hospital in South Korea. He led the group of researchers, which also included colleagues from Pusan National University School of Medicine, Pusan National University Yangsan Hospital and T-Stem Co., Ltd.

The team recruited 38 patients (29 men and nine women) with AGA and assigned half to an intervention group that received the ADSC-CE topical solution and half as a control group that received a placebo. Twice daily, each patient applied the ADSC-CE topical solution or placebo to their scalp using their fingers.

At the end of 16 weeks, the group that received the ADSC-CEs had a significant increase in both hair count and follicle diameter, reported the studys senior author, Young Jin Tak, M.D., Ph.D.

Dr. Lee added, Our findings suggest that the application of the ADSC-CE topical solution has enormous potential as an alternative therapeutic strategy for hair regrowth in patients with AGA, by increasing both hair density and thickness while maintaining adequate treatment safety. The next step should be to conduct similar studies with large and diverse populations in order to confirm the beneficial effects of ADSC-CE on hair growth and elucidate the mechanisms responsible for the action of ADSC-CE in humans.

For the millions of people who suffer from male-pattern baldness, this small clinical trial offers hope of a future treatment for hair regrowth, said Anthony Atala, M.D., Editor-in-Chief ofSTEM CELLS Translational Medicineand director of the Wake Forest Institute for Regenerative Medicine. The topical solution created from proteins secreted by stem cells found in fat tissue proves to be both safe and effective. We look forward to further findings that support this work.

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Reference: A Randomized, Double-blind, Vehicle-Controlled Clinical Study of Hair Regeneration Using Adipose-Derived Stem Cell Constituent Extract in Androgenetic Alopecia by Young Jin Tak, Sang Yeoup Lee, A Ra Cho and Young Sil Kim, 18 May 2020, STEM CELLS Translational Medicine.DOI: 10.1002/sctm.19-0410

AboutSTEM CELLS Translational Medicine:STEM CELLS Translational Medicine(SCTM), co-published by AlphaMed Press and Wiley, is a monthly peer-reviewed publication dedicated to significantly advancing the clinical utilization of stem cell molecular and cellular biology. By bridging stem cell research and clinical trials, SCTM will help move applications of these critical investigations closer to accepted best practices. SCTM is the official journal partner of Regenerative Medicine Foundation.

About AlphaMed Press: Established in 1983, AlphaMed Press with offices in Durham, NC, San Francisco, CA, and Belfast, Northern Ireland, publishes two other internationally renowned peer-reviewed journals:STEM CELLS, celebrating its 38th year, is the worlds first journal devoted to this fast paced field of research.The Oncologist, also a monthly peer-reviewed publication, entering its 25th year, is devoted to community and hospital-based oncologists and physicians entrusted with cancer patient care. All three journals are premier periodicals with globally recognized editorial boards dedicated to advancing knowledge and education in their focused disciplines.

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Coronavirus immunity passports could create a world of ‘us and them’. But here’s why they make sense – Genetic Literacy Project

Dividing groups of people into us and them isnt usually a good idea, but in the scary new world of COVID-19, it makes a certain sense. Issuing immunity licenses aka passports or certificates to people whose blood contains neutralizing antibodies against the novel coronavirus may be a safer way to reopen parts of the economy than letting unchecked crowds spill onto beaches, pack into subway cars, and fill eateries, stadiums, and concert venues.

Immunity licenses would give holders certain time-limited work and social freedoms, joining larger gatherings or returning to nonessential jobs, wrote Mark A. Hall, of the Wake Forest University Schools of Law and Medicine and David M. Studdert, from Stanford University Schools of Law and Medicine, in a recent Viewpoint in JAMA.

License holders could safely:

Getting an immunity license should be free. The Coronavirus Aid, Relief and Economic Security (CARES) Act requires private and public insurers to pay for all professional SARS-CoV-2 testing, including antibody tests, and reimburse hospitals for testing uninsured patients. And licenses wont be needed indefinitely. Theyre a bridge to gradually reawaken the economy until a combination of vaccines and recovery build towards herd immunity if that happens.

The coming of immunity licenses is almost inevitable, said Ezekiel Emanuel, an oncologist and bioethicist at the University of Pennsylvania during a webinar that JAMA held, upon publication of a Viewpointhe wrote with Govind Persad, from the University of Denver.

Countries like Chile and Germany have already said they would do this. If New Zealand becomes virus-free, theyre going to only want people coming in who can demonstrate a license or do a 14-day quarantine. The UK too is discussing an immunity-based license. Its going to be travel that forces the US to adopt the idea, Emanuel said.

On the surface, the idea of distinguishing those who have recovered from those who are susceptible to infection may seem like a ticket to discrimination, a literal status symbol. Would holding a license become part of a job application, a dating profile, a metro card, or a stamp on an airline ticket like TSA precheck?

More nefariously, would not having an immunity license become like wearing a scarlet letter as Hester Prynne did in Nathaniel Hawthornes classic tale to mark her as an adulteress, or Jewish people being forced to wear yellow starsin Nazi Germany?

Dr. Emanuel doesnt see it that way:

An immunity passport enhances the liberty of those people whove been exposed to and recovered from COVID-19, but it doesnt diminish the liberty of those who are nave to the virus.

But those not holding licenses might not agree.

Comparison to Nazi Germany, which Dr. Emanuel was asked about during the webinar, is a false dichotomy, he said. We have to recognize the difference between having a star because youre Jewish and having an immunity passport because youve recovered from COVID-19. The first is whats legally called invidious discrimination taking an irrelevant factor and excluding you from benefits and rights in society, and eventually sending you to concentration camps. Thats very different from an immunity passport not based on a characteristic like race, religion, or gender, but upon recovering from an infection and becoming immune so you cant pass it on.

Emanuel compared an immunity document to the necessity of having a drivers license. Driving a car poses a lethal threat to self and others. We test people, make distinctions in gradations you need a license to drive a bus or truck or motorcycle. Similarly, with an immunity passport, you get certified, but its time-limited because we dont know how long immunity will last. Natural immunity to SARS lasts up to 2 years and to MERSup to 3 years.

Widespread use of immunity licenses also depends upon having enough accurate serology testing to reliably detect neutralizing antibodies. And we still dont know whether reinfection happens.

In a report in Nature Medicine, Joshua Weitz, from the Georgia Institute of Technology, and his team coin the term shield immunity to describe using the short-term immunity of the recently-recovered to temporarily protect the vulnerable by replacing them in parts of the outside world.

Our epidemiological intervention computational model describes ways in which serological tests used to identify individuals who have been infected by and recovered from COVID-19 could help both reduce future transmission and foster increased economic engagement, said Weitz.

The model considers a population of a specific size against shielding strategies of varying strengths to predict number of lives saved. Strength refers to the proportion of protected individuals who substitute in society for infected individuals in a particular role such as recovered health care workers.

The metrics are clear. In a population of 10 million citizens, intermediate shielding with worst-case viral transmission can reduce 71,000 deaths to 58,000. But enhanced shielding more protected people replacing vulnerable ones would cut deaths down to 20,000.

Even better would be teaming shielding with continuing some social distancing as the economy reopens.

Documents similar to immunity licenses or passports are already in use. For example, students, teachers, and educational support staff need proof of vaccination to go to school. International travelrequires a slew of vaccinations. And of course health care workers need them.

But an immunity license for COVID-19 would differ from one for, say, yellow fever or hepatitis, in three ways, Hall and Studdert argued.

First, we know so little about the new virus compared to other pathogens. Secondly, immunity is possible only through infection and recovery, not also through a vaccine. People are vaccinated against yellow fever and hepatitis B, for example.

Thirdly, the conditioned privileges could include a greater range of fundamental civil liberties and opportunities, like freedom of association, worship, work, education, and travel, wrote Hall and Studdert.

As the idea of immunity licenses gains traction, some people are antsy about waiting for the particulars to be worked out. Knowing they were sick, some individuals might start going out more, assuming immunity even if theyd never had a diagnostic PCR-based test or one for protective antibodies. Wrote Hall and Studdert:

People will begin to self-certify, with much less accuracy and credibility than if certification were official. The rapidly unfolding situation raises a host of important legal, ethical, and policy concerns that will not wait for greater scientific certainty.

Emanuel agreed. Imagine being a parent of a child going to school, or hiring a nanny. Youd do your own immunity-based passport. If it starts out haphazardly, were not going to get an organized system, he warned.

I remember back in the 1960s, in that slice of time when youngsters progressed through a series of infectious diseases measles, mumps, rubella, and chickenpox many parents intentionally exposed their kids to sick friends to get the diseases over with. The practice of pox parties diminished when the public realized that these diseases can be deadly, and with the arrival of vaccines.

Physicians today fear coronavirus parties.

We are a society based on individual rights, and we want people to make choices about risk. We allow extreme sports, skiing, bungee jumping. We allow them to drive cars. We wont get rid of pox parties entirely, but we dont want to incentivize behavior that has serious complications, said Emanuel, who admitted to having had pox parties for his now-grown sons.

But the initial thinking that kids arent likely to contract or get very sick from COVID-19 has been changing. Young people can suffer strokes. And the recent emergence of multisystem inflammatory syndromein children weeks after the acute sickness, or even in asymptomatic kids, is a good reason not to intentionally expose a child.

The fact that the virus is affecting communities of color and povertyconsiderably more than other areas is undisputed. Reasons are many: access to health care, living in crowded conditions, higher prevalence of underlying conditions that elevate risk of infection. But these higher-risk groups may also disproportionately benefit from immunity licenses.

The licenses will actually correct some disparities and even operate more as a leveler than a class divider, said Hall and Studdert. That assumes antibody testing is available to all.

Emanuel offered an example. African-Americans are 45 to 50% of the Washington, DC population, but in terms of deaths from COVID-19, they account for around 80%. It is a horrible disparity. But immunity passports would then allow these African-Americans exposed to the virus to participate in employment. Theres no discrimination in an immunity-based passport. Its based on whether youve recovered or not.

Rolling out immunity licenses will also require safeguards. They must be hard to forge or counterfeit, a nonhackable electronic certification, said Emanuel, comparing the challenge to the FAA certifying pilots. States in the end will have this responsibility, he added.

Concludes Weitz, We dont have a silver bullet. Until we have a vaccine, we will have to use a combination of strategies to control COVID-19.

Ricki Lewis is the GLPs senior contributing writer focusing on gene therapy and gene editing. She has a PhD in genetics and is a genetic counselor, science writer and author of The Forever Fix: Gene Therapy and the Boy Who Saved It, the only popular book about gene therapy. BIO. Follow her at her website or Twitter @rickilewis

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Coronavirus immunity passports could create a world of 'us and them'. But here's why they make sense - Genetic Literacy Project

Scientists race to find a cure or vaccine for the coronavirus. Here are the top drugs in development – CNBC

A researcher of the Openlab genetic and cell technologies laboratory of the Kazan Federal University working with biomaterial.

Yegor Aleyev | TASS via Getty Images

Health officials and scientists across the world are racing to develop vaccines and discover effective treatments against the coronavirus, which has infected more than 4.2 million people worldwide in as little as four months, according to data compiled by Johns Hopkins University.

There are no proven, knockout treatments and U.S. health officials say a vaccine could take at least a year to 18 months.

On May 1, theFood and Drug Administration granted emergency use authorizationfor Gilead Sciences' antiviral drug remdesivir. This after a government-run clinical trial found Covid-19 patients who took remdesivir usually recovered after 11 days. That is four days faster than those who didn't take the drug. The EUA means doctors in the U.S. will be allowed to use remdesivir on patients hospitalized with Covid-19 even though it has not been formally approved by the agency.

Even if the drug wins final approval, infectious disease specialists and scientists say researchers will need an arsenal of medications to fight this respiratory virus, which can also attack the cardiovascular, nervous, digestive and other major systems of the body.

Below is a list of the leading vaccines and drugs in development to battle Covid-19.

Nicolas Asfouri | AFP | Getty Images

Moderna

The National Institutes of Health, an agency within the Department of Health and Human Services, has been fast-tracking work with biotech company Moderna to develop a vaccine to prevent Covid-19.The company began the first phase 1 human trialon45 volunteers testing a vaccine to prevent the disease in March and has been approved to soon start its phase 2, which would expand the testing to 600 people, by late May or June. If all goes well, its vaccine could be in production as early as July.

Scientist Xinhua Yan works in the lab at Moderna in Cambridge, Massachusetts, on Feb. 28, 2020. Moderna has developed the first experimental coronavirus medicine, but an approved treatment is more than a year away.

David L. Ryan | Boston Globe | Getty Images

Moderna's potential vaccine contains genetic material called messenger RNA, or mRNA, that was produced in a lab. The mRNA is a genetic code that tells cells how to make a protein and was found in the outer coat of the new coronavirus, according to researchers at the Kaiser Permanente Washington Health Research Institute. The mRNA instructs the body's own cellular mechanisms for making proteins to create those that mimic the virus proteins, thereby producing an immune response.

Johnson & Johnson

Johnson & Johnson began Covid-19 vaccine development in January. J&J's lead vaccine candidate will enter a phase 1 human clinical study by September, the company announced in March, and clinical data on the trial is expected before the end of the year. If the vaccine works well, the company said it could produce600 million to 900 million doses by April 2021.

The company said it is using the same technologies it used to make its experimental Ebola vaccine, which was provided to people in the Democratic Republic of Congo in late 2019. It involves combing genetic material from the coronavirus with a modified adenovirus that is known to cause common colds in humans.

Inovio Pharmaceutical

Inovio began its early stage clinical trials for a potential vaccine on April 6,making it the second potential Covid-19 vaccine to undergo human testing after Moderna. It says it will enroll up to 40 healthy adult volunteers in Pennsylvaniaand Missouri and expects initial immune responses and safety data by late summer. Inovio made its potential vaccine by adding genetic material of the virus inside synthetic DNA, which researchers hope will cause the immune system to make antibodies against it.

Oxford University

A coronavirus vaccine developed by researchers at Oxford University began phase 1 human trials on April 23. British Health Minister Matt Hancock saidthat he wouldprovide 20 million, ($24.5 million), to help fund the Oxford project. The team said it aims to produce 1 million doses by September.

General view of the sign for University of Oxford, Old Road Campus and Trials clinic on May 02, 2020 in Oxford, England.

Catherine Ivill | Getty Images

Oxford researchers are calling their experimental vaccineChAdOx1 nCoV-19, and it's a kind ofrecombinant viral vector vaccine. Like J&J's team, the researchers will place genetic material from the coronavirus into another virus that's been modified. They will then inject the virus into a human, hoping to produce an immune response.

Pfizer

Pharmaceutical giant Pfizer,which is working alongside German drugmaker BioNTech, began testing an experimental vaccine to combat the coronavirus in the U.S. on May 5.The U.S.-based drugmaker hopes to produce "millions" of vaccines by the end of this year and expects to increase to "hundreds of millions" of doses next year. The experimental vaccine uses mRNA technology, similar to Moderna. The mRNA is a genetic code that tells cells what to build in this case, an antigen that may induce an immune response for the virus.

In this photo illustration the American multinational pharmaceutical corporation Pfizer logo seen displayed on a smartphone with a computer model of the COVID-19 coronavirus on the background.

Budrul Chukrut | SOPA Images | Getty Images

Sanofi and GSK

Sanofi and GSKannouncedApril14 that they had entered an agreement to jointly create a Covid-19 vaccineby the end of next year.The companies plan to start clinical trials in the second half of 2020 and, if successful, produce up to 600 million doses next year. To make it, Sanofi said it will repurpose its SARS vaccine candidate that never made it to market while GSK will provide pandemic adjuvant technology, which is meant to enhance the immune response in vaccines.

Novavax

Novavax announced on April 8 it found a coronavirus vaccine candidate and would start human trials in May with preliminary results expected in July. The potential vaccine, which is being calledNVX-CoV2373, is usingadjuvant technology and will attempt to neutralize the so-called spike protein, found on the surface of the coronavirus, which is used to enter the host cell.

Vials of investigational coronavirus disease (COVID-19) treatment drug remdesivir are capped at a Gilead Sciences facility in La Verne, California, U.S. March 18, 2020. Picture taken March 18, 2020.

Gilead Sciences Inc | Reuters

Gilead Sciences

The FDA granted emergency use authorization for Gilead's remdesivir drug to treat Covid-19 on May 1. The National Institute of Allergy and Infectious Diseases released results from its study showing patients who took remdesivir usually recovered faster than those who didn't take the drug. Even though remdesivir was granted for emergency use, there are still several ongoing clinical trials testing whether it's effective in stopping the coronavirus from replicating.

Remdesivir has shown some promise in treating SARS and MERS, which are also caused by coronaviruses. Some health authorities in the U.S., China and other parts of the world have been using remdesivir, which was tested as a possible treatment for the Ebola outbreak, in hopes that the drug can improve the outcomes for Covid-19 patients. The company said it expects to produce more than 140,000 rounds of its 10-day treatment regimen by the end of May and anticipates it can make 1 million rounds by the end of this year.

New York state and others

Hydroxychloroquine is a decades-old malaria drug touted by PresidentDonald Trumpas a potential "game-changer."

The drug is proven to work in treating Lupus and rheumatoid arthritis, but not Covid-19. A handful of small studies on its use in coronavirus patients published in France and China had raised hope that the drug might help fight the virus. However, hydroxychloroquine, which is available as a generic drug and is also produced under the brand name Plaquenil by French drugmaker Sanofi, can have serious side effects, including muscle weakness and heart arrhythmia.

A bottle of Prasco Laboratories Hydroxychloroquine Sulphate is arranged for a photograph in the Queens borough of New York, U.S., on Tuesday, April 7, 2020.

Christopher Occhicone | Bloomberg | Getty Images

The FDA issueda warning against takingthe drug outside a hospital or formal clinical trial setting after it became aware of reports of "serious heart rhythm problems" in patients.

On March 24, researchers at NYU Langone in New York launchedone of the nation's largest hydroxychloroquine clinical studiesafter federal health regulators fast-tracked approvals for coronavirus research, allowing scientists across the nation to skip through months of red tape. It's one of more than a dozen formal studies in the U.S. looking at treatments for the coronavirus,according to ClinicalTrials.gov.

But the early results aren't so promising. An observational study published in thejournal JAMA Network Open on Monday and run by the New York State Department of Health, in partnership with the University of Albany, found that it didn't help coronavirus patients. Worse yet, when taken with azithromycin which French researchers credited with speeding recovery times it put patients at significantly higher risk of cardiac arrest.

Zhejiang Hisun Pharmaceutical

Favipiravir is an anti-flu drug sold byFujifilm Holding under the name Avigan. Researchers in China are testing the drug to see if it's effective in fighting the coronavirus. Most of favipiravir's preclinical data is derived from its influenza and Ebolaactivity; however, the agent also demonstrated broad activity against other RNA viruses, according to researchers in Japan.

Regeneron and Sanofi

Regeneron and Sanofi started clinical trials of rheumatoid arthritis drug Kevzara in Covid-19 patients in March.The drug inhibits a pathway thought to contribute to the lung inflammation in patients with the most severe forms of Covid-19.

The companies announced last month that Kevzara showed promise for treating the sickest coronavirus patients in a clinical trial but it wasn't beneficial for patients with less-advanced disease, prompting the companies to stop testing the medicine in that group.

Eli Lilly

Eli Lilly, in partnership with National Institute of Allergy and Infectious Diseases, is seeing if its rheumatoid arthritis drugbaricitinib is effective against the coronavirus.The company theorizes that baricitinib's anti-inflammatory effects could curb the body's reaction to the virus.

Eli Lilly, AstraZeneca and Regeneron

While some drugmakers are looking for vaccines to stop the virus, Eli Lilly, AstraZeneca and Regeneron, among other companies, are working on so-called antibody treatments, which are made to act like immune cells and may provide protection after exposure to the virus. Earlier this month,Regeneron said its treatment could be available for use by the end of this summer or fall.

Original post:

Scientists race to find a cure or vaccine for the coronavirus. Here are the top drugs in development - CNBC

WHITEHALL ANALYTICA THE AI SUPERSTATE: Part 2 Is COVID-19 Fast-Tracking a Eugenics-Inspired Genomics Programme in the NHS? – Byline Times

Nafeez Ahmed explores the troubling implications and assumptions of the Governments AI-driven gene programme.

In Part 1 of this investigation, I looked at how the convergence of an AI Superstate and corporate interests with health data lies at the heart of a new frontier for profit and surveillance. But the Governments response during the COVID-19 pandemic has revealed something even more profoundly disturbing: a fascination with genomics which moves from a merely descriptive tool to something so prescriptive it verges on eugenics.

The NHSX app is simply one project with a questionable design which appears to result from the Governments much wider project to remake the NHS.

At the core of the new NHSX AI drive is the goal of predictive, preventive, personalised and participatory medicine, according to an NHSX document published in October 2019. Pivotal to this AI-driven transformation is genetics:

Key to unlocking the benefits of precision medicine with AI is the use of genomic data generated by genome sequencing. Machine learning is already being used to automate genome quality control. AI has improved the ability to process genomes rapidly and to high standards and can also now help improve genome interpretation.

The NHS Genomic Medicine Service is starting with a focus on cancer, rare and inherited diseases,but its broader goal is far more comprehensive. Initially, the hope is that genomics will expand to cover other areas, such as pharmacogenomics, which looks at how an individuals genes influence a particular biological process that mediates the effects of a medicine, according to The Pharmaceutical Journal.

But the end-goal is to convert the NHS into a health service oriented fundamentally around the role of genetics in disease. The aspiration is that from 2020, and by 2025, genomic medicine will be an embedded part of routine care to enable better prediction and prevention of disease and fewer adverse drug reactions. The GMS aims to complete five million genomic analyses and five million early disease cohorts over the next five years.

By 2025, genomic technologies will be embedded through multiple clinical pathways and included as a fundamental part of clinical training. As a result, it is hoped that there will be a new taxonomy of medicine based on the underlying drivers of disease.

But, this entire premise is deeply questionable. There is little evidence that the underlying drivers of disease are primarily genetic.

Last December, a study in the journal PLOS One found that genetics usually explains no more than 5-10% of the risk for several common diseases. The study examined data from nearly 600 earlier studies identifying associations between common variations in the DNA sequence and more than 200 medical conditions. But its conclusion was stark: more than 95% of diseases or disease risks including Alzheimers, autism, asthma, juvenile diabetes, psoriasis, and so on could not be predicted accurately from the DNA sequence. A separate meta-analysis of two decades of DNA science corroborated this finding.

The implication is startling: that the entire premise for the billions of pounds this Government is investing in building a new privatised NHS infrastructure for AI-driven genomic medicine is scientifically unfounded.

The obsession with genetics can be traced directly back to the Prime Ministers chief advisor, Dominic Cummings.

Cummings set out his vision for the NHS in a February 2019 blog, which although previously reported on has not been fully appreciated for its astonishingly direct implications. While focusing on disease risk, the blog flagged-up Cummings hopes that a new NHS genomics prediction programme would ultimately allow the UK to, not just prevent diseases, but to do so before birth in effect a nod toward the selective breeding techniques at the core of eugenics.

They are using the COVID-19 crisis to erect a corporate superstate powered by mass surveillance and AI. Their grim ambition is to reach into the very DNA of every British citizen.

His vision for what a genomics-focused NHS would look like bears startling resemblance to the core ideas of eugenics the discredited pseudoscience aiming to improve the genetic quality of a human population by selecting for superior groups and excluding those with inferior genes. Its worst manifestations were exemplified by the Nazis.

In the blog, Cummings wrote:

Britain could contribute huge value to the world by leveraging existing assets, including scientific talent and how the NHS is structured, to push the frontiers of a rapidly evolving scientific field genomic prediction. He called for free universal SNP [single-nucleotide polymorphis] genetic sequencing as part of a shift to genuinely preventive medicine, to be rolled-out across the UK. This approach holds the promise of revolutionising healthcare in ways that give Britain some natural advantages over Europe and America.

Later in the post, Cummings allowed himself to speak more directly to what natural advantages could actually entail. He claimed that a combination of AI-driven machine learning with very large genetic sampling could enable the precise prediction of complex traits such as general intelligence and most diseases.

The two scientists Cummings cited as the primary sources for his vision were educational psychologist Robert Plomin and physicist Steven Hsu.

Plomin, described by Cummings as the worlds leading expert on the subject, is a renowned scientist. But he also has a history of association with the eugenics movement, according to Dr David King, founder of Human Genetics Alert and previously a molecular biologist. (Sir David King, the former chief scientific adviser to the UK Government, has also criticised the genome sequencing goldrush).*

When The Bell Curve a book advocating the genetic inferiority of African Americans was published, Plomin was a key signatory to a statement defending the science behind the book, explained Dr David King in a paper for the non-profit watchdog Human Genetics Alert. The statement carefully avoided explicitly endorsing The Bell Curves racist conclusions (aptly summarised by Francis Wheen as black people are more stupid than white people: always have been, always will be. This is why they have less economic and social success), while failing to repudiate them. Plomins fellow co-signatories included several self-proclaimed scientific racists, Philippe Rushton and Richard Lynn. Plomin has also published papers with the American Eugenics Society and spoken at several meetings of the British Eugenics Society (the latter rebranded itself as the Galton Institute in 1989) both of which advocated racial science.

In December 2013, Plomin was called as an expert witness to the House of Commons Education Select Committee, where he called for the Government to focus on the heritability of educational attainment. Twenty-five minutes into the session, Dominic Raab who as Foreign Secretary and First Secretary has stood in for Boris Johnson during his period of absence due to COVID-19 prompted Plomin to focus more specifically on explaining his views about genetics, intelligence and socio-economic status.

Just two months before Plomins parliamentary testimony, a 237-page dossier by Cummings then a top advisor to Education Secretary Michael Gove was leaked to the press. The paper claimed that genetics plays a bigger role in a childs IQ than teaching and called for giving specialist education as per Eton to the top 2% in IQ. Pete Shanks of the Centre for Genetics and Society described Cummings policy proposal as a blatantly eugenic association of genes with intelligence, intelligence with worth, and worth with the right to rule.

The Cummings dossier which cites Plomin extensively further reveals that, according to Cummings, he had invited Plomin into the DfE [Department for Education] to explain the science of IQ and genetics to officials and ministers.

The Education Select Committees report shows that, at the time of Plomins testimony, the Government was resistant to these views. But, the position appears to have changed since then, with figures such as Cummings, Raab and Gove now at the seat of power under Prime Minister Boris Johnson.

Plomin would go on to work with Steven Hsu, who was involved in a major Chinese genome sequencing project based on thousands of samples from very high-IQ people around the world. The goal was to identify genes that can predict intelligence. Hsu went on to launch his own company, Genomic Prediction. In slide presentations about his work from 2012, Hsu approvingly quoted British eugenicist Ronald Fisher, closing his slides with the following quotation: but such a race will inevitably arise in whatever country first sees the inheritance of mental characters elucidated. Hsus slides, wrote David King, include plans for a eugenic breeding scheme using embryo selection to improve the overall IQ of the population.

Yet, on his blog, Cummings confirmed that Hsu has recently attended a conference in the UK where he presented some of these ideas to UK policy-makers. Among the ideas Hsu presented to Cummings colleagues in Government was that the UK could become the world leader in genomic research by combining population-level genotyping with NHS health records. Hsu further claimed that risk prediction for common diseases was already available to guide early interventions that save lives and money.

Hopefully the NHS and Department for Health will play the Gretzky game, take expert advice from the likes of Plomin and Hsu and take this opportunity to make the UK a world leader in one of the most important frontiers in science, enthused Cummings.

Plomins claim that intelligence is determined primarily by genes contradicts a vast body of scientific literature, and is largely overblown. One of the latest studies debunking Cummings hopes was led by the University of Bristol and published in March. Based on a sample size of 3,500 children, the study found that polygenic scores (which combine information from all genetic material across the entire genome) have limited use for accurately predicting individual educational performance or for personalised education.

The study did not dismiss a role for genes outright, noting genetic scores modestly predictededucational achievement. The problem was that these predictions were less accurate than using standard information known to predicteducational outcomes, such as achievement at younger ages, parents educational attainment or family socio-economic position.

Last November, Hsus Genomic Prediction began touting new report cards to its customers. The cards displayed alleged results of genetic tests containing warnings that embryos might have low intelligence, grow up to be short, or have other conditions such as diabetes. But, according to the MIT Technology Review, the company has struggled both to validate its predictions and to interest fertility centres in them. In the month prior to Hsus grand announcement, the first major study to test the empirical viability of screening embryos, led by statistical geneticist Shai Carmi of the Hebrew University of Jerusalem, concluded that the technology is not plausible.

The lack of scientific substantiation has not stopped Cummings from suggesting a more interventionist vision for the NHS, which could be accused of paving the way for a new form of eugenics. In his February 2019 blog, he wrote: We can imagine everybody in the UK being given valuable information about their health for free,truly preventive medicinewhere we target resources at those most at risk, and early (evenin utero) identification of risks. This passage appears to nod to the core eugenics notion of selective breeding using embryo selection. Cummings even went further to endorse the goal of editing genes to fix problems.

In a further telling but slightly more well-known passage, Cummings characterised the genomics programme as a precursor to more realistic views about IQ and social mobility: It ought to go without saying that turning this idea into a political/government success requires focus on A) the NHS, health, science, NOT getting sidetracked into B) arguments about things like IQ and social mobility. Over time, the educated classes will continue to be dragged to more realistic views on (B) but this will be a complex process entangled with many hysterical episodes. (A) requires ruthless focus.

This passage affirms that Cummings approach is deliberately deceptive. The focus on health and the NHS is revealed as a cover for a longer-term vision to usher in more realistic views about things like IQ and social mobility. The passage also lifts the rock on Cummings weakest point that he fears that public attention on these more realistic views could sidetrack the broader strategy before it reaches fruition.

In the words of Dr David King, Cummings deference to Hsu, who openly advocated eugenics breeding programmes, suggests that the Prime Ministers chief advisor clearly favours this strategy for Britain; of course, this is precisely what all the European countries were trying to achieve in the heyday of eugenics to overcome their imperialist competitors by improving the national stock.

This, it seems, is the essence of Cummings ambition to use the NHS genomics prediction programme as a mechanism to provide Britain natural advantages over Europe and America.

And in this context, it is impossible to ignore the implications of Cummings appointment of Andrew Sabisky to a senior role advising Boris Johnson. When Johnsons spokespeople were asked repeatedly whether the Prime Minister would condemn Sabiskys sympathies for racist eugenics, he repeatedly refused. Sabisky later stepped away from the role.

The COVID-19 pandemic has now provided the Government with the opportunity to double down on its goals of extending genome sequencing across the UK population.

While genomic sequencing of the Coronavirus is undoubtedly an important scientific task to map and understand it, the crisis fits neatly into Cummings call for a ruthless focus on the NHS as a vehicle for Britains genetic enhancement.

On 23 March, when the UK finally instituted a lockdown at least three weeks after being informed that hundreds of thousands of people (and potentially up to a million) people were at risk of death from its previous policy of herd immunity, the Government launched a new scientific research consortium coordinated by Cambridge University along with the Wellcome Sanger Institute, the NHS and Public Health England.

The consortium would gather samples from patients confirmed with COVID-19 and send them to genetic sequencing centres across the country to analyse the whole genetic code of the samples. The project was billed breathlessly as an essential step in being able to control the pandemic and prevent further spread.

Unsurprisingly, it has done no such thing. Instead, six weeks later, the UK has ended up with the highest COVID-19 fatality rate in Europe.

As the death toll approaches the same level of British civilian casualties during the Second World War, the Governments strategy has privileged ambiguous, extortionate high technology solutions, pouring hundreds of millions of pounds into powerful private sector players with no transparency or due process. Meanwhile, traditional, proven, public health strategies such as better border controls, or extensive contact tracing and testing by scaling up local capacity, were inexplicably delayed for months.

On 13 March, the Government launched a new partnership between the NHS, Genomics England, the GenOMICC consortium, and US biotech giant Illumina, to conduct a nationwide human whole genome sequencing study targeting COVID-19 patients in 170 intensive care units.

The Governments new genome sequencing partner, Illumina, has previously produced genetic sequencing systems marketed to police agencies in China to facilitate its genetic profiling of the minority Uyghur population in Xinjang the largest system of discriminatory, ethnically-targeted biometric surveillance using DNA ever created.

It is difficult to avoid the conclusion that Dominic Cummings and his fellow ideologues in Government are hell-bent on pursuing a pseudo-scientific vision that has been years in the making.They are using the COVID-19 crisis to erect a corporate superstate powered by mass surveillance and AI. Their grim ambition is to reach into the very DNA of every British citizen.

Dominic Cummings was contacted for this article, but is yet to reply.

*This article was corrected to remove a confusion between Sir David King, the former government chief scientific adviser, and Dr David King, the molecular biologist who isthefounder and Director of Human Genetics Alert.

Continued here:

WHITEHALL ANALYTICA THE AI SUPERSTATE: Part 2 Is COVID-19 Fast-Tracking a Eugenics-Inspired Genomics Programme in the NHS? - Byline Times

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CRISPR And CRISPR-Associated (Cas) Genes Market Table of Content

Table of Contents 1 CRISPR And CRISPR-Associated (Cas) Genes Market Overview1.1 Product Overview and Scope of CRISPR And CRISPR-Associated (Cas) Genes1.2 CRISPR And CRISPR-Associated (Cas) Genes Segment by Type1.2.1 Global CRISPR And CRISPR-Associated (Cas) Genes Sales Growth Rate Comparison by Type (2021-2026)1.2.2 Genome Editing1.2.3 Genetic engineering1.2.4 gRNA Database/Gene Librar1.2.5 CRISPR Plasmid1.2.6 Human Stem Cells1.2.7 Genetically Modified Organisms/Crops1.2.8 Cell Line Engineering1.3 CRISPR And CRISPR-Associated (Cas) Genes Segment by Application1.3.1 CRISPR And CRISPR-Associated (Cas) Genes Sales Comparison by Application: 2020 VS 20261.3.2 Biotechnology Companies1.3.3 Pharmaceutical Companies1.3.4 Academic Institutes1.3.5 Research and Development Institutes1.4 Global CRISPR And CRISPR-Associated (Cas) Genes Market Size Estimates and Forecasts1.4.1 Global CRISPR And CRISPR-Associated (Cas) Genes Revenue 2015-20261.4.2 Global CRISPR And CRISPR-Associated (Cas) Genes Sales 2015-20261.4.3 CRISPR And CRISPR-Associated (Cas) Genes Market Size by Region: 2020 Versus 2026 2 Global CRISPR And CRISPR-Associated (Cas) Genes Market Competition by Manufacturers2.1 Global CRISPR And CRISPR-Associated (Cas) Genes Sales Market Share by Manufacturers (2015-2020)2.2 Global CRISPR And CRISPR-Associated (Cas) Genes Revenue Share by Manufacturers (2015-2020)2.3 Global CRISPR And CRISPR-Associated (Cas) Genes Average Price by Manufacturers (2015-2020)2.4 Manufacturers CRISPR And CRISPR-Associated (Cas) Genes Manufacturing Sites, Area Served, Product Type2.5 CRISPR And CRISPR-Associated (Cas) Genes Market Competitive Situation and Trends2.5.1 CRISPR And CRISPR-Associated (Cas) Genes Market Concentration Rate2.5.2 Global Top 5 and Top 10 Players Market Share by Revenue2.5.3 Market Share by Company Type (Tier 1, Tier 2 and Tier 3)2.6 Manufacturers Mergers & Acquisitions, Expansion Plans2.7 Primary Interviews with Key CRISPR And CRISPR-Associated (Cas) Genes Players (Opinion Leaders) 3 CRISPR And CRISPR-Associated (Cas) Genes Retrospective Market Scenario by Region3.1 Global CRISPR And CRISPR-Associated (Cas) Genes Retrospective Market Scenario in Sales by Region: 2015-20203.2 Global CRISPR And CRISPR-Associated (Cas) Genes Retrospective Market Scenario in Revenue by Region: 2015-20203.3 North America CRISPR And CRISPR-Associated (Cas) Genes Market Facts & Figures by Country3.3.1 North America CRISPR And CRISPR-Associated (Cas) Genes Sales by Country3.3.2 North America CRISPR And CRISPR-Associated (Cas) Genes Sales by Country3.3.3 U.S.3.3.4 Canada3.4 Europe CRISPR And CRISPR-Associated (Cas) Genes Market Facts & Figures by Country3.4.1 Europe CRISPR And CRISPR-Associated (Cas) Genes Sales by Country3.4.2 Europe CRISPR And CRISPR-Associated (Cas) Genes Sales by Country3.4.3 Germany3.4.4 France3.4.5 U.K.3.4.6 Italy3.4.7 Russia3.5 Asia Pacific CRISPR And CRISPR-Associated (Cas) Genes Market Facts & Figures by Region3.5.1 Asia Pacific CRISPR And CRISPR-Associated (Cas) Genes Sales by Region3.5.2 Asia Pacific CRISPR And CRISPR-Associated (Cas) Genes Sales by Region3.5.3 China3.5.4 Japan3.5.5 South Korea3.5.6 India3.5.7 Australia3.5.8 Taiwan3.5.9 Indonesia3.5.10 Thailand3.5.11 Malaysia3.5.12 Philippines3.5.13 Vietnam3.6 Latin America CRISPR And CRISPR-Associated (Cas) Genes Market Facts & Figures by Country3.6.1 Latin America CRISPR And CRISPR-Associated (Cas) Genes Sales by Country3.6.2 Latin America CRISPR And CRISPR-Associated (Cas) Genes Sales by Country3.6.3 Mexico3.6.3 Brazil3.6.3 Argentina3.7 Middle East and Africa CRISPR And CRISPR-Associated (Cas) Genes Market Facts & Figures by Country3.7.1 Middle East and Africa CRISPR And CRISPR-Associated (Cas) Genes Sales by Country3.7.2 Middle East and Africa CRISPR And CRISPR-Associated (Cas) Genes Sales by Country3.7.3 Turkey3.7.4 Saudi Arabia3.7.5 U.A.E 4 Global CRISPR And CRISPR-Associated (Cas) Genes Historic Market Analysis by Type4.1 Global CRISPR And CRISPR-Associated (Cas) Genes Sales Market Share by Type (2015-2020)4.2 Global CRISPR And CRISPR-Associated (Cas) Genes Revenue Market Share by Type (2015-2020)4.3 Global CRISPR And CRISPR-Associated (Cas) Genes Price Market Share by Type (2015-2020)4.4 Global CRISPR And CRISPR-Associated (Cas) Genes Market Share by Price Tier (2015-2020): Low-End, Mid-Range and High-End 5 Global CRISPR And CRISPR-Associated (Cas) Genes Historic Market Analysis by Application5.1 Global CRISPR And CRISPR-Associated (Cas) Genes Sales Market Share by Application (2015-2020)5.2 Global CRISPR And CRISPR-Associated (Cas) Genes Revenue Market Share by Application (2015-2020)5.3 Global CRISPR And CRISPR-Associated (Cas) Genes Price by Application (2015-2020) 6 Company Profiles and Key Figures in CRISPR And CRISPR-Associated (Cas) Genes Business6.1 Caribou Biosciences6.1.1 Corporation Information6.1.2 Caribou Biosciences Description, Business Overview and Total Revenue6.1.3 Caribou Biosciences CRISPR And CRISPR-Associated (Cas) Genes Sales, Revenue and Gross Margin (2015-2020)6.1.4 Caribou Biosciences Products Offered6.1.5 Caribou Biosciences Recent Development6.2 Addgene6.2.1 Addgene CRISPR And CRISPR-Associated (Cas) Genes Production Sites and Area Served6.2.2 Addgene Description, Business Overview and Total Revenue6.2.3 Addgene CRISPR And CRISPR-Associated (Cas) Genes Sales, Revenue and Gross Margin (2015-2020)6.2.4 Addgene Products Offered6.2.5 Addgene Recent Development6.3 CRISPR THERAPEUTICS6.3.1 CRISPR THERAPEUTICS CRISPR And CRISPR-Associated (Cas) Genes Production Sites and Area Served6.3.2 CRISPR THERAPEUTICS Description, Business Overview and Total Revenue6.3.3 CRISPR THERAPEUTICS CRISPR And CRISPR-Associated (Cas) Genes Sales, Revenue and Gross Margin (2015-2020)6.3.4 CRISPR THERAPEUTICS Products Offered6.3.5 CRISPR THERAPEUTICS Recent Development6.4 Merck KGaA6.4.1 Merck KGaA CRISPR And CRISPR-Associated (Cas) Genes Production Sites and Area Served6.4.2 Merck KGaA Description, Business Overview and Total Revenue6.4.3 Merck KGaA CRISPR And CRISPR-Associated (Cas) Genes Sales, Revenue and Gross Margin (2015-2020)6.4.4 Merck KGaA Products Offered6.4.5 Merck KGaA Recent Development6.5 Mirus Bio LLC6.5.1 Mirus Bio LLC CRISPR And CRISPR-Associated (Cas) Genes Production Sites and Area Served6.5.2 Mirus Bio LLC Description, Business Overview and Total Revenue6.5.3 Mirus Bio LLC CRISPR And CRISPR-Associated (Cas) Genes Sales, Revenue and Gross Margin (2015-2020)6.5.4 Mirus Bio LLC Products Offered6.5.5 Mirus Bio LLC Recent Development6.6 Editas Medicine6.6.1 Editas Medicine CRISPR And CRISPR-Associated (Cas) Genes Production Sites and Area Served6.6.2 Editas Medicine Description, Business Overview and Total Revenue6.6.3 Editas Medicine CRISPR And CRISPR-Associated (Cas) Genes Sales, Revenue and Gross Margin (2015-2020)6.6.4 Editas Medicine Products Offered6.6.5 Editas Medicine Recent Development6.7 Takara Bio USA6.6.1 Takara Bio USA CRISPR And CRISPR-Associated (Cas) Genes Production Sites and Area Served6.6.2 Takara Bio USA Description, Business Overview and Total Revenue6.6.3 Takara Bio USA CRISPR And CRISPR-Associated (Cas) Genes Sales, Revenue and Gross Margin (2015-2020)6.4.4 Takara Bio USA Products Offered6.7.5 Takara Bio USA Recent Development6.8 Thermo Fisher Scientific6.8.1 Thermo Fisher Scientific CRISPR And CRISPR-Associated (Cas) Genes Production Sites and Area Served6.8.2 Thermo Fisher Scientific Description, Business Overview and Total Revenue6.8.3 Thermo Fisher Scientific CRISPR And CRISPR-Associated (Cas) Genes Sales, Revenue and Gross Margin (2015-2020)6.8.4 Thermo Fisher Scientific Products Offered6.8.5 Thermo Fisher Scientific Recent Development6.9 Horizon Discovery Group6.9.1 Horizon Discovery Group CRISPR And CRISPR-Associated (Cas) Genes Production Sites and Area Served6.9.2 Horizon Discovery Group Description, Business Overview and Total Revenue6.9.3 Horizon Discovery Group CRISPR And CRISPR-Associated (Cas) Genes Sales, Revenue and Gross Margin (2015-2020)6.9.4 Horizon Discovery Group Products Offered6.9.5 Horizon Discovery Group Recent Development6.10 Intellia Therapeutics6.10.1 Intellia Therapeutics CRISPR And CRISPR-Associated (Cas) Genes Production Sites and Area Served6.10.2 Intellia Therapeutics Description, Business Overview and Total Revenue6.10.3 Intellia Therapeutics CRISPR And CRISPR-Associated (Cas) Genes Sales, Revenue and Gross Margin (2015-2020)6.10.4 Intellia Therapeutics Products Offered6.10.5 Intellia Therapeutics Recent Development6.11 GE Healthcare Dharmacon6.11.1 GE Healthcare Dharmacon CRISPR And CRISPR-Associated (Cas) Genes Production Sites and Area Served6.11.2 GE Healthcare Dharmacon CRISPR And CRISPR-Associated (Cas) Genes Description, Business Overview and Total Revenue6.11.3 GE Healthcare Dharmacon CRISPR And CRISPR-Associated (Cas) Genes Sales, Revenue and Gross Margin (2015-2020)6.11.4 GE Healthcare Dharmacon Products Offered6.11.5 GE Healthcare Dharmacon Recent Development 7 CRISPR And CRISPR-Associated (Cas) Genes Manufacturing Cost Analysis7.1 CRISPR And CRISPR-Associated (Cas) Genes Key Raw Materials Analysis7.1.1 Key Raw Materials7.1.2 Key Raw Materials Price Trend7.1.3 Key Suppliers of Raw Materials7.2 Proportion of Manufacturing Cost Structure7.3 Manufacturing Process Analysis of CRISPR And CRISPR-Associated (Cas) Genes7.4 CRISPR And CRISPR-Associated (Cas) Genes Industrial Chain Analysis 8 Marketing Channel, Distributors and Customers8.1 Marketing Channel8.2 CRISPR And CRISPR-Associated (Cas) Genes Distributors List8.3 CRISPR And CRISPR-Associated (Cas) Genes Customers 9 Market Dynamics 9.1 Market Trends 9.2 Opportunities and Drivers 9.3 Challenges 9.4 Porters Five Forces Analysis 10 Global Market Forecast10.1 Global CRISPR And CRISPR-Associated (Cas) Genes Market Estimates and Projections by Type10.1.1 Global Forecasted Sales of CRISPR And CRISPR-Associated (Cas) Genes by Type (2021-2026)10.1.2 Global Forecasted Revenue of CRISPR And CRISPR-Associated (Cas) Genes by Type (2021-2026)10.2 CRISPR And CRISPR-Associated (Cas) Genes Market Estimates and Projections by Application10.2.1 Global Forecasted Sales of CRISPR And CRISPR-Associated (Cas) Genes by Application (2021-2026)10.2.2 Global Forecasted Revenue of CRISPR And CRISPR-Associated (Cas) Genes by Application (2021-2026)10.3 CRISPR And CRISPR-Associated (Cas) Genes Market Estimates and Projections by Region10.3.1 Global Forecasted Sales of CRISPR And CRISPR-Associated (Cas) Genes by Region (2021-2026)10.3.2 Global Forecasted Revenue of CRISPR And CRISPR-Associated (Cas) Genes by Region (2021-2026)10.4 North America CRISPR And CRISPR-Associated (Cas) Genes Estimates and Projections (2021-2026)10.5 Europe CRISPR And CRISPR-Associated (Cas) Genes Estimates and Projections (2021-2026)10.6 Asia Pacific CRISPR And CRISPR-Associated (Cas) Genes Estimates and Projections (2021-2026)10.7 Latin America CRISPR And CRISPR-Associated (Cas) Genes Estimates and Projections (2021-2026)10.8 Middle East and Africa CRISPR And CRISPR-Associated (Cas) Genes Estimates and Projections (2021-2026) 11 Research Finding and Conclusion 12 Methodology and Data Source 12.1 Methodology/Research Approach 12.1.1 Research Programs/Design 12.1.2 Market Size Estimation 12.1.3 Market Breakdown and Data Triangulation 12.2 Data Source 12.2.1 Secondary Sources 12.2.2 Primary Sources 12.3 Author List 12.4 DisclaimerAbout Us:QYResearch always pursuits high product quality with the belief that quality is the soul of business. Through years of effort and supports from huge number of customer supports, QYResearch consulting group has accumulated creative design methods on many high-quality markets investigation and research team with rich experience. Today, QYResearch has become the brand of quality assurance in consulting industry.

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Researchers: Disease affecting kids could be in the genes – Newsday

The key to understanding and fighting the mysterious COVID-19-related inflammatory illness that is targeting children across the state could be in their genes.

The New York Genome Center is analyzingblood samples from the young patients with the hopes of finding genetic markers specific to the disease known as "pediatric multi-system inflammatory syndrome associated with COVID-19."

The state is investigating 102 cases of children who have the illness, which shows symptoms similar to Kawasaki disease or toxic shock syndrome. Three people, including an 18-year-old girl from Suffolk County, have died from the syndrome.

"This approach is widely used to study the genetic basis of all diseases, said Tom Maniatis, Evnin Family scientific director and chief executive officer of the New York Genome Center. We are trying to see if there are anygenetic clues to what might be causing this syndromein children.

If we can detect and understand thegenetic basis for predisposition, and how the immune system is affected in the disease, it might be possible to develop strategies for the clinical care of these children, he added.

Gov.Andrew M. Cuomo announced last week the state Department of Health was partnering with the Genome Center and The Rockefeller University to conduct a genome and RNA sequencing study of the illness, which hasbeen identified in 14 other states, including neighboring New Jersey and Connecticut, as well as five European countries.

Cuomo said Wednesday that60% of children with the illness have tested positive for COVID-19 and 40% had the antibody, meaning they may have been exposed to the coronavirus weeks before. Of those affected, 71% became seriously ill and were placed in intensive care units. He said 43% of those minors remain hospitalized and 19% had to be intubated.

According to a racial and ethnic breakdown of cases on thestate health department's website, 25% were white, 23% black, 20% other, 3% Asian and 31% unknown. In addition, 35% were Hispanic/Latino, 40% non Hispanic and 25% unknown.

Officials at Cohen Childrens Medical Center in New Hyde Park said they are seeing as many as two or three children a day with symptoms of the syndrome: fever and severe abdominal pain, rashes and red lips, eyes and tongue.

Experts believethe patients bodies might be having an extreme reaction to COVID-19, the disease caused by the novel coronavirus.

Whats so striking about this phenomena is that we all thought that most children were relatively safe, considering that they have the lowest mortality rate of any of the categories of COVID patients, Maniatis said.

A genome is an organisms complete set of DNA, including its genes, with all of the information needed to build and maintain that organism, according to the Bethesda, Maryland-based National Institutes of Health.

Researchers will look through the genome of patients in an effort to find DNA sequences that vary from the standard.

By comparing the childrens DNA sequence to the standard, we might be able to identify a variant that is not seen normally in most individuals, Maniatis said. And if you can show that it happens enough, you can begin to conclude that statistically its likely the DNA sequence change is associated with the disease."

The next step is RNA sequencing, which could provide insights into identification of altered immune pathways that are known to operate during virus infections.

Similar sequencing research conducted in the past led scientists to discover a gene mutation in people with blood cancer that impacted their immune system. A drug calledGleevec was developed to correct that mutation.

The Feinstein Institutes for Medical Research in Manhasset plans to participate in the study, said Dr. Peter Gregersen, professor of molecular medicine at Feinstein, the research arm of Northwell Health.

He said understanding the genetic variations of COVID-19 and the related illness thats attacking children is key to finding effective treatment.

We know age, sex and certain underlying conditions play a role, but genetic variations have something to do with this as well, Gregersen said. A lot of variations are unexplained. We know there is a huge variation, and some people dont get sick at all, while others have a devastating illness.

Maniatis said a vital part of the investigation is the collaboration with Jean-Laurent Casanova, head of the St. Giles Laboratory of Human Genetics of Infectious Diseases at The Rockefeller University.

He is one of the worlds experts in this field, and he established an international consortium directed toward understanding exceptional cases of clinical manifestations, Maniatis said. With Jean-Laurents participation, the search would extend from our efforts in New York and New Jersey to include researchers around the world and that will increase the statistical significance of any finding.

Lisa joined Newsday as a staff writer in 2019. She previously worked at amNewYork, the New York Daily News and the Asbury Park Press covering politics, government and general assignment.

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Researchers: Disease affecting kids could be in the genes - Newsday

From Competition To Sharing: How Her Childrens Rare Disease Led Sharon Terry To Revolutionize Medical Research – Forbes

Sharon Terry, President and CEO of Genetic Alliance.

Ashoka Fellow Sharon Terry looks back at 25 years of impact that led her from being a homeschooling mom to a genetic researcher and global health leader.

Sharon, in 1994 your two children were diagnosed with a rare genetic disease. That propelled you from a homeschooling mom with a degree in theology to a self-taught genetic researcher with now multiple scientific discoveries. It sounds like a naive question but: How did you do this?

Well, when my kids were diagnosed with this rare disease, I quickly learned that no one knew anything about it. The research available wasnt good, no doctor could really help us. The fear that something was going to happen to my children drove me and trying to keep ahead of the disease.My husband and I realized we would have to start to do research on the disease ourselves and figure out a way forward. We had to turn to ourselves for help, there was no other way.

Where did you get the confidence to do this?

Good question. I didnt really piece the dots together until much later, but I think one thing that ironically helped me was that I had had a very abusive childhood. I had to learn how to survive early. And from that terrible situation grew a confidence. I somehow knew, having survived my childhood years, I could overcome anything else.

You boldly asked Harvard to lend you bench space in their laboratories at night.

Yes. It worked!

And you identified a major problem in scientific research the lack of sharing.

Yes. I quickly learned that one of the biggest impediments was that scientists don't share, they don't collaborate, competition is their driving force. I saw all these researchers that had collected data, but they would hoard it, and not let another researcher see it. So I had to think of ways to break through that system and build a new model one that would encourage accelerated academic collaboration.

How did you do that?

I tracked down individuals suffering from the same condition around the world, and invited them to donate tissue, blood, health records, descriptions of their experience, to set up a database that would invite scientists to collaboratively pursue research on the disease. I knew if I could make a central repository of blood and tissue and DNA, then I could set the rules of the game to be different from what scientists were used to. And I decided my rules were going to be: If you come to my well, you will have to share with the community and with everybody else who takes anything out of the well."

And do you think it was key that you outcompeted them from the get-go with a central repository that was bigger than what they had?

Yes, that is certainly one way to look at it. If, for example, I had only come up with 100 data sets and they had 100, then they would have said, "Eh, well, I don't want to play by your rules." But they knew that we were going to be bigger than them. Because we were open, we were people-centered, and they were regional and closed. I think also people trusted us faster. I was a mom with two kids who had this disease, and was in the same boat they were in.

And your goal was not to outcompete other scientists, but to serve people with diseases.

Right. They knew that we would be in the game longer. A lot of scientists do two, three years of research on one condition, and then they go on to the next disease. In contrast, people knew I would probably work on this condition for the rest of my life.

And they were right. Though in addition, you also included many other genetic diseases into your work.

Correct, when I joined Genetic Alliance in 1996, my goal was to replicate my work and use theblueprint I had created for all sorts of other diseases. Which we did. Today, after almost 25 years, we have over 10,000 organizations that interact with us, and dozens of disease groups that are very, very active, working side by side with us, partnering on research.

A key part of your initial success was to patent the gene you discovered that caused your childrens disease, paradoxically to preserve its open accessibility.

Yes. I was concerned that others might patent the gene and restrict access. I had seen a lot on the way: researchers trying to steal my data, to thaw my samples so theyd be useless to me. When we were succeeding in sequencing the gene, I knew I had to go first. I got the patent and then I turned the patent over to the foundation I had set up. And the foundation licensed it to researchers for a dollar back in the days when we had to license it. Now its free and open, so that doesnt matter anymore.

How do you ensure privacy, and that the benefits of the research get distributed back to the community that contributed the data and samples in the first place?

Any data or samples you share your experience of living with your disease, your electronic health record, and your genomic information is encrypted, stored on the platform and never leaves the system. In lay terms, you keep a string on your data. You always know where it is, you know who's looking at it. Researchers cannot export your data. Neither can they access just your data, they only get access to a big pool of aggregate data. And the fee they pay, based on their size and capacity, and anything they find out based on the research they do, gets passed back and redistributed to the pool in terms of shares in this public benefit corporation established by LunaDNA. Those who contribute data are the shareholders in the B-corp. They receive dividends based on their shares. And, this model cannot be changed without going back the Securities and Exchange Commission with a new plan and then reconsenting everyone.

So patients and nonprofits get remunerated for gains that researchers make based on the data they contributed.

Yes, that happens, and I am very delighted.

What is different for parents or for families with genetic diseases nowadays compared towhen you started?

Today, we have created an infrastructure you can plug into. We created a directory calledDisease InfoSearch, which allows anyone to look up a disease as soon as they're diagnosed, so they get all the support information, all the research information in one place. Furthermore, its easier to take action even when you start from a green field. Lets say you're a mom and a dad, your kid gets diagnosed with a genetic disease, perhaps no one else has done research on it. What we will help you with is to set up a biobank, set up a registry, set up a research consortium, and we help you decide where you want to go, how you're going to get researchers interested.

How have you responded to COVID-19?

We set up aCOVID-19 registry, built on our platform. Any organization gets a branded entry point, and the underlying backend is our registry. But your data is yours. It will not be shared unless you say it can be, and then it will not be ever shared individually, so no one will know your name, your age, etc, and it will never be exported.The communities that are building portals on the platform have a lot of questions. If I have a genetic disease that has lung implications, am I at higher risk of COVID-19? How many of my people have had COVID-19? What kind of services should a non-profit be thinking of giving?We don't have results yet because it's only been up a few weeks, but well have some insights soon.

What is the big opportunity in the field of medical research?

I dearly hope it's going to be that we people take control of what's going to happen with our data and our health. My dream is an encompassing registry, a repository of everyones health information and genotype, where everyone has a string on their data, but it is all available for research. That we overcome the silos that keep us from sharing, and build a common infrastructure for the common good. You can see the complications of the current system in the slow COVID-19response: As much as everyone wants to share, there's no way to share, because the various silos have all kept their data separate from one another, and the federal government doesn't want to go against free enterprise. And my hope is that in 10 years, this will have changed.

I like to say that in another 10 years, smart girl scouts will find the solutions to diseases. We won't be spending one billion dollars with a 95% failure rate, fueled by the goals of big pharmaceuticals. Instead, we'll be just having really smart people play with data and come up with solutions, because information will be freely available, it will be in abundance like air, and we will all win.

___

Sharon F. Terry is President and CEO of Genetic Alliance, an enterprise engaging individuals, families and communities to transform health.Genetic Alliance works to provide programs, products and tools for advocacy organizations and ordinary people to take charge of their health and to further biomedical research. As just a Mom with a masters degree in Theology, she cofounded PXE International, a research advocacy organization for the genetic condition pseudoxanthoma elasticum (PXE), in response to the diagnosis of PXE in her two children in 1994.She is a co-discoverer of the ABCC6 gene, and conducts clinical trials.She is the author of 150 peer-reviewed papers, of which 30 are clinical PXE studies. Her story is the topic of herTED TalkandTED Radio Hour. She is co-inventor of the Program for Engaging Everyone Responsibly (PEER), a cross condition people-centered registry system. She was named one of FDAs 30 Heroes for the Thirtieth Anniversary of the Orphan Drug Act in 2013.In 2019, she won the Luminary Award from the Precision Medicine World Conference.Terry is an Ashoka Fellow since 2009.She is an avid student and facilitator ofGestalt Awareness Practice, offering workshops and individual facilitation. Her daughter and son are why she started down this path. They, their wives, and her granddaughter ground and enliven her.

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From Competition To Sharing: How Her Childrens Rare Disease Led Sharon Terry To Revolutionize Medical Research - Forbes

Infection rates may have links to cancer – Medical News Today

New research suggests the prevalence of infection has links to the development of some types of cancer.

A new study has suggested that before developing some forms of cancer, people experienced increased rates of infectious diseases, such as influenza and pneumonia.

The study, published in the journal Cancer Immunology Research, might help develop diagnostic methods for detecting cancers.

Previous research has indicated that there is a link between immunity, inflammation, and cancer.

Inflammation can promote the development of cancers. This can compromise a persons immune system, which can, in turn, increase inflammation.

Dr. Shinako Inaida, a visiting researcher at the Graduate School of Medicine at Kyoto University in Japan and the corresponding author of the study, explains. Cancer can develop in an inflammatory environment caused by infections, immunity disruption, exposure to chemical carcinogens, or chronic or genetic conditions.

An individuals immunity is thought to be a factor in the development of cancer, but additional research is needed to understand the relationship [between] precancerous immunity, infections, and cancer development. This information may contribute to efforts to prevent or detect cancer.

Consequently, it may be valuable to investigate the relationship between immunity, inflammation, and cancers.

The researchers wanted to understand the relationship between the prevalence of specific infectious diseases that could cause inflammation and cancer development.

To investigate, the authors took their information from a 7-year Japanese social health insurance system database.

The researchers looked at data from 50,749 participants. All the participants were over the age of 30 and did not have any detected immunodeficiency.

The case group comprised 2,354 participants who had developed a form of cancer in the 7th year of the study. The control group consisted of 48,395 people who had no cancer diagnosis during the 7 years of the study, plus an additional final year.

The authors then calculated the prevalence of influenza, gastroenteritis, hepatitis, and pneumonia infections for the two groups.

The authors found a clear link between the prevalence of the four illnesses and the later development of cancer.

The case group experienced significantly higher infection rates than the control group in the 6 years before cancer diagnosis.

Members of the case group experienced higher rates of infection in the year before their cancer diagnosis than those in the control group. During this year, the case group experienced an 18% greater infection of influenza, 46.1% of gastroenteritis, 232.1% of hepatitis, and 135.9% for pneumonia than the control group.

The authors also noted that there was a relationship between different infections and different cancers.

For example, people who developed male germ cell cancers were more likely to have experienced influenza. People who developed stomach cancer were more likely to have had pneumonia, and people who developed blood or bone cancers were more likely to have had hepatitis.

However, as Dr. Inaida points out, [i]nterestingly, we found that infection afflicting a specific organ did not necessarily correlate with increased risk of cancer in the same organ.

The authors point out that the study had some limitations. For example, the data provided limited information on underlying genetic and medical conditions, as well as environmental exposures and different lifestyles. These may have affected the chances of infection and developing cancer.

Nonetheless, by making clear an association between infections, inflammation, immunity, and the development of cancers, future research can look in more detail at the precise mechanisms that govern these relationships.

This may then open the door to better diagnostic methods.

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Infection rates may have links to cancer - Medical News Today

Management of Fertility and Hormonal Health in Women at Risk for Hereditary Gynecologic Cancers – Endocrinology Advisor

Hereditary cancer syndromes account for approximately 5% to 10% of all cancers, including those of the female reproductive organs.1 It is important to identify patients at risk for inherited cancer syndromes to manage and prevent various syndrome-associated malignancies.

The management of women at increased risk for hereditary gynecologic cancer specifically has to take into consideration unique concerns regarding fertility and hormonal health, with the use of appropriate fertility preservation strategies and hormone therapy, according to an evidence-based review by the Society of Gynecologic Oncology and American Society for Reproductive Medicine published jointly in Gynecologic Oncology and Fertility & Sterility.2

The most common conditions associated with gynecologic cancers include hereditary breast and ovarian cancer and hereditary nonpolyposis colorectal cancer, also known as Lynch syndrome.2 Other genetic cancer syndromes that have been linked to increased risk for gynecologic malignancy include Peutz-Jeghers syndrome and Cowden syndrome.1

Hereditary breast and ovarian cancer accounts for approximately 5% of breast cancers and 10% to 25% of ovarian cancers.2 Mutations of the genes breast cancer 1 (BRCA1) and 2 (BRCA2) account for the majority of hereditary ovarian, tubal, and peritoneal cancers.3

Several other pathogenic variants are associated with an increased risk for ovarian cancer but not breast cancer, including variants in BRIP1, RAD51C, and RAD51D. Other pathogenic variants that are associated with an increased risk for breast cancer without a significantly increased risk for ovarian cancer include variants in TP53, CDH1, CHEK2, and ATM.2

Lynch syndrome is associated with increased risk for various solid malignancies other than gynecologic cancers, especially colorectal cancer, with Lynch genes varying in penetrance.2

The International Federation of Gynecology and Obstetrics (FIGO) guidelines detail criteria for genetic risk assessment in hereditary breast and ovarian cancer, based on personal or family history of ovarian and breast cancer, age at diagnosis of the breast or ovarian cancer, or having a close relative with a known mutation or a family history indicative of Lynch syndrome.4

Once a mutation is identified, the patient should be counseled regarding risk-reducing surgery, other risk-reduction strategies, and altered screening.

Screening: Although early detection of malignancies may improve prognosis, there are no effective screening tests for ovarian cancer, even in those at high risk for the malignancy. Transvaginal ultrasound and the cancer antigen 125 (CA 125) test may have a role in these cases.2

Chemoprevention: Several classes of drugs have been investigated for chemoprevention of ovarian cancer, but only oral contraceptives were found to potentially reduce risk for the malignancy. However, several studies have reported a possible increased risk for breast cancer with oral contraceptive in the general population and in women with BRCA1 or BRCA2 mutations.2

Risk-reducing surgery: Women with BRCA1 or BRCA2 mutations should be offered risk-reducing salpingo-oophorectomy by age 35 years or when childbearing is complete, but some countries recommend surgery at age 40 years or at an age that is 5 years younger than the youngest affected family member.4 Women with Lynch syndrome should be offered prophylactic total hysterectomy and bilateral salpingo-oophorectomy after the completion of childbearing, especially after age 40 years, as these measures have been shown to decrease the risk for endometrial and ovarian cancer in this patient population.2

There are multiple fertility-preservation and family-building strategies that can be used to help women achieve their goals, including oocyte and/or embryo cryopreservation; use of donor oocytes, donor embryos, and/or gestational carriers; and adoption.2

Women with BRCA1 or BRCA2 pathogenic variants should be referred early to reproductive endocrinologists, as discussions with physicians and ovarian reserve testing may help inform patients decisions on if and when to pursue fertility preservation.2

Patients have the option to cryopreserve and store oocytes and/or embryos using assisted reproductive technology. Although embryo cryopreservation is an effective strategy for fertility preservation, the success rate is dependent on multiple factors. The use of fertility drugs is not associated with a greater risk for invasive breast, ovarian, or uterine cancer in the general population. There is also no known increased risk for breast cancer with fertility medications in BRCA mutation carriers, but there are limited data on the risk for ovarian cancer in these patients.2

Additional options for parenthood include hormonally priming the uterus for embryo transfer after risk-reducing salpingo-oophorectomy. Even women who have undergone hysterectomy but who have retained ovaries can have children using their own gametes through in vitro fertilization with a gestational carrier. Uterine transplantation is still a novel procedure and its role in fertility preservation has not yet been determined.2

Embryo biopsies for preimplantation genetic testing (PGT) should be offered to carriers of known pathogenic gene variants. Analysis for monogenic/single gene defects (PGT-M) can aid in selecting embryos for intrauterine transfer and serve as an alternative to prenatal testing. However, one study found that only approximately one-third of high-risk women would theoretically use PGT-M themselves.2

Chorionic villus sampling and amniocentesis may be used to assess fetal karyotype and certain chromosomal abnormalities, but as of 2018, it is still considered a screening test primarily for aneuploidy that should not be used for prenatal diagnosis of a cancer risk gene.5

Surgical intervention can result in menopausal symptoms at a young age, including vasomotor symptoms, cognitive changes, increased risk for cardiovascular disease, and osteoporosis. Hormonal therapy may alleviate some of these symptoms, but its use in patients at greater risk for gynecologic and breast cancers is controversial and limited data are available on the safety of hormonal therapy for women with BRCA1 or BRCA2 mutations or those with Lynch syndrome. As the benefits of hormone therapy may outweigh the risks secondary to premature estrogen loss, this option should be considered for women without a personal history of breast cancer.2

Nonhormonal options to reduce vasomotor symptoms include selective serotonin reuptake inhibitors, alpha-2 adrenergic agonists, dietary and lifestyle changes, and alternative medicine approaches.2

Providers who care for women at risk for hereditary gynecologic cancers must consider the impact of these conditions on reproductive and hormonal health, stated the authors of the Society of Gynecologic Oncology and American Society for Reproductive Medicine review. These considerations include discussions about options for cancer prevention, fertility preservation and family planning, and management of early surgical menopause in these patients.

References

1. Ballinger LL. Hereditary gynecologic cancers: risk assessment, counseling, testing and management. Obs Gynecol Clin N Am. 2012;39(2):165-181.

2. Chen L-M, Blank SV, Burton E, Glass K, Penick E, Woodard T. Reproductive and hormonal considerations in women at increased risk for hereditary gynecologic cancers: Society of Gynecologic Oncology and American Society for Reproductive Medicine evidence-based review. Fertil Steril. 2019;112(6):1034-1042.

3. Shaw PA, Clarke BA. Prophylactic gynecologic specimens from hereditary cancer carriers. Surg Pathol. 2016;9(2):307-328.

4. Mutch D, Denny L, Quinn M; for the FIGO Committee on Gynecologic Oncology. Hereditary gynecologic cancers. Int J Gynecol Obstet. 2014;124(3):189-192.

5. American College of Obstetricians and Gynecologists Committee on Practice Bulletins. Practice bulletin No. 163 summary: screening for fetal aneuploidy. Obs Gynecol. 2016;127(5):979-981.

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Management of Fertility and Hormonal Health in Women at Risk for Hereditary Gynecologic Cancers - Endocrinology Advisor

Twin peeks: Stanford inherits twin registry, expanding research options – Stanford Medical Center Report

fTwin studies compare similarities and differences between identical twins with those between fraternal twins. Stronger similarities between identical twins than between fraternal twins are assumed to be rooted in their genes. Significant differences between twin siblings, whether identical or fraternal, point to environmental influences.

Understanding the environmental versus the genetic contribution is a leg up in a long climb. If you find genetic influences dominate, you can drop your search for environmental causes and go after the genes responsible. If theres only a weak genetic basis, you can skip the gene hunt and start tracking down suspected environmental causes. Either way, you save time and money.

It was that economy that spurred the creation of the SRI Twin Registry 25 years ago.

In 1995, SRI researcher Gary Swan, PhD, initiated the registry to further his nicotine metabolism, addiction and cessation research.

Finding more effective ways to help smokers quit has been a major theme of my career, said Swan, who for many years directed SRIs Center for Health Science. Relapse rates following smoking cessation can be as high as 70% among smokers who want to quit.

Now an adjunct lecturer affiliated with the Stanford Prevention Research Center, Swan has authored or co-authored hundreds of papers tied at least in part to the study of twins. These studies allowed him to show, among other things, that about 50% of addiction is genetic, suggesting that treatments to aid smoking cessation can be tailored to individuals rates of nicotine metabolism.

Several Stanford scientists have used the SRI Twin Registry. About a decade ago, Martin Angst, MD, professor of anesthesiology, perioperative and pain medicine, wanted to know whether patients responsiveness to the analgesic effects of opioids varied because of genetic influences. Angst recruited participants from the registry to find out. In a couple of papers published in 2012, he concluded that of five distinct dimensions of opioids action analgesia, euphoria, nausea, respiratory depression and addiction only one of them, nausea, varied in degree largely due to genetic influences.

Meanwhile, Angst told Davis about the SRI Twin Registry. Davis was contemplating a study on the relative contributions of the environment and genes to immune responsiveness.

The twins in the registry ranged from infancy to 90 years old. This allowed Davis to see whether similarities the researchers observed in the immune responses of young twins were stronger than those found in older twins, which would indicate that twins diverging environments, as they moved away from home and from each other, affected their immune response to influenza vaccination.

In 2015, Davis reported inCellthat the environmental contribution in many ways dwarfed genetic factors.

While there are larger twin registries in the United States and one in China with half a million registrants its the only twin registry in Northern California.

But with Swans retirement in 2014, SRI gradually deprioritized the twin registry. In January 2019, with Swans blessing, Lisa Jack, a senior project manager at SRI, asked Davis if he could take over the registry. He responded enthusiastically.

By November, the transfer was a done deal, and the ITI Institute was actively recruiting twin pairs. In late October, the institute sent emails to most of the intact twin pairs from the SRI registry, offering them a mug emblazoned with a colorful logo: Stanford Twins Registry.

But only if they sign up, Davis said.

So far,600 individuals from the SRI registry and about 500 brand-new recruits have climbed aboard.

Davis wants to get the word out to other Stanford researchers, too. In mid-2019, Philip Grant, MD, assistant professor of infectious diseases and the Stanford Twin Registrys newly appointed director, sent out an anticipatory notice alerting the institutes faculty of the registrys impending transfer.

That was a trial run, Davis said. We want to reach the whole community.

Having the registry reside on campus should mean reduced overhead and less paperwork, making it easier for Stanford scientists of all stripes to explore genetic versus environmental influences on all sorts of human traits and outcomes.

Theres a lot of value in having it here, said Michael Snyder, PhD, professor and chair of genetics and the Stanford W. Ascherman, MD, FACS, Professor in Genetics. Having the registry at Stanford will put it right in front of our researchers faces.

You never know all the possibilities until people show up and start doing things, Davis said. People will find all kinds of ways to study twins thattheyhavent thought of yet.

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Twin peeks: Stanford inherits twin registry, expanding research options - Stanford Medical Center Report

Individualized mosaics of microbial strains transfer from the maternal to the infant gut – Newswise

Newswise BIRMINGHAM, Ala. Microbial communities in the intestine also known as the gut microbiome are vital for human digestion, metabolism and resistance to colonization by pathogens. The gut microbiome composition in infants and toddlers changes extensively in the first three years of life. But where do those microbes come from in the first place?

Scientists have long been able to analyze the gut microbiome at the level of the 500 to 1,000 different bacterial species that mainly have a beneficial influence; only more recently have they been able to identify individual strains within a single species using powerful genomic tools and supercomputers that analyze massive amounts of genetic data.

Researchers at the University of Alabama at Birmingham now have used their microbiome fingerprint method to report that an individualized mosaic of microbial strains is transmitted to the infant gut microbiome from a mother giving birth through vaginal delivery. They detailed this transmission by analyzing existing metagenomic databases of fecal samples from mother-infant pairs, as well as analyzing mouse dam and pup transmission in a germ-free, or gnotobiotic, mouse model at UAB, where the dams were inoculated with human fecal microbes.

The results of our analysis demonstrate that multiple strains of maternal microbes some that are not abundant in the maternal fecal community can be transmitted during birth to establish a diverse infant gut microbial community, said Casey Morrow, Ph.D., professor emeritus in UABs Department of Cell, Developmental and Integrative Biology. Our analysis provides new insights into the origin of microbial strains in the complex infant microbial community.

The study used a strain-tracking bioinformatics tool previously developed at UAB, called Window-based Single-nucleotide-variant Similarity, or WSS. Hyunmin Koo, Ph.D., UAB Department of Genetics and Genomics Core, led the informatics analysis. The gnotobiotic mouse model studies were led by Braden McFarland, Ph.D., assistant professor in the UAB Department of Cell, Developmental and Integrative Biology.

Morrow and colleagues have used this microbe fingerprint tool in several previous strain-tracking studies. In 2017, they found that fecal donor microbes used to treat patients with recurrent Clostridium difficile infections remained in recipients for months or years after fecal transplants. In 2018, they showed that changes in the upper gastrointestinal tract through obesity surgery led to the emergence of new strains of microbes. In 2019, they analyzed the stability of new strains in individuals after antibiotic treatments, and earlier this year, they found that adult twins, ages 36 to 80 years old, shared a certain strain or strains between each pair for periods of years, and even decades, after they began living apart from each other.

In the current study, several individual-specific patterns of microbial strain-sharing were found between mothers and infants. Three mother-infant pairs showed only related strains, while a dozen other infants of mother-infant pairs contained a mosaic of maternal-related and unrelated microbes. It could be that the unrelated strains came from the mother, but they had not been the dominant strain of that species in the mother, and so had not been detected.

Indeed, in a second study using a dataset from nine women taken at different times in their pregnancies showed that strain variations in individual species occurred in seven of the women.

To further define the source of the unrelated strains, a mouse model was used to look at transmission from dam to pup in the absence of environmental microbes. Five different females were given transplants of different human fecal matter to create five unique humanized-microbiome mice, which were bred with gnotobiotic males. The researchers then analyzed the strains found in the human donors, the mouse dams and their mouse pups. They found four different patterns: 1) The pups strain of a particular species was related to the dams strain; 2) The pups strain was related to both the dams strain and the human donors strain; 3) The pups strain was related to the human donors strain, but not to the dams strain; and, importantly, 4) No related strains for a particular species were found between the pup, the dam and the human donor. Since these animals were bred and raised in germ-free conditions, the unrelated strains in the pups came from minor, undetected strains in the dams.

The results of our studies support a reconsideration of the contribution of different maternal microbes to the infant enteric microbial community, Morrow said. The constellation of microbial strains that we detected in the infants inherited from the mother was different in each mother-infant pair. Given the recognized role of the microbiome in metabolic diseases such as obesity and type 2 diabetes, the results of our study could help to further explain the susceptibility of the infant to metabolic disease found in the mother. Co-authors with Koo, McFarland and Morrow in the study, An individualized mosaic of maternal microbial strains is transmitted to the infant gut microbial community, published in Royal Society Open Science, are Joseph A. Hakim, UAB School of Medicine; David K. Crossman and Michael R. Crowley, UAB Department of Genetics; J. Martin Rodriguez, UAB Department of Medicine, Division of Infectious Diseases; and Etty N. Benveniste, UAB Department of Cell, Developmental and Integrative Biology.

Support came from the University of Alabama School of Medicine, National Institutes of Health grants CA194414 and NS116559, a UAB Neuro-Oncology Support Fund award, and an American Cancer Society Institutional Research Grant through the ONeal Comprehensive Cancer Center at UAB.

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Individualized mosaics of microbial strains transfer from the maternal to the infant gut - Newswise

The Falsehoods of the ‘Plandemic’ Video – FactCheck.org

The first installment of a documentary called Plandemic stormed through social media this week, promising viewers on its website that the film will expose the scientific and political elite who run the scam that is our global health system. The video appeared across platforms, with individual uploads each garnering hundreds of thousands of views.

But the viral video, running nearly 26 minutes, weaves a grand conspiracy theory by using a host of false and misleading claims about the novel coronavirus pandemic andits origins, vaccines, treatments for COVID-19, and more.

The video is largely an interview with Judy Mikovits, a former chronic fatigue researcher who has lobbed a number of accusations against National Institute of Allergy and Infectious Diseases Director Dr. Anthony Fauci. Mikovits was an author on a controversial 2009 study linking a retrovirus to chronic fatigue syndrome that was published in the journal Science, and then retracted in late 2011 after labs were unable to replicate the results and other issues were brought to light.

That same year, in September 2011, Mikovits was fired from her position as research director at the Whittemore Peterson Institute in Nevada and arrested two months later after the institute alleged she stole a laptop, flash drives and other property with institute information. While Mikovits claims in the documentary that she was held in jail despite being charged with nothing, a criminal complaint from November 2011 shows she was charged with two felonies related to the stolen property. The charges were later dropped.

What followed was a years-long legal battle in which Whittemore won a civil judgment against Mikovits; Mikovits filed for bankruptcy; and Mikovits alleged that Whittemore defrauded the government by misusing federally funded research materials. The latter case was dismissed this year.

Mikovits recently co-authored a book with self-described anti-vaxxerKent Heckenlively, with a forward by vaccine skeptic Robert Kennedy Jr., and has spoken at events aimed at discrediting vaccines.

In the video, she claims, And they will kill millions as they already have with their vaccines. Its unclear what vaccines shes referring to, but vaccines have been credited with saving millions of lives. For instance, according to one estimate by researchers with the Centers for Disease Control and Prevention and the World Health Organization, the measles vaccine has saved more than 20 million lives across the globe from 2000 to 2016 alone.

In the sections below, we break down eight of the false, misleading and unfounded claims aired in Plandemic.

The first part of the video focuses largely on two sweeping, but unrelated, accusations against Fauci, who also has been a fixture at the White House briefings on COVID-19.

Without offering any evidence, the video claims that Fauci was part of a cover-up and that he worked with other doctors to take credit and make money on the AIDS epidemic.

Filmmaker Mikki Willis sets the tone for this section of the video, saying to Mikovits, So Anthony Fauci, the man who is heading the pandemic task force, was involved in a cover-up. Willis, a former model, has a large following on YouTube, where he has previously claimed the novel coronavirus was intentionally released.

He directed the cover-up, Mikovits says. And, in fact, everybody else was paid off, and paid off big time.

But at no point in the video does anyone explain what Fauci supposedly covered up.

We asked Mikovits in a phone interview to explain. She said it was a reference to her 2009research paperthat was laterretracted. Mikovits holds Fauci responsible and claims it was part of a cover-up on the part of the medical establishment to keep hidden her research linking a mouse retrovirus to chronic fatigue syndrome. In the years since the research was first published, Mikovits has expanded its reach, suggesting that it could apply also to prostate cancer, lymphoma, and autism.

The NIAID funded Mikovits initial research related to chronic fatigue syndrome, and, after she was fired, another researcher at Whittemore was awarded the remaining grant money. But there is no evidence that Fauci, personally, had anything to do with it. And the journal that published the paper made no mention of Fauci in its retraction. Rather, it explained it was fully retracting the paper because the results couldnt be replicated, even in the same lab, and there is evidence of poor quality control in a number of specific experiments in the Report.

As for the claim about the AIDS epidemic,that goes back much further. In the early 1980s, Mikovits was working as a technician at the National Cancer Institute. She claimsthat the lab she was in had identified the HIV virus from blood and saliva samples and prepared a paper detailing those findings that was slated for publication.

But, she says in the video, referencing one of the pioneers of AIDS research, Dr. Robert Gallo,Fauci holds up the paper for several months, while Robert Gallo writes his own paper and takes all the credit.

Mikovits could not provide the name of her labs paper or the journal that was going to publish it when we spoke to her, so we couldnt check on that. But heres what we do know about the timeline for AIDS research in the early 1980s:

1981 The Centers for Disease Control and Prevention published an article in its Morbidity and Mortality Weekly Report describing a rare lung infection in five young gay men in Los Angeles. Fauci would later recall seeing that article, saying in a 2011 interview, I remember putting the issue to the side of my desk, thinking, Wow, what a bizarre curiosity. One month later, in July, a second MMWR report came to my desk, and this time, an additional 26 men had it, again all gay, all seemingly healthy, and not only in LA, but now also in San Francisco and New York City. I remember reading it very clearly. It was the first time in my medical career I actually got goose pimples. I knew something was very wrong. It changed the direction of my career.

1982 The CDC used the term AIDS, Acquired Immune Deficiency Syndrome, for the first time.

1983 A group of French researchers identified the virus now known as HIV. Twenty-five years later, Franoise Barr-Sinoussi and Luc Montagnier were awarded the Nobel Prize for that discovery.

1984 A team led by Gallo at the National Cancer Institute published research showing that HIV causes AIDS.

Beyond the unsupported claim that Fauci who didnt become the director of NIAID until 1984 stymied early AIDS research at the National Cancer Institute, Mikovits also claims that he has profited from the epidemic.

Referring vaguely to patents, Mikovits says in the video that Fauci was working with other researchers to take credit and make money on the AIDS epidemic. Its true that Faucis name appears on at least six patents related to AIDS research. But its less clear how much he has profited from them. In 2005, the Health and Human Services Department was criticized for not disclosing how much government scientists were collecting from patent royalties. At the time, Fauci expressed concern over the potential for the appearance of a conflict of interest and said that he donated all of his royalty money to charity.

Mikovits makes a claim that numerous scientists have refuted: that the novel coronavirus was manipulated in a laboratory and is not naturally occurring.

So its very clear this virus was manipulated, these, this family of viruses was manipulated and studied in a laboratory where the animals were taken into the laboratory, she says in the video. And this is what was released, whether deliberate or not, that cannot be naturally occurring. Somebody didnt go to a market, get a bat. The virus didnt jump directly to humans. Thats not how it works. Thats accelerated viral evolution. If it was a natural occurrence, it would take it up to 800 years to occur. This occurred from SARS-1 within a decade. That is not naturally occurring.

The exact origin of the coronavirus is not known, but scientists have said the genetic features of SARS-CoV-2 indicate it was neither created in a lab nor manipulated.

Our analyses clearly show that SARS-CoV-2 is not a laboratory construct or a purposefully manipulated virus, said an article published in Nature Medicine in March. Instead, the authors said its plausible that the coronavirus originated in one of two ways: natural selection in an animal host before zoonotic transfer, which refers to the spread of disease from animals to humans, or natural selection in humans following zoonotic transfer.

The authors said the possibility of an inadvertent laboratory release of SARS-CoV-2 cannot be ruled out, but they do not believe that any type of laboratory-based scenario is plausible because they had observed all notable SARS-CoV-2 features in related coronaviruses in nature.

In a statement in April, University of Sydney professor Edward Holmes, who was involved in mapping the genome of the coronavirus that causes COVID-19, likewise said: Coronaviruses like SARS-CoV-2 are commonly found in wildlife species and frequently jump to new hosts. This is also the most likely explanation for the origin of SARS-CoV-2.

Holmes said there is unfounded speculation that a bat coronavirus named RaTG13, which was being kept at the Wuhan Institute of Virology, was the origin of the new coronavirus. But, he explained, that is not the case, for several reasons.

In summary, the abundance, diversity and evolution of coronaviruses in wildlife strongly suggests that this virus is of natural origin, Holmes said. He added that more sampling of other animals is needed to resolve the exact origins of SARS-CoV-2.

Mikovits also may give viewers a false impression when she says the novel coronavirus occurred from SARS-1, which is a different coronavirus that caused a global outbreak in 2003.

SARS-CoV, or severe acute respiratory syndrome, is similar but distinct from SARS-CoV-2. The viruses share about 79% of the same genetic make-up, but SARS-CoV-2 is even more closely related (96%) to the bat coronavirus from which Holmes has said SARS-CoV-2 wasnt derived.

Weve already written about a bogus analysis that suggested the new coronavirus could have leaked from a Chinese lab because a portion of its genome is similar to part of a viral vector that was used in previous research on SARS.

Kristian Andersen, the director of infectious disease genomics at the Scripps Research Translational Institute, told us in an email that analysis was completely wrong.

Also on the issue of the Wuhan lab, the video shows a clip claiming that $3.7 million flowed from the National Institutes of Health here in the U.S. to the Wuhan lab in China and that NIAID had already been conducting experiments with the Wuhan lab in the past in regard to coronavirus.

Thats misleading.

The project referenced, as other fact-checkers have previously reported, is actually funding from NIAID to EcoHealth Alliance, a U.S.-based nonprofit that researches emerging infectious diseases. The project was done to examine the risk of future coronavirus (CoV) emergence from wildlife using in-depth field investigations across the human-wildlife interface in China, in particular the risk posed by bats, according to a 2014 description.

NIH records show the project was awarded nearly $3.4 million altogether. Most of the funding was through a five-year grant awarded in 2014, Robert Kessler, an EcoHealth spokesman, said in an email to us. The group was renewed for a second five-year grant in 2019 and received $292,161 but NIH recently terminated the grant.

Of that money, only $600,000 (from the first grant) was given to the Wuhan Institute of Virology, Kessler said. The Wuhan lab was a collaborator that was pre-approved by NIH and the State Department, he added, and one that researchers used to conduct genetic analyses of the viruses.

In each of nearly 30 countries around the world where we work, we collaborate with local institutions, all of which are pre-approved by our federal funders, EcoHealth said in an April 28 statement about the terminated funding. Its been EcoHealth Alliances position for the past 15 years that coronaviruses present a clear and immediate threat to our safety. That seems clearer now than ever before.

The group said its research aimed to analyze the risk of coronavirus emergence and help in designing vaccines and drugs to protect us from COVID-19 and other coronavirus threats. In fact, genetic sequences of two bat coronaviruses that we discovered with this grant have been used as lab tools to test the breakthrough antiviral drug Remdesivir.

So its incorrect, and also lacks context, to claim NIAID gave $3.7 million to the Wuhan lab.

Mikovits falsely claims that if youve ever had a flu vaccine, you were injected with coronaviruses.

Shes wrong, Dr. Paul A. Offit, director of the Vaccine Education Center at Childrens Hospital of Philadelphia, told us in a phone interview. Thats not true.

This person doesnt know what she is talking about, Dr. Lee Riley, professor and chair of the Division of Infectious Disease and Vaccinology at the University of California, Berkeley School of Public Health, told us in an email, adding, I think this person is just seeking publicity.

In an interview, we asked Mikovits what support she had for the claim, and she didnt provide any. She only said that flu vaccines are cultured in chicken eggs and dog kidney cells, and those animals have coronaviruses. Its an extreme leap to then claim animal strains of coronaviruses end up in vaccines tested and approved for people. Mikovits further said she attributes the spread of the novel coronavirus worldwide at least in part to the use of the flu vaccine.

As weve explained before, coronaviruses are a diverse family of viruses, and some, such as canine coronavirus, infect animals. Those arent the same as SARS-CoV-2, the coronavirus that causes COVID-19.

As for influenza vaccines, most are made using hens eggs, Offit explained, and about 10% of vaccines in the U.S. are cell-culture vaccines, which use mammalian cells instead of eggs. Specifically, the process uses Madin-Darby Canine Kidney, or MDCK, cells.

These lines have been around for a long time, Offit said. This is a well-tested cell line that does not contain coronavirus and would never be allowed to.

On its website, the Centers for Disease Control and Prevention has more information on how egg-based and cell-based influenza vaccines are manufactured. A cell-based method that also used eggs at the beginning of the process received Food and Drug Administration approval in 2012, and a fully cell-based process got FDA approval in 2016.

The CDC notes that once vaccines are manufactured, FDA tests and approves the vaccines prior to release and shipment.

This cell-based technology has been used in other U.S. vaccines, including vaccines for rotavirus, polio, smallpox, hepatitis, rubella and chickenpox, the CDC says.

Mikovits also repeats the unsubstantiated claim that the flu vaccines increase the odds by 36% of getting COVID-19, which weve previously covered.

Experts say that there has been no study linking the flu shot to elevated risk for the novel coronavirus. The military study cited by Mikovits involved four types of seasonal coronaviruses thatcausecommon colds, not SARS-CoV-2.

More than that, the results in the study that indicate a flu-vaccinated person had an increased likelihood of testing positive for a seasonal coronavirus do not appear to be adjusted for age groups or seasons. Those factors could affect someones chances of getting a specific virus, regardless of whether or not theyve been vaccinated for the flu.

Multiple scientists have pointed out the same issue in other fact-checks, too, and have debunked the erroneous suggestion that the study looked at SARS-CoV-2.

The Military Health System told us in a statement that the study does not show or suggest that influenza vaccination predisposes in any way, the potential for infection with the more severe forms of coronavirus, such as COVID-19. MHS further said it remains essential for people to obtain the seasonal flu shot each year as it becomes available.

The video makes the unsubstantiated claim that the antimalarial drug hydroxychloroquine is the most effective medication to treat COVID-19, citing a survey of doctors.

Shortly after that, Mikovits says hydroxychloroquine is effective against these families of viruses, referring to the family of coronaviruses, such as COVID-19, but they keep it from the people.

We have covered this ground before when President Donald Trump encouraged the off-label use of chloroquineand its derivativehydroxychloroquine for treatment of COVID-19 patients. Both drugs are used to treat malaria, lupus and rheumatoid arthritis.

But there is only limited evidence that hydroxychloroquine is effective for COVID-19, and it carries potential health risks.

The National Institutes of Health says there is insufficient clinical data to recommend either for or against using chloroquine or hydroxychloroquine for the treatment of COVID-19.

Despite insufficient clinical data, the Food and Drug Administration issued an emergency use authorization, or EUA, order on March 28 that allowed for the drugs to be used as a treatment for some hospitalized COVID-19 patients.

A little less than a month later, the FDA issueda warning against using hydroxychloroquine or chloroquine for COVID-19 outside of the hospital setting or a clinical trial due to risk of heart rhythm problems. The warning came a few days after astudyfoundthat patients at Veterans Health Administration medical centers treated with hydroxychloroquine had an increased mortality risk compared with those that were not treated with the drug.

In the video, Mikovits says, The AMA was saying doctors will lose their license if they use hydroxychloroquine, the anti-malarial drug thats been on the list of essential medicine worldwide for 70 years. Dr. Fauci calls that anecdotal. Its not storytelling if we have thousands of pages of data saying its effective against these families of viruses. This is essential medicine and they keep it from the people.

Its not true that the American Medical Association told doctors they will lose their license if they use hydroxychloroquine for COVID-19. The AMA issued a statement saying it opposed purchasing excessive amounts of chloroquine or hydroxychloroquine for possible COVID-19 treatment. But it also said, Novel off-label use of FDA-approved medications is a matter for the physicians or other prescribers professional judgment.

As for hydroxychloroquines effectiveness against coronaviruses, we have written that at least two studies show that it has antiviral activity against the novel coronavirus in cells grown in the lab. But there is only anecdotal evidence that the drug works in people.

Trump cited in a tweet the results of a small clinical trial in France, but the International Society of Antimicrobial Chemotherapy, which publishes the journal in which the study appeared, later issued a statement that said the article does not meet the Societys expected standard, especially relating to the lack of better explanations of the inclusion criteria and the triage of patients to ensure patient safety.

We cover this more extensively in our story Trump Hypes Potential COVID-19 Drugs, But Evidence So Far Is Slim.

In attacking public health measures taken to address the pandemic in the U.S., Mikovits wrongly suggests that using masks could lead to people infecting themselves with their own breath. Wearing the mask literally activates your own virus, Mikovits said. Youre getting sick from your own reactivated coronavirus expressions and if it happens to be SARS-CoV-2, then youve got a big problem.

Experts were perplexed by what she meant and said the implication that simply breathing through a mask could lead to self-infection doesnt square with science.

Linsey Marr, a professor of civil and environmental engineering at Virginia Tech who studies airborne disease transmission, told us: If youre shedding (breathing out) virus, then youre already infected. Even without a mask, infected people who are shedding virus probably rebreathe some of their own viruses, but there are already billions times more viruses in your body. Hopefully, the mask is protecting other people from your exhalations.

And Lisa Brosseau, an expert on respiratory protection and infectious diseases and a certified industrial hygienist, said in an email that viruses are not activated by anything, as Mikovits suggests.

Viruses instead require living cells in order to replicate, but their viability or ability to replicate isnt affected whether someone is wearing a mask or not, said Brosseau, a former professor at the University of Illinois at Chicago. If anything, viruses in the environment can be rendered non-viable by exposure to certain temperature and relative humidity conditions.

There is nothing magical about our breath that activates or reactivates a virus, Brosseau said.

As weve previously written, while there is little research on cloth masks, the hope is that they can help prevent individuals, even those who do not feel sick, from unknowingly spreading COVID-19 to others. Brosseau said people should frequently wash cloth masks, though, and stressed that masks are not a substitute for social distancing. The CDC notesthe same.

Mikovits says in the video: In 1999, I was working in Fort Detrick and my job was to teach Ebola how to infect human cells without killing them. Ebola couldnt infect human cells until we took it in the laboratories and taught them.

Its not clear what she meant by that, and she didnt explain when we asked about her claim.

But the suggestion that Ebola, which includes six species of ebolaviruses, didnt infect people until 1999, or later, is false.

The first two species, Zaire ebolavirus and Sudan ebolavirus, were discovered after outbreaks in 1976 in Central Africa. Combined, those two viruses, which scientists believe may have come from bats or nonhuman primates (such as chimpanzees, apes, monkeys, etc.), killed about 430 people that year, according to the CDC.

Zaire ebolavirus which is also linked to the largest Ebola outbreak which began in West Africa in 2014 is said to have initially spread in 1976 through the use of contaminated needles and syringes at a hospital in the village where the first infected person was treated. And the Sudan ebolavirus is believed to have started with workers in a cotton factory.

In fact, the CDC says four of the six species of ebolavirus Zaire ebolavirus, Sudan ebolavirus, Ta Forest ebolavirus (formerly Cte dIvoire ebolavirus) and Bundibugyo ebolavirus are known to cause disease in people. And three of the four species were discovered prior to 1999.

A fifth species, Reston ebolavirus, was first discovered in 1989 in research monkeys imported into the U.S. from the Philippines. That species is known to cause disease in nonhuman primates and pigs, but not in people, the CDC says. There have been cases in which individuals developed Reston ebolavirus antibodies, but did not experience symptoms.

The sixth species, Bombali ebolavirus, was discovered in 2018 in a bat in Sierra Leone. It also is not known to infect humans.

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The Falsehoods of the 'Plandemic' Video - FactCheck.org

Its in your genes Whether Covid lands you in hospital or not depends on your body – ThePrint

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When some people become infected with the coronavirus, they only develop mild or undetectable cases of COVID-19. Others suffer severe symptoms, fighting to breathe on a ventilator for weeks, if they survive at all.

Despite a concerted global scientific effort, doctors still lack a clear picture of why this is.

Could genetic differences explain the differences we see in symptoms and severity of COVID-19?

To test this, we used computer models to analyze known genetic variation within the human immune system. The results of our modeling suggest that there are in fact differences in peoples DNA that could influence their ability to respond to a SARS-CoV-2 infection.

When a virus infects human cells, the body reacts by turning on what are essentially anti-virus alarm systems. These alarms identify viral invaders and tell the immune system to send cytotoxic T cells a type of white blood cell to destroy the infected cells and hopefully slow the infection.

But not all alarm systems are created equal. People have different versions of the same genes called alleles and some of these alleles are more sensitive to certain viruses or pathogens than others.

To test whether different alleles of this alarm system could explain some of the range in immune responses to SARS-CoV-2, we first retrieved a list of all the proteins that make up the coronavirus from an online database.

We then took that list and used existing computer algorithms to predict how well different versions of the anti-viral alarm system detected these coronavirus proteins.

Also read: Worlds most accurate antibody test has arrived. Or has it?

The part of the alarm system that we tested is called the human leukocyte antigen system, or HLA. Each person has multiple alleles of the genes that make up their HLA type. Each allele codes for a different HLA protein. These proteins are the sensors of the alarm system and find intruders by binding to various peptides chains of amino acids that make up parts of the coronavirus that are foreign to the body.

Once an HLA protein binds to a virus or piece of a virus, it transports the intruder to the cell surface. This marks the cell as infected and from there the immune system will kill the cell.

In general, the more peptides of a virus that a persons HLAs can detect, the stronger the immune response. Think of it like a more sensitive sensor of the alarm system.

The results of our modeling predict that some HLA types bind to a large number of the SARS-CoV-2 peptides while others bind to very few. That is to say, some sensors may be better tailored to SARS-CoV-2 than others. If true, the specific HLA alleles a person has would likely be a factor in how effective their immune response is to COVID-19.

Because our study only used a computer model to make these predictions, we decided to test the results using clinical information from the 2002-2004 SARS outbreak.

Whats next?

We found similarities in how effective alleles were at identifying SARS and SARS-CoV-2. If an HLA allele appeared to be bad at recognizing SARS-CoV-2, it was also bad at recognizing SARS. Our analysis predicted that one allele, called B46:01, is particularly bad with regards to both SARS-CoV-2 and SARS-CoV. Sure enough, previous studies showed that people with this allele tended to have more severe SARS infections and higher viral loads than people with other versions of the HLA gene.

Based on our study, we think variation in HLA genes is part of the explanation for the huge differences in infection severity in many COVID-19 patients. These differences in the HLA genes are probably not the only genetic factor that affects severity of COVID-19, but they may be a significant piece of the puzzle. It is important to further study how HLA types can clinically affect COVID-19 severity and to test these predictions using real cases. Understanding how variation in HLA types may affect the clinical course of COVID-19 could help identify individuals at higher risk from the disease.

To the best of our knowledge, this is the first study to evaluate the relationship between viral proteins across a wide range of HLA alleles. Currently, we know very little about the relationship between many other viruses and HLA type. In theory, we could repeat this analysis to better understand the genetic risks of many viruses that currently or could potentially infect humans.

Austin Nguyen, PhD Candidate in Computational Biology and Biomedical Engineering, Oregon Health & Science University; Abhinav Nellore, Assistant Professor of Biomedical Engineering & Surgery, Oregon Health & Science University, and Reid Thompson, Assistant Professor of Radiation Medicine, Oregon Health & Science University

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

Also read: After HCQ, its time for azithromycin and pneumonia drug combo to go under clinical trial

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Its in your genes Whether Covid lands you in hospital or not depends on your body - ThePrint

FDA approves Tabrecta, first targeted therapy to treat metastatic NSCLC – The Cancer Letter

publication date: May. 8, 2020

FDA has granted accelerated approval to Tabrecta (capmatinib) for adult patients with metastatic non-small cell lung cancer whose tumors have a mutation that leads to mesenchymal-epithelial transition exon 14 skipping as detected by an FDA-approved test.

Tabrecta is the first FDA-approved therapy to treat NSCLC with specific mutations (those that lead to mesenchymal-epithelial transition or MET exon 14 skipping).

Tabrecta is sponsored by Novartis.

FDA also approved the FoundationOne CDx assay (Foundation Medicine, Inc.) as a companion diagnostic for Tabrecta. Most patients had tumor samples that were tested for mutations that lead to MET exon 14 skipping using local tests and confirmed with the F1CDx, which is a next-generation sequencing based in vitro diagnostic device capable of detecting several mutations, including mutations that lead to MET exon 14 skipping.

Lung cancer is increasingly being divided into multiple subsets of molecularly defined populations with drugs being developed to target these specific groups, Richard Pazdur, director of the FDA Oncology Center of Excellence and acting director of the Office of Oncologic Diseases in the FDAs Center for Drug Evaluation and Research, said in a statement. Tabrecta is the first approval specifically for the treatment of patients with non-small cell lung cancer whose tumors have mutations that lead to MET exon 14 skipping. This patient population now has an option for a targeted therapy, which they didnt have prior to today.

Efficacy was demonstrated in the GEOMETRY mono-1 trial (NCT02414139), a multicenter, non-randomized, open-label, multicohort study enrolling 97 patients with metastatic NSCLC with confirmed MET exon 14 skipping. Patients received Tabrecta 400 mg orally twice daily until disease progression or unacceptable toxicity.

The main efficacy outcome measures were overall response rate (ORR) determined by a blinded independent review committee using RECIST 1.1 and response duration. Among the 28 treatment-nave patients, the ORR was 68% (95% CI: 48, 84) with a response duration of 12.6 months (95% CI: 5.5, 25.3). Among the 69 previously treated patients, the ORR was 41% (95% CI: 29, 53) with a response duration of 9.7 months (95% CI: 5.5, 13.0).

FDA approves daratumumab and hyaluronidase-fihj for multiple myeloma

FDA has approved daratumumab and hyaluronidase-fihj (Darzalex Faspro) for adult patients with newly diagnosed or relapsed/refractory multiple myeloma. This new product allows for subcutaneous dosing of daratumumab.

Darzalex Faspro is sponsored by Janssen Biotech Inc.

Daratumumab and hyaluronidase-fihj is approved for the following indications that intravenous daratumumab had previously received:

in combination with bortezomib, melphalan and prednisone in newly diagnosed patients who are ineligible for autologous stem cell transplant,

in combination with lenalidomide and dexamethasone in newly diagnosed patients who are ineligible for autologous stem cell transplant and in patients with relapsed or refractory multiple myeloma who have received at least one prior therapy,

in combination with bortezomib and dexamethasone in patients who have received at least one prior therapy,

as monotherapy, in patients who have received at least three prior lines of therapy including a proteasome inhibitor and an immunomodulatory agent or who are double-refractory to a PI and an immunomodulatory agent.

Efficacy of daratumumab and hyaluronidase-fihji (monotherapy) was evaluated in COLUMBA (NCT03277105), an open-label non-inferiority trial randomizing 263 patients to daratumumab and hyaluronidase-fihj and 259 to intravenous daratumumab (daratumumab IV). The trials co-primary endpoints were overall response rate and pharmacokinetic endpoint of the maximum Ctrough on cycle 3, day 1 pre-dose. Daratumumab and hyaluronidase-fihj was non-inferior to daratumumab IV in evaluating these two endpoints.

The ORR was 41.1% for daratumumab and hyaluronidase-fihj and 37.1% for daratumumab IV with a risk ratio of 1.11 (95% CI: 0.89, 1.37). The geometric mean ratio comparing daratumumab and hyaluronidase-fihj to daratumumab IV for maximum Ctrough was 108% (90% CI: 96,122).

Efficacy of daratumumab and hyaluronidase-fihj in combination with VMP (D-VMP) was evaluated in a single-arm cohort of PLEIADES (NCT03412565), a multi-cohort, openlabel trial. Eligible patients were required to have newly diagnosed multiple myeloma and were ineligible for transplant. The major efficacy outcome measure, ORR, was 88.1% (95% CI: 77.8, 94.7).

Efficacy of daratumumab and hyaluronidase-fihj in combination with Rd (D-Rd) was evaluated in a single-arm cohort of this trial. Eligible patients had received at least one prior line of therapy. ORR was 90.8% (95% CI: 81.0, 96.5).

FDA accepts NDA for CC-486 in AML indication

FDA has accepted a New Drug Application for CC-486, an investigational oral hypomethylating agent, for the maintenance treatment of adult patients with acute myeloid leukemia who achieved complete remission, or CR with incomplete blood count recovery, following induction therapy with or without consolidation treatment, and who are not candidates for, or who choose not to proceed to, hematopoietic stem cell transplantation.

CC-486 is sponsored by Bristol Myers Squibb. FDA granted the application Priority Review and set a Prescription Drug User Fee Act goal date of Sept. 3, 2020.

The NDA submission was based on the efficacy and safety results of the phase III QUAZAR AML-001 study, which met the primary endpoint of improved overall survival for patients receiving AML maintenance treatment with CC-486 versus placebo.

Often, newly diagnosed adult patients with AML achieve a complete response with induction therapy, however many patients will relapse and experience a poor outcome. Patients in remission are seeking treatment options that decrease the likelihood of relapse and extend overall survival, Noah Berkowitz, senior vice president of Global Clinical Development, Hematology, at Bristol Myers Squibb, said in a statement.

CC-486 is an investigational therapy that is not approved for any use in any country.

Caris Life Sciences submits two PMA applications to FDA for whole exome and whole transcriptome sequencing

Caris Life Sciences has submitted two Pre-Market Approval applications for MI Exome CDx and MI Transcriptome CDx to FDA.

MI Exome CDx, whole exome sequencing (DNA), and MI Transcriptome CDx, whole transcriptome sequencing (RNA), are precision medicine assays that include key companion diagnostic biomarkers with therapy claims, and detect all classes of alterations including genomic signatures for microsatellite instability, tumor mutation burden, and loss of heterozygosity.

MI Exome CDx is a next-generation sequencing-based test utilizing DNA isolated from formalin-fixed paraffin embedded tumor tissue specimens for the qualitative detection of genomic alterations. MI Exome CDx can identify genetic variants (single nucleotide variants, insertions and deletions), copy number alterations, MSI, TMB and LOH.

MI Transcriptome CDx is a next-generation sequencing-based test that utilizes RNA isolated from formalin-fixed paraffin embedded tumor tissue specimens for the qualitative detection of genomic and transcriptomic alterations. MI Transcriptome CDx is a broad, multi-gene panel utilized to identify gene fusions, transcript variants, genetic variants (single nucleotide variants, insertions and deletions), and gene expression changes. FDA granted MI Transcriptome CDx received Breakthrough Device designation in 2019.

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FDA approves Tabrecta, first targeted therapy to treat metastatic NSCLC - The Cancer Letter

Research into the health of unborn babies receives government funding – UNSW Newsroom

A research project that will examine the feasibility of genomic testing has received funding from the Australian Government Medical Research Futures Fund (MRFF).

The two-year project, PreGen, will be led by Associate Professor Tony Roscioli from UNSW Medicine, who is an expert in genomics at Neuroscience Research Australia (NeuRA) and New South Wales Health Pathology.

The funding received will allow PreGen to perform genomic tests in families seen at ten of Australias largest maternity centres. This will assess the benefits made available from antenatal genomic testing.

We do not currently have easily accessible accredited antenatal genomic testing in Australia. Pregnancy abnormalities identified on ultrasound are therefore not usually investigated further with genomic testing to try to find the cause, A/Prof. Roscioli said.

The grant will help to improve knowledge about the conditions causing malformations, improve available testing and promote international collaborations to understand the genetic conditions that may occur in babies.

Prenatal genomic testing allows the cause of some abnormalities to be identified. This information helps families consider available options and could allow clinicians to better manage a babys health after the birth.

There is huge demand for this technology from families and doctors, A/Prof. Roscioli said.

The project will also create training positions to build the workforce required to perform and analyse the results quickly. Further, PreGen will evaluate the psychological support families may require when undergoing genomic testing.

The priorities will be to set up antenatal genomic testing safely around Australia and to expand knowledge about genetic conditions in babies. We will evaluate the counselling that is required to support families appropriately, he said.

UNSW Deputy Vice-Chancellor (Research) Professor Nicholas Fisk, in noting that this grant represented a quantum leap for prenatal genetics, said that rolling out exome and genome sequencing was exactly the sort of translation the MRFF was designed for.

Prof. Fisk,a former President of the International Fetal Medicine Society, said: Fetal abnormalities occur in up to one in 20 pregnancies - this exemplary hi-tech model of care will help parents and their clinicians understand whether imaging findings are just isolated or part of more complex disorders.

PreGen will compliment a related multicentre MRFF grant, Mackenzies Mission, also run out of the Randwick Health Precinct, attesting to UNSWs national leadership in this area.

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Research into the health of unborn babies receives government funding - UNSW Newsroom

New medical foundation invests in COVID-19 research funding – News – The University of Sydney

Snow Medical founder Terry Snow said: COVID-19 has had a devastating effect on Australia and the world this is the biggest thing to hit the globe since 1945 and it will have a lasting impact for years to come. Government has stepped up and now is the time for the community to play a role. All these measures are aimed at getting Australians back to work, making treatment more effective and efficient and getting our economy working again.

Snow Medical chair, Tom Snow, added: We want to help Australias best and brightest to focus their efforts on this huge national and global challenge.

This consortium is particularly notable because of its national reach and collaborative networks it draws on research expertise from over 15 universities and medical research institutes, their affiliated public hospitals, state health departments, public health authorities, pathology services and the Australian Red Cross Blood Service to provide a truly national picture and coordinated approach to beating COVID-19.

Professor Tania Sorrell who is director of the University of Sydneys Marie Bashir Institute for Infectious Diseases and Biosecurity, Infectious Diseases Group head in The Westmead Institute of Medical Research and the lead investigator in CREID said: This very generous donation will help Australia lead in the fight to contain the spread of COVID-19 in the community, better protect health care workers, and offer the best care to individual patients.

Critically, the vision of Snow Medical has enabled CREID and APPRISE to leverage the joint power of their national research networks in the fight against COVID-19.

Professor Sharon Lewin, director of the Peter Doherty Institute for Infection and Immunity (Doherty Institute), a joint venture of the University of Melbourne and The Royal Melbourne Hospital, and chief investigator for APPRISE said: The large injection of funds supports the development of critical national platforms for the current pandemic while building capacity for future pandemics."

Infectious diseases physician and trials expert at the University of Sydneys Faculty of Medicine and Health, Professor Tom Snelling, who will be leading the data science project, said: Australias brisk and effective response to COVID-19 is the envy of many countries but we cant afford to become complacent. This donation will give researchers a critical boost in their race to find and implement science-driven solutions for the pandemic.

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New medical foundation invests in COVID-19 research funding - News - The University of Sydney