Category Archives: Transhuman News

JERUSALEM, Feb. 3, 2022 /PRNewswire/ --The Hadassah Cancer Research Institute at the Hadassah University Medical Center in Jerusalem, announced today that using artificial intelligence (AI), researchers have developed, an algorithm to identify, with an unprecedented 96.5% level of accuracy, all possible deleterious mutations of TP53 gene which are commonly found in 50% of tumors. This breakthrough can potentially lead to improved genetic screening and consultation and to improved precision medicine for cancer patients.

This groundbreaking algorithm was trained using AI, huge cancer and normal genomics databases coupled with computational and experimental parameters specific to TP53 gene. Prof. Thierry Soussi (Sorbonne Universit, Paris, France), a world leading researcher of TP53 gene, lent his expertise to an international research collaboration, led by Dr. Shai Rosenberg, aimed at increasing identification of variants posing risk of developing cancer from variants that are not, from 190 (in the ClinVar database) to all 2,314 possible missense variants.

This gene-specific, AI approach can be generalized to other cancer genes and thus, contribute to more accurate genetic screening and consultation. Additionally, it can lead to more effective precision medicine for oncological patients by the creation of customized cancer treatment decision support systems that are able to identify and discern the important mutations that require treatment from the total number of somatic mutations of the tumor.

"The research and technology behind this breakthrough not only provide life-saving screening for carriers of previously unknown cancerous mutations who may be at increased risk, but it is also critical for genomic analysis of somatic mutation profiles in all tumors," said Prof. Michal Lotem, MD, Head of the Center for Melanoma and Cancer Immunotherapy, Dept. of Oncology.

"Hadassah Medical Center has been at the forefront of promoting technological innovation in medicine in order to provide patients in our care with the most advanced treatment options," said Prof. Aron Popovtzer a Professor of Radiation Oncology and Head of the Sharett Institute of Oncology. "Following this important milestone, Dr. Rosenberg's research group will continue actively working to develop similar models for additional cancer genes."

Read the full articleby Dr. Rosenberg, published in the prestigious - Briefings in Bioinformatics Journal. Dr. Rosenberg is a physician-researcher at Hadassah Medical Center. He is a senior Neuro-Oncologist and heads the Laboratory for Computational Biology of Cancer. He is a graduate of the Rothschild Excellence Program and the Technion's MD-PhD Program. He heads the Sagol program for dual degree in Medicine and Computer Science in the Faculty of Medicine in the Hebrew University.

This research is funded by Israel Academy of Sciences and Humanities, Trudy Mandel Louis Charitable Trust, Y.M.H and Hadassah-France. The research of Professor Soussi by Hadassha France.

For more information on the Hadassah Cancer Research Institute, contact:Amalia HerszkowiczHadassah Research Institute (HCRI)[emailprotected]

SOURCE Hadassah Cancer Research Institute

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Predictive-AI Algorithm Used to Successfully Identify Common Cancerous Gene Mutations Demonstrated at Hadassah Cancer Research Institute - PRNewswire

The CGTs gaining marketing authorisation in Europe and the US each year can currently be counted in single digitals, but hundreds of potential new CGTs are in the pipeline. According to the AMR report, 136 of the 956 unique therapies under development are already in the phase three stage of clinical trials commonly the last stage of clinical trials where the safety and effectiveness of the proposed new treatments is compared to existing treatments.

Much of the research ongoing is focused on delivering new cancer treatments, but CGTs have potential utility across other areas of medicine. The AMR report highlights the efforts being undertaken by medical researchers across industry, academia and government to develop new CGTs to address problems such as heart failure, rare genetic diseases, and neuromuscular diseases, for example.

Research overseen by the Massachusetts Institute of Technologys Center for Biomedical Innovation, published in 2018, projects that around 500,000 patients in the US will have been treated with between 40 and 60 approved CGTs by 2030.

CGTs are often developed to treat small patient populations at high cost. This poses a problem for budget-constrained health systems in terms of fitting the therapies within existing reimbursement models in a way which enables the developers of the therapies to obtain a fair return on their investment. A lack of harmonisation over the way each country approaches reimbursement creates uncertainty for researchers and their financial backers.

In addition, small biotech companies behind CGTs must navigate a complex regulatory framework and find infrastructure solutions to scale-up the manufacturing of approved treatments.

The challenges facing the CGT sector are well-recognised by policy makers, and efforts to resolve them are underway across Europe at EU level, EU27 member state level and within the UK alone to address them. We have set out examples of the initiatives we think could be taken forward.

Covid-19 has shown how collaborative, concerted efforts can drive innovation forward. There is an opportunity for stakeholders across the CGT sector to come together differently, perhaps in a pre-competitive way, to help drive economies that reduce costs.

The BioPharmaceutical industry has historically turned to industry-wide collaboration through organisations such as the Innovative Medicines Initiative (IMI) and the Pistoria Alliance to address resource-wasting replication of pre-competitive research activities and solve bottlenecks in drug discovery and development across diseases. CGT should be no exception.

An international group of senior researchers is lobbying the G7 to reform the way they manage collaboration on emerging technologies. The proposed framework would produce model, multilateral agreements on sharing and exploiting emerging technologies, including CGTs, that companies, universities and governments could follow; reducing uncertainty about IP, standardisation, data sharing, researcher mobility and other contentious issues.

Standardisation will cut development time and costs of CGTs too. Companies are already working with regulators and standard setting bodies, such as the International Organization for Standardisation, to agree regulatory standards. Various groups globally are discussing harmonisation of best practices to eliminate or reduce costs. In time, standardisation will facilitate technology platforms that are able to target many different diseases; viral-vector platforms that target a range of diseases in gene therapy are already in development.

Innovative payment models are already being used by health systems across Europe for CGTs to address affordability. As the pipeline of CGTs approaching market is increasing, there is a growing awareness and acknowledgment that outcomes-based reimbursement (OBR) schemes offer a potentially effective mechanism to reduce the long-term data uncertainty and have the potential to ensure greater access and reward for efficacious therapeutic innovation.

One of the takeaways from NICEs regenerative medicines study in 2016 is that outcomes-based payments increased the probability of a therapy being cost-effective but without the risk of eroding product value, unlike upfront discounts. When evaluating an OBR scheme it will be important to consider the feasibility of patient follow-up and the availability of a suitable data collection infrastructure, such as a patient registry. Covid-19 sped the adoption of digitally-enabled processes and CGT companies can leverage new practices such as remote monitoring for long-term patient follow-up. Clearly different CGTs may call for different pricing models in different markets.

The ability to combine clinical trial data and real world data is seen by many as one of the most critical transformations occurring in CGT development. Looking to strike a careful balance between the benefits of early access and the potential, still-unknown, long-term safety risks, regulators including the European Medicines Agency (EMA) and Medicines & Healthcare products Regulatory Agency (MHRA) in the UK are already performing accelerated assessment and granting approvals for CGTs on the condition that real-world evidence (RWE), based on real-world data, is periodically submitted thereafter.

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Cell and gene therapies: our eyes to the future - Pinsent Masons

Researchers have discovered a mechanism that may explain why people with COVID-19 lose their sense of smell.

Published online February 1 in the journal Cell, the new study finds that infection with the pandemic virus, SARS-CoV-2, indirectly dials down the action of olfactory receptors, proteins on the surfaces of nerve cells in the nose that detect the molecules associated with odors.

Led by researchers from NYU Grossman School of Medicine and Columbia University, the new study may also shed light on the effects of COVID-19 on other types of brain cells and other lingering neurological effects of COVID-19 such as brain fog, headaches, and depression.

Experiments showed that the presence of the virus near nerve cells (neurons) in olfactory tissue brought an inrushing of immune cells, microglia, and T cells that sense and counter infection. Such cells release proteins called cytokines that changed the genetic activity of olfactory nerve cells, even though the virus cannot infect them, say the study authors. Where immune cell activity would dissipate quickly in other scenarios, in the brain, according to the teams theory, immune signaling persists in a way that reduces the activity of genes needed for the building of olfactory receptors.

Our findings provide the first mechanistic explanation of smell loss in COVID-19 and how this may underlie long COVID-19 biology, says co-corresponding author Benjamin tenOever, PhD, professor in the Departments of Medicine and Microbiology at NYU Langone Health. The work, in addition to another study from the tenOever group, also suggests how the pandemic virus, which infects less than 1 percent of cells in the human body, can cause such severe damage in so many organs.

One unique symptom of COVID-19 infection is loss of smell without the stuffy nose seen with other infections like the common cold, researchers say. In most cases, the smell loss lasts only a few weeks, but for more than 12 percent of people with COVID-19, olfactory dysfunction persists in the form of ongoing reduction in the ability to smell (hyposmia) or changes in how a person perceives the same smell (parosmia).

To gain insight into COVID-19induced smell loss, the current authors explored the molecular consequences of SARS-CoV-2 infection in golden hamsters and in olfactory tissue taken from 23 human autopsies. Hamsters represent a good model, being mammals that both depend more on the sense of smell than humans, and that are more susceptible to nasal cavity infection.

The study results build on the discovery over many years that the process that turns on genes involves complex 3D relationships, where DNA sections become more or less accessible to the cells gene-reading machinery based on key signals, and where some DNA chains loop around to form long-range interactions that enable the stable reading of genes. Some genes operate in chromatin compartmentsprotein complexes that house the genesthat are open and active, while others are compacted and closed, as part of the nuclear architecture.

In the current study, experiments confirmed that SARS-CoV-2 infection, and the immune reaction to it, decreases the ability of DNA chains in chromosomes that influence the formation of olfactory receptor building to be open and active, and to loop around to activate gene expression. In both hamster and human olfactory neuronal tissue, the research team detected persistent and widespread downregulation of olfactory receptor building. Other work posted by these authors suggests that olfactory neurons are wired into sensitive brain regions, and that ongoing immune cell reactions in the nasal cavity could influence emotions, and the ability to think clearly (cognition), consistent with long COVID.

Experiments in hamsters recorded over time revealed that downregulation of olfactory neuron receptors persisted after short-term changes that might affect the sense of smell had naturally recovered. The authors say this suggests that COVID-19 causes longer-lasting disruption in chromosomal regulation of gene expression, representing a form of nuclear memory that could prevent the restoration of olfactory receptor transcription even after SARS-CoV-2 is cleared.

The realization that the sense of smell relies on fragile genomic interactions between chromosomes has important implications, says Dr. tenOever. If olfactory gene expression ceases every time the immune system responds in certain ways that disrupts inter-chromosomal contacts, then the lost sense of smell may act as the canary in the coal mine, providing early signals that the COVID-19 virus is damaging brain tissue before other symptoms present, and suggesting new ways to treat it.

In a next step, the team is presently seeing whether treating hamsters with long COVID with steroids can restore restrain damaging immune reactions (inflammation) to protect nuclear architecture.

Along with Dr. tenOever, authors of the current study from the Department of Microbiology at NYU Langone Health were Justin Frere, Rasmus Moeller, Skyler Uhl, and Daisy Hoagland. Also leading the study were corresponding authors Jonathan Overdevest and Stavros Lomvardas from the Mortimer B. Zuckerman Mind Brain Behavior Institute at Columbia University. Additional contributors included Marianna Zazhytska, Albana Kodra, Hani Shayya, Stuart Firestein, Peter Canoll, and James Goldman. Also making important contributions were study authors John Fullard and Panos Roussos of the Icahn School of Medicine at Mt. Sinai; Arina Omer of Baylor Genetics in Houston; and Qizhi Gong of the Department of Cell Biology and Human Anatomy, School of Medicine, University of California at Davis.

Funding for the study was provided by National Institutes of Health grants NIDCD 3R01DC018744-01S1 and U01DA052783, as well as a Howard Hughes Medical Institute Faculty Scholars award and the Zegar Family Foundation.

Greg WilliamsPhone: 212-404-3500gregory.williams@nyulangone.org

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Mechanism Revealed Behind Loss of Smell with COVID-19 - NYU Langone Health

DUBLIN, Feb. 3, 2022 /PRNewswire/ -- The "Precision Medicine Software Market - Global Outlook & Forecast 2022-2027" report has been added to ResearchAndMarkets.com's offering.

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The precision medicine software market size was valued at USD 1,344.28 million in 2021 and is expected to reach USD 2,657.21 million by 2027, growing at a CAGR of 12.03% during the forecast period.

Favorable government initiatives and the adoption of big data analytics and related software continue to drive precision medicine software industry growth. Precision medicine software is one of the fast-growing healthcare systems IT industry segments, driven predominantly by genomics, drug discovery & development, clinical research, and big data analytics.

Start-ups are leveraging many software and machine learning algorithms to help solve major and complex problems such as reducing R&D activities timeline and billion dollars of expenditure during drug development processes.

PRECISION MEDICINE SOFTWARE MARKET SEGMENTATION

The on-cloud segment will witness an absolute growth of more than 100% in the forecast period. Cloud technology supports the industry with an agile and mountable provider engagement model. This provides better outcomes by pushing crucial information to clinicians while pulling vital, real-world insight back from key experts in the field.

Precision oncology has the highest share in Precision medicine practices by application. Oncology is the leading and fastest-growing therapeutic area in the life sciences industry. New treatments are being established at a remarkable pace, with more than 1100 oncology therapeutics in clinical development in the US alone.

GEOGRAPHICAL OUTLOOK

North America: North America made remarkable progress post the Human Genome Project in genome sequencing and precision medicine. The region is actively engaged in developing and commercializing cell and gene therapies with ICT and genome sequencing. This will drive demand in the precision medicine software industry.

Europe: The European Commission has been a driver for developing PM approaches to be readily implemented in healthcare practice. Its efforts started in 2010 with a series of workshops exploring different research areas that can contribute to developing precision medicine.

APAC: The region will likely witness a dramatic rise and innovation in precision medicine. China has already begun to make significant progress in genomics research, announcing its precision medicine initiative in 2016 with an investment of around USD 9 billion by 2030.

Story continues

VENDOR LANDSCAPE

The key players in the precision medicine software market are Syapse, AccessDx Laboratory, Fabric Genomics, Foundation Medicine, Intel, and International Business Machines (IBM).

Companies are resolving to inorganic growth approaches. AccessDx Holdings acquired 2bPrecise to create the industry's most advanced precision medicine enablement solution.

KEY HIGHLIGHTS

Blockchain technology, which works on shared ledgers and distributed networks, can ensure the data is secured and used ethically while prohibiting mishandling. Thus, blockchain technology has a huge scope in the precision medicine market.

Start-ups and scaleups are developing research platforms and techniques to better understand the underlying causes of cancer. For instance, US-America start-up OncXerna creates an RNA expression biomarker panel that permits clinical researchers to develop algorithms for effective treatment using RNA signature derived from biomarker panels.

AI leverages sophisticated computation and deep learning to overcome the obstacles involved in sizeable disparate data sets and generate insights to enable the system to learn and reason. Over the last few years, AI approaches have been used in neurodevelopmental disorders, specifically autism spectrum disorder, epileptic encephalopathy, intellectual disability, attention deficit hyperactivity disorder (ADHD), and rare genetic disorders.

KEY GROWTH FACTORS

Technological Advancements for Improvement of Precision Medicine Delivery

Increased Adoption of Cloud-Based Platform

The emergence of Local & Regional Start-Ups

Prevalence of Cancer, Genetic and Rare Diseases

Increased Partnership Among Software and Pharmaceutical Companies

Key Vendors

AccessDx Laboratory

Fabric Genomics

Foundation Medicine

Intel

IBM

Syapse

Other Prominent Vendors

GenomOncology

Koninklijke Philips

LifeOmic

NantHealth

PhenoTips

PierianDx

Qiagen

Roper Technologies

SOPHiA GENETICS

Translational Software

Key Topics Covered:

1 Research Methodology

2 Research Objectives

3 Research Process

4 Scope & Coverage4.1 Market Definition4.2 Base Year4.3 Scope Of The Study

5 Report Assumptions & Caveats5.1 Key Caveats5.2 Currency Conversion5.3 Market Derivation

6 Market at a Glance

7 Introduction7.1 Overview

8 Market Opportunities & Trends8.1 Technological Advances In Precision Medicine Delivery8.2 Increased Adoption Of Cloud-Based Platforms8.3 Emergence Of Local & Regional Start-UPS8.4 Artificial Intelligence In Precision Medicine

9 Market Growth Enablers9.1 High Prevalence Of Cancer, Genetic, & Rare Diseases9.2 Increased Partnerships Among Software & Pharmaceutical Companies9.3 Paradigm Shift Toward Tailored Disease Treatment

10 Market Growth Restraints10.1 High R&D & Implementation Cost Of Precision Medicine10.2 Dearth Of Skilled Professionals10.3 Lack Of Security & Storage For Large Volumes Of Sequenced Data

11 Market Landscape11.1 Market Overview11.2 Market Size & Forecast11.2.1 Geography Insights11.2.2 Deployment Insights11.2.3 Application Insights11.2.4 End-User Insights11.3 Five Forces Analysis

12 Deployment12.1 Market Snapshot & Growth Engine12.2 Market Overview12.3 On-Premise12.4 Cloud

13 Application13.1 Market Snapshot & Growth Engine13.2 Market Overview13.3 Precision Oncology13.4 Pharmacogenomics13.5 Rare Disease

14 End-User14.1 Market Snapshot & Growth Engine14.2 Market Overview14.3 Healthcare Providers14.4 Research Labs14.5 Pharma & Biotech Companies

15 Geography15.1 Market Snapshot & Growth Engine15.2 Geographic Overview

For more information about this report visit https://www.researchandmarkets.com/r/udylyk

Media Contact:

Research and Markets Laura Wood, Senior Manager press@researchandmarkets.com

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Global Precision Medicine Software Market Report 2022: Market was Valued at $1,344.28 Million in 2021 and is Expected to Reach $2,657.21 Million by...

A new study confirms that G207, a genetically engineered virus developed at UAB, may be a beneficial therapy for brain tumors.

A new study confirms that G207, a genetically engineered virus developed at UAB, may be a beneficial therapy for brain tumors.A new study provides additional evidence of the efficacy of virotherapy for glioblastoma, the most deadly type of brain tumor. The research findings, published Feb. 1, 2022, inClinical Cancer Research, indicate that an oncolytic herpes simplex virus, G207, appears to boost immune response and that this is associated with better overall survival for patients with glioblastoma.

The study, from investigators at theUniversity of Alabama at BirminghamandNationwide Childrens Hospital, builds on previous trials of G207. The current study further examined findings from an earlier Phase 1b study of six patients with glioblastoma recurrence. The earlier study indicated G207 was well tolerated by the patients. Overall survival, a secondary outcome, was generally but not uniformly improved in the study.

In this study, we sought to identify biological differences that could describe the variable survival duration associated with G207 virotherapy, said James Markert, M.D., Ph.D., chair of theDepartment of Neurosurgeryat UABsHeersink School of Medicineand a study co-author.

We performed RNA sequencing from pre- and post-G207 treatment tumor biopsies to investigate changes in gene expression during the treatment interval. We hypothesized that gene expression indicative of an active immune response would be characteristic of patients with improved survival.

The research team found that the adaptive immune response differed between patients and indicated there was an association with this immune response and increased length of survival in patients with recurrent glioblastoma after treatment with G207.

Glioblastomas are central nervous system tumors that are uniformly fatal with median survival of 12 to 15 months from initial diagnosis and four to six months after recurrence. The standard medical care including surgical removal of the tumor, chemotherapy and radiation currently offers limited survival benefit.

Markert, who is a senior scientist in the O'Neal Comprehensive Cancer Center, says previous research has confirmed that glioblastomas have an immunosuppressive quality, meaning they inhibit the bodys immune system from attacking and destroying the tumor. This allows the tumor to evade the immune system and continue to grow and spread. Chemotherapy and radiation therapy, necessary treatments for the tumor, unfortunately exacerbate suppression of the immune response.

Immunotherapies are an evolving strategy for cancer treatment. They are designed to stimulate the immune system to attack tumor cells and have led to remarkable responses in many cancers.

Oncolytic virotherapy, in particular, involves genetically engineered viruses designed to selectively replicate in tumor cells, relieving immunosuppression in the tumor microenvironment and enhancing antitumor immune responses.

Markert first became interested in genetically engineered viruses while a neurosurgical resident in a Boston laboratory more than 30 years ago. The lab was involved in testing the first genetically engineered herpes virus as an anti-cancer drug, based on a suitable candidate initially constructed to serve as a vaccine against herpes. The realization followed that the virus might be effective as a means to destroy brain tumors.

In 2001, Markert and his colleagues published initial results of G207, indicating it was safe to use as a sole therapy as well as in combination with radiation for malignant gliomas.

For the current study, Katherine Miller, Ph.D., a research assistant professor in the Institute for Genomic Medicine at Nationwide Childrens and the Ohio State University College of Medicine, looked at RNA extracted from the patients before and after treatment with G207. Analysis of 770 immune response genes representing 24 different immune cell types revealed that G207 treatment, more than any other component, had the greatest effect on immune gene expression changes.

They also examined which immune cell types were enriched in the post-G207 samples. Looking at 109 marker genes specific to 24 major immune-cell populations to assign cell type scores, they found that nearly all post-G207 samples had a higher abundance of immune cells relative to pre-G207 samples.

Specifically, G207 treatment significantly increased the cytotoxic, T-cell, natural killer, macrophage, neutrophil and dendritic cell scores, said study co-author Kevin Cassady, M.D., professor of pediatrics at theOhio State University College of Medicineand aninfectious diseases physicianat Nationwide Childrens Hospital. We also found that G207 reduced the number of dysfunctional T cells, known as exhausted T cells in that they become tolerant of the tumor they are supposed to attack. Exhausted T cells are one contributor to a poor immune response.

The investigators also looked to see whether there was a direct correlation between the post-G207 treatment gene expression levels and survival.

We detected approximately 500 genes that significantly correlated with patient survival and demonstrated that approximately 50 percent of these genes were related to immune response pathways and functions, Markert said. Our analysis of immune-cell populations after treatment with G207 revealed associations with patient survival and identified important mechanistic events related to cellular immune infiltrate changes including an increase in the myeloid, cytotoxic and T-cell populations, suggesting a relationship between immune gene response and survival duration.

The authors suggest that the gene sets identified permit further examination of gene expression response predictors when evaluating the impact of different recombinant oncolytic viruses. Currently, there are numerous active oncolytic viral clinical trials ongoing, five of which involve the treatment of central nervous system tumors using recombinant herpes virus vectors of various designs.

Malignant glioma is one of the most devastating forms of cancer, Cassady said. Survival after diagnosis is often no more than a few years and is frequently measured in months. Our hope is that these genetically engineered viruses will ultimately extend lifespan and improve quality of life for patients with these malignant brain tumors.

This research was supported by grants from the National Cancer Institute, part of the National Institutes of Health.

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Study supports virotherapy as a potential treatment for brain tumors - The Mix

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REDWOOD CITY, Calif. & RESEARCH TRIANGLE PARK, N.C.--(BUSINESS WIRE)--Kriya Therapeutics, Inc., a fully integrated company pioneering novel technologies and therapeutics in gene therapy, announced today that it has appointed Maan Muhsin, M.D., as President and Chief Medical Officer of Kriya Oncology, the companys oncology therapeutic area division. Dr. Muhsin will lead overall strategic, development, and partnership activities to accelerate and expand Kriyas portfolio of transformative gene therapies for cancers of high unmet need.

Maan brings a wealth of experience in the development of novel oncology therapies across a number of modalities, said Shankar Ramaswamy, M.D., Co-Founder and Chief Executive Officer of Kriya. He is uniquely positioned to accelerate the expansion and clinical translation of our growing pipeline of gene therapies that can be combined with existing and emerging standards of care in oncology. We are keen to bring forward in vivo gene therapy as a new modality to treat cancer, and Maan is a leader with an exceptional track record that will help us achieve this goal.

Dr. Muhsin previously served as Chief Medical Officer at Medicenna Therapeutics where he designed and executed clinical trials of the companys solid tumor programs. Prior to joining Medicenna, he served as Medical Lead, Oncology Clinical Development for Nektar Therapeutics where he oversaw the progression of the PIVOT-12 and REVEAL clinical studies for metastatic melanoma and advanced and local solid tumors, respectively. Dr. Muhsin has held roles of increasing responsibility at HUYA Bioscience International where he served as the Senior Vice President, Oncology Clinical Development, and at Halozyme Therapeutics where he served as Senior Medical Director, Oncology Clinical Development. He also worked in the U.S. Army Combat Support Hospitals (CSH) and held other positions within the Medical Brigade and the Medical Command under the United States Department of Defense (DoD). Dr. Muhsin completed his medical education at the Baghdad University School of Medicine and completed postgraduate education in oncology drug development at Tufts University Center for the Study of Drug Development (CSDD).

I am excited to join Kriya and look forward to advancing its promising portfolio of gene therapies in oncology, said Dr. Muhsin. While the management of cancer has come a long way in the last decade, I believe in the potential to further enhance the treatment of patients with the incorporation of rationally engineered gene therapies that can transform treatment paradigms for a wide array of cancers. I look forward to leveraging Kriyas fully-integrated gene therapy engine to deliver a pipeline of novel medicines with the potential to significantly impact the lives of cancer patients.

About Kriya

Kriya is a fully integrated company pioneering novel technologies and therapeutics in gene therapy. The company aims to revolutionize how gene therapies are designed, developed, and manufactured, improving speed to market and delivering significant reductions in cost. Kriya is organized into four principal business units: Kriya Technologies, Kriya Therapeutics, Kriya R&D, and Kriya Manufacturing. The company is advancing a deep and diversified pipeline of innovative gene therapies in multiple therapeutic area divisions, with current pipeline programs in ophthalmology, oncology, rare disease, and chronic disease. Kriya was founded by pioneers in the biopharmaceutical industry and is backed by leading life sciences and technology investors. The company has core operations in Silicon Valley, California and Research Triangle Park, North Carolina. For more information, please visit http://www.kriyatx.com and follow on LinkedIn.

View source version on businesswire.com: https://www.businesswire.com/news/home/20220203005305/en/

Danielle CanteyCanale Communicationsdanielle.cantey@canalecomm.com(619) 826-4657

Source: Kriya Therapeutics, Inc.

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Kriya Announces the Appointment of Ma'an Muhsin, MD, as President and Chief Medical Officer of Its Oncology Therapeutic Area Division -...

Several years ago, in a lab meeting, one of Nikolaus Schultzs postdoctoral fellows posed a question: Do you think its possible to predict, based on the genomic profile of an individual tumor, which organs it might metastasize to?

And just like that, a research project was born.

Dr. Schultz is a computational oncologist in the Department of Epidemiology and Biostatistics at Memorial Sloan Kettering Cancer Center. He also serves as Head of Knowledge Systems in the Marie-Jose and Henry R. Kravis Center for Molecular Oncology. In these dual roles, he has gained a wealth of experience sequencing the DNA in patients tumors and using this information to help physicians guide treatment.

MSK computational oncologists Francisco Sanchez-Vega and Nikolaus Schultz

Every person with advanced cancer who is treated at MSK undergoes genetic sequencing of their tumor with MSK-IMPACT, a tool that looks for mutations in 400-plus cancer-associated genes. Since sequencing started in 2014, MSK has compiled genetic tumor profiles from more than 50,000 patients. This vast repository represents a goldmine for biologists interested in asking questions about the relationships between tumor mutations and cancer progression.

Dr. Schultz and Francisco Sanchez-Vega the curious postdoc who originally posed the question about metastasis and who is now an Assistant Attending Computational Oncologist at MSK realized that they could use computational techniques to search this mountain of data for clues. Specifically, they could ask whether particular mutations (or groups of mutations) correlate with the spread of cancer to particular organs, across many different types of cancer.

That was six years ago. Now, in a paper published February 3, 2022, in the journal Cell, Drs. Schultz and Sanchez-Vega and their team, including postdoctoral researchers Bastien Nguyen and Christopher Fong, and 71 other MSK scientists present the results of their investigation.

To the question of whether its possible to look at an individual tumor and, based on its genomic profile alone, predict its precise future metastatic trajectory, the answer is clearly no.

VIDEO | 01:38

Learn about metastasis, which is the spreading of cancer from its original location to a new location. Memorial Sloan Kettering researchers are making advances in understanding the three stages of metastasis.

While we found some gene mutations to be slightly more common in tumor samples with specific metastatic transitions, we found no single gene that, when mutated, will predict with absolute certainty whether or not a tumor will metastasize to a particular organ, Dr. Schultz says.

The study was revealing in other ways: At a very high level, what the data are telling us is that metastatic disease is genomically different from primary disease, Dr. Schultz says.

For example, in many cancer types, metastatic tumors have more of what geneticists call DNA copy-number changes compared with primary tumors. A DNA copy-number change is when a particular segment of DNA is present in greater or fewer than the normal number of copies. These copy-number changes, when observed in primary tumors, were an indicator of metastatic potential, Dr. Schultz points out.

In addition, he notes, some cancer-driving mutations were detected at different frequencies in metastases compared with primary tumors across a variety of cancer types.

Dr. Schultz likens the extensive dataset his team has curated to The Cancer Genome Atlas (TCGA) project, in which he was also involved. An important goal of TCGA was to assemble a valuable dataset and get it out into the world so that others could mine it, he says.

To help researchers mine these new data for insights, the team is making them publicly available through the cBioPortal for Cancer Genomics as MSK-MET (Memorial Sloan Kettering Metastatic Events and Tropisms).

The dataset includes information on genetic changes and clinical outcomes from 25,000 patients across 50 different cancer types.

Because no single mutation or set of mutations stood out as reliable predictors of metastatic behavior across tumor types, the new study may add support to an emerging framework in cancer science that views metastasis the cause of 90% of cancer deaths as not primarily driven by genetic mutations. Rather, epigenetic changes that occur in cancer cells as a consequence of their interactions with normal cells in the surrounding environment could be more to blame. (Epigenetic changes are ones that alter what genes are turned on or off in a cell without altering the DNA sequence as a mutation would.) These changes may underlie the ability of metastatic cells to adapt to otherwise hostile tissue environments.

To the question of whether its possible to look at an individual tumor and, based on its genomic profile alone, predict its precise future metastatic trajectory, the answer is clearly no.

Recent discoveries from other investigators at MSK including Joan Massagu, Karuna Ganesh, Charles Sawyers, Kat Hadjantonakis, and Dana Peer have pointed to a kind of epigenetically driven identity switching that enables cancer cells to assume more developmentally primitive states and thereby grow in new parts of the body.

Exploring the ramifications of these and other findings will be the focus of MSKs new Marie-Jose and Henry R. Kravis Cancer Ecosystems Project, which launches today.

Currently, genetic sequencing of tumors with MSK-IMPACT can inform whether or not a specific patient should receive a specific drug based on a single genomic alteration. For example, if someone is found to have a mutation in the BRAF gene, they might be a good candidate for a targeted drug called vemurafenib.

But Dr. Schultz points out that there is potentially much more information to be found in the mass of sequencing data and associated patient clinical data that could inform treatment decisions.

When properly mined, this data could tell us a lot more about prognosis of these patients, whether or not their tumors will metastasize, maybe even to what tissues, he says. This information might determine how these patients get monitored in the future. We can learn about what treatments they might be more sensitive to or less sensitive to. I think that theres enormous potential for personalized medicine that goes beyond the single biomarker, and therefore justification to keep sequencing more patients with broader sequencing panels to increase our power to make new discoveries.

Key Takeaways

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The Mystery of Metastasis: Can a Tumors Genetic Mutations Predict Whether and Where Cancer Will Spread? - On Cancer - Memorial Sloan Kettering

DUBLIN, Feb. 1, 2022 /PRNewswire/ -- The "Cell & Gene Therapy Market - Global Outlook & Forecast 2022-2027" report has been added to ResearchAndMarkets.com's offering.

The cell and gene therapy market size was valued at USD 4.99 billion in 2021 and is expected to reach USD 36.92 billion by 2027, growing at a CAGR of 39.62 % during the forecast period

In the cell and gene therapy field, gene therapy gathered the pace last from 2 decades because of the discovery of several genes responsible for mutation in various diseases. The advancement in the cell & gene therapy field and innovative technologies give the new era for biological therapeutics. Also, PRIME Designation and marketing authorization for products provide a new opportunity for the manufacturer's financing and revenue generation.

KEY HIGHLIGHTS

As per the American Society of Cell + Gene Therapy report in 2021, increasing the number of cellular and gene therapy products, application rate and products in clinical trials drive the market growth.

As per the Dive Biopharma report 2021, biotech companies who actively engaged in regenerative medicines and therapies reported USD 14 billion funding only in six months of 2021 which was reported to be USD 19.9 billion for the overall year.

CELL AND GENE THERAPY MARKET SEGMENTATION

Increasing application of gene therapies in diseases diagnosis and rapidly growing new drugs applications will give new market space in upcoming years. In 2020, around USD 2.3 billion funding was reported only from private companies for gene therapies. By 2025, the FDA is expected to approve 10?20 products each year, driving the global cell and gene therapy manufacturing market.

In 2020, Medicine in Development Report 2020, around 176 products were reported in cancer therapies in development procedures.

GEOGRAPHICAL OUTLOOK

North America: High economic status and high expenditure on healthcare services drive the cell and gene therapy market in North America. National Health Institutes, industries, academic institutes, and hospitals are the significant contributors of sponsorship and financial funding for cell and gene therapy products.

Europe: The increasing funding for cell and gene therapy drives the cell and gene therapy market growth consistently in Europe. Around USD 2.6 billion financings were reported in Europe for CGTs in 2020, which increased by 103% compared to previous years. In the cell therapy segment, USD 1.8 billion and in gene therapy, USD 2.3 billion funding accounted in 2020, which increased by 196% and 111% growth respectively

VENDOR LANDSCAPE

The key players in the cell and gene therapy market are Gilead Sciences, Novartis, Smith Nephew, Amgen, Organogenesis, Roche (Spark Therapeutics), Dendreon, Vericel, and Bristol-Myers Squibb Company.

An increasing number of mergers and acquisitions gives new potential to market growth. Gilead Sciences acquired Kite Pharma in 2020. Also, Novartis acquired Avexis in 2018, and Smith & Nephew acquired Osiris Therapeutics.

MAJOR GROWTH FACTORS

KEY VENDORS

OTHER PROMINENT VENDORS

UPCOMING VENDORS

Key Topics Covered:

1 Research Methodology

2 Research Objectives

3 Research Process

4 Scope & Coverage4.1 Market Definition4.2 Base Year4.3 Scope of The Study

5 Report Assumptions & Caveats5.1 Key Caveats5.2 Currency Conversion5.3 Market Derivation

6 Market at a Glance

7 Introduction7.1 Overview7.1.1 Cell & Gene Therapy Approved Products 2020-20217.2 Cell & Gene Therapy Phase-III Products7.3 Road Map of Cell & Gene Therapy

8 Market Opportunities & Trends8.1 Rising Number of Mergers & Acquisitions8.2 Expansion of CGT Manufacturing Plants8.3 Expanding Applications for Cell & Gene Therapies8.4 Growing Demand for Car T-Cell Therapies

9 Market Growth Enablers9.1 New Product Approvals & Increasing Pipeline of Products9.2 Prime Designation & Funding Support For CGT9.3 Rising Use of CGT Products for Disease Care9.4 Increasing Use of CGT Products for Disease Treatment

10 Market Restraints10.1 High Cost of Cell & Gene Therapies10.2 Ethical Issues Regarding Genetical Material10.3 Stringent Regulation for CGT Approvals

11 Market Landscape11.1 Market Overview11.2 Market Size & Forecast11.3 Five Forces Analysis

12 Therapy12.1 Market Snapshot & Growth Engine12.2 Market Overview12.3 Gene Therapy12.4 Cell Therapy

13 Application13.1 Market Snapshot & Growth Engine13.2 Market Overview13.3 Oncology13.4 Genetic Disorders13.5 Dermatology13.6 Musculoskeletal Diseases13.7 Other Diseases

14 End-User14.1 Market Snapshot & Growth Engine14.2 Market Overview14.3 Hospitals14.4 Cancer Care Centers14.5 Wound Care Centers14.6 Other End-Users

15 Geography15.1 Market Snapshot & Growth Engine15.2 Geographic Overview15.2.1 Global Cell & Gene Therapy Market by Geography

For more information about this report visit https://www.researchandmarkets.com/r/z7gm5

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Global Cell & Gene Therapy Market Research Report 2022: Expanding Application for Cell & Gene Therapies & Growing Demand for CAR T- Cell...

The authors would like to thank the participants of the individual studies contributing to the BCAC, GECCO, CORECT, CCFR, INTEGRAL-ILCCO, PRACTICAL, Finngen, BioBank Japan, Asia Colorectal Cancer Consortium, ICBP, DIAGRAM, CARDIoGRAMplusC4D, and MEGASTROKE consortia and the Genetic Epidemiology Research on Adult Health, UK Biobank, and the Korean National Cancer Center CRC Study 2. The authors would also like to acknowledge the investigators of these consortia and studies for generating the data used for this analysis. The authors would like to acknowledge the following investigators of the OncoArray and GAME-ON1KG INTEGRAL-ILCCO analyses: Maria Teresa Landi, Victoria Stevens, Ying Wang, Demetrios Albanes, Neil Caporaso, Paul Brennan, Christopher I Amos, Sanjay Shete, Rayjean J Hung, Heike Bickebller, Angela Risch, Richard Houlston, Stephen Lam, Adonina Tardon, Chu Chen, Stig E Bojesen, Mattias Johansson, H-Erich Wichmann, David Christiani, Gadi Rennert, Susanne Arnold, John K. Field, Loic Le Marchand, Olle Melander, Hans Brunnstrm, Geoffrey Liu, Angeline Andrew, Lambertus A Kiemeney, Hongbing Shen, Shan Zienolddiny, Kjell Grankvist, Mikael Johansson, M Dawn Teare, Yun-Chul Hong, Jian-Min Yuan, Philip Lazarus, Matthew B Schabath, Melinda C Aldrich. Cancer consortia-specific funding and acknowledgments is presented in S1 Text.

http://practical.icr.ac.uk/

Rosalind A. Eeles1,2, Christopher A. Haiman3, Zsofia Kote-Jarai1, Fredrick R. Schumacher4,5, Sara Benlloch6,1, Ali Amin Al Olama6,7, Kenneth Muir8,9, Sonja I. Berndt10, David V. Conti3, Fredrik Wiklund11, Stephen Chanock10, Ying Wang12, Victoria L. Stevens12, Catherine M. Tangen13, Jyotsna Batra14,15, Judith A. Clements14,15, APCB BioResource (Australian Prostate Cancer BioResource)14,15, Henrik Grnberg11, Nora Pashayan16,17, Johanna Schleutker18,19, Demetrius Albanes10, Stephanie Weinstein10, Alicja Wolk20, Catharine M. L. West21, Lorelei A. Mucci22, Graldine Cancel-Tassin23,24, Stella Koutros10, Karina Dalsgaard Srensen25,26, Eli Marie Grindedal27, David E. Neal28,29,30, Freddie C. Hamdy31,32, Jenny L. Donovan33, Ruth C. Travis34, Robert J. Hamilton35,36, Sue Ann Ingles37, Barry S. Rosenstein38,39, Yong-Jie Lu40, Graham G. Giles41,42,43, Adam S. Kibel44, Ana Vega45,46,47, Manolis Kogevinas48,49,50,51, Kathryn L. Penney52, Jong Y. Park53, Janet L. Stanford54,55, Cezary Cybulski56, Brge G. Nordestgaard57,58, Sune F. Nielsen57,58, Hermann Brenner59,60,61, Christiane Maier62, Jeri Kim63, Esther M. John64, Manuel R. Teixeira65,66,67, Susan L. Neuhausen68, Kim De Ruyck69, Azad Razack70, Lisa F. Newcomb54,71, Davor Lessel72, Radka Kaneva73, Nawaid Usmani74,75, Frank Claessens76, Paul A. Townsend77,78, Jose Esteban Castelao79, Monique J. Roobol80, Florence Menegaux81, Kay-Tee Khaw82, Lisa Cannon-Albright83,84, Hardev Pandha78, Stephen N. Thibodeau85, David J. Hunter86, Peter Kraft87, William J. Blot88,89, Elio Riboli90

1 The Institute of Cancer Research, London, SM2 5NG, UK

2 Royal Marsden NHS Foundation Trust, London, SW3 6JJ, UK

3 Center for Genetic Epidemiology, Department of Preventive Medicine, Keck School of Medicine, University of Southern California/Norris Comprehensive Cancer Center, Los Angeles, CA 90015, USA

4 Department of Population and Quantitative Health Sciences, Case Western Reserve University, Cleveland, OH 441067219, USA

5 Seidman Cancer Center, University Hospitals, Cleveland, OH 44106, USA

6 Centre for Cancer Genetic Epidemiology, Department of Public Health and Primary Care, University of Cambridge, Strangeways Research Laboratory, Cambridge CB1 8RN, UK

7 University of Cambridge, Department of Clinical Neurosciences, Stroke Research Group, R3, Box 83, Cambridge Biomedical Campus, Cambridge CB2 0QQ, UK

8 Division of Population Health, Health Services Research and Primary Care, University of Manchester, Oxford Road, Manchester, M13 9PL, UK

9 Warwick Medical School, University of Warwick, Coventry, CV4 7AL, UK

10 Division of Cancer Epidemiology and Genetics, National Cancer Institute, NIH, Bethesda, Maryland, 20892, USA

11 Department of Medical Epidemiology and Biostatistics, Karolinska Institute, SE-171 77 Stockholm, Sweden

12 Department of Population Science, American Cancer Society, 250 Williams Street, Atlanta, GA 30303, USA

13 SWOG Statistical Center, Fred Hutchinson Cancer Research Center, Seattle, WA 98109, USA

14 Australian Prostate Cancer Research Centre-Qld, Institute of Health and Biomedical Innovation and School of Biomedical Sciences, Queensland University of Technology, Brisbane QLD 4059, Australia

15 Translational Research Institute, Brisbane, Queensland 4102, Australia

16 Department of Applied Health Research, University College London, London, WC1E 7HB, UK

17 Centre for Cancer Genetic Epidemiology, Department of Oncology, University of Cambridge, Strangeways Laboratory, Worts Causeway, Cambridge, CB1 8RN, UK

18Institute of Biomedicine, University of Turku, Finland

19 Department of Medical Genetics, Genomics, Laboratory Division, Turku University Hospital, PO Box 52, 20521 Turku, Finland

20 Department of Surgical Sciences, Uppsala University, 75185 Uppsala, Sweden

21 Division of Cancer Sciences, University of Manchester, Manchester Academic Health Science Centre, Radiotherapy Related Research, The Christie Hospital NHS Foundation Trust, Manchester, M13 9PL UK

22 Department of Epidemiology, Harvard T. H. Chan School of Public Health, Boston, MA 02115, USA

23 CeRePP, Tenon Hospital, F-75020 Paris, France

24 Sorbonne Universite, GRC n5, AP-HP, Tenon Hospital, 4 rue de la Chine, F-75020 Paris, France

25 Department of Molecular Medicine, Aarhus University Hospital, Palle Juul-Jensen Boulevard 99, 8200 Aarhus N, Denmark

26 Department of Clinical Medicine, Aarhus University, DK-8200 Aarhus N

27 Department of Medical Genetics, Oslo University Hospital, 0424 Oslo, Norway

28 Nuffield Department of Surgical Sciences, University of Oxford, Room 6603, Level 6, John Radcliffe Hospital, Headley Way, Headington, Oxford, OX3 9DU, UK

29 University of Cambridge, Department of Oncology, Box 279, Addenbrookes Hospital, Hills Road, Cambridge CB2 0QQ, UK

30 Cancer Research UK, Cambridge Research Institute, Li Ka Shing Centre, Cambridge, CB2 0RE, UK

31 Nuffield Department of Surgical Sciences, University of Oxford, Oxford, OX1 2JD, UK

32 Faculty of Medical Science, University of Oxford, John Radcliffe Hospital, Oxford, UK

33 Population Health Sciences, Bristol Medical School, University of Bristol, BS8 2PS, UK

34 Cancer Epidemiology Unit, Nuffield Department of Population Health, University of Oxford, Oxford, OX3 7LF, UK

35 Dept. of Surgical Oncology, Princess Margaret Cancer Centre, Toronto ON M5G 2M9, Canada

36 Dept. of Surgery (Urology), University of Toronto, Canada

37 Department of Preventive Medicine, Keck School of Medicine, University of Southern California/Norris Comprehensive Cancer Center, Los Angeles, CA 90015, USA

38 Department of Radiation Oncology and Department of Genetics and Genomic Sciences, Box 1236, Icahn School of Medicine at Mount Sinai, One Gustave L. Levy Place, New York, NY 10029, USA

39 Department of Genetics and Genomic Sciences, Icahn School of Medicine at Mount Sinai, New York, NY 100295674, USA

40 Centre for Cancer Biomarker and Biotherapeutics, Barts Cancer Institute, Queen Mary University of London, John Vane Science Centre, Charterhouse Square, London, EC1M 6BQ, UK

41 Cancer Epidemiology Division, Cancer Council Victoria, 615 St Kilda Road, Melbourne, VIC 3004, Australia

42 Centre for Epidemiology and Biostatistics, Melbourne School of Population and Global Health, The University of Melbourne, Grattan Street, Parkville, VIC 3010, Australia

43 Precision Medicine, School of Clinical Sciences at Monash Health, Monash University, Clayton, Victoria 3168, Australia

44 Division of Urologic Surgery, Brigham and Womens Hospital, 75 Francis Street, Boston, MA 02115, USA

45 Fundacin Pblica Galega Medicina Xenmica, Santiago de Compostela, 15706, Spain

46 Instituto de Investigacin Sanitaria de Santiago de Compostela, Santiago De Compostela, 15706, Spain

47 Centro de Investigacin en Red de Enfermedades Raras (CIBERER), Spain

48 ISGlobal, Barcelona, Spain

49 IMIM (Hospital del Mar Medical Research Institute), Barcelona, Spain

50 CIBER Epidemiologa y Salud Pblica (CIBERESP), 28029 Madrid, Spain

51 Universitat Pompeu Fabra (UPF), Barcelona, Spain

52 Channing Division of Network Medicine, Department of Medicine, Brigham and Womens Hospital/Harvard Medical School, Boston, MA 02115, USA

53 Department of Cancer Epidemiology, Moffitt Cancer Center, 12902 Magnolia Drive, Tampa, FL 33612, USA

54 Division of Public Health Sciences, Fred Hutchinson Cancer Research Center, Seattle, Washington, 981091024, USA

55 Department of Epidemiology, School of Public Health, University of Washington, Seattle, Washington 98195, USA

56 International Hereditary Cancer Center, Department of Genetics and Pathology, Pomeranian Medical University, 70115 Szczecin, Poland

57 Faculty of Health and Medical Sciences, University of Copenhagen, 2200 Copenhagen, Denmark

58 Department of Clinical Biochemistry, Herlev and Gentofte Hospital, Copenhagen University Hospital, Herlev, 2200 Copenhagen, Denmark

59 Division of Clinical Epidemiology and Aging Research, German Cancer Research Center (DKFZ), D-69120, Heidelberg, Germany

60 German Cancer Consortium (DKTK), German Cancer Research Center (DKFZ), D-69120 Heidelberg, Germany

61 Division of Preventive Oncology, German Cancer Research Center (DKFZ) and National Center for Tumor Diseases (NCT), Im Neuenheimer Feld 460, 69120 Heidelberg, Germany

62 Humangenetik Tuebingen, Paul-Ehrlich-Str 23, D-72076 Tuebingen, Germany

63 The University of Texas M. D. Anderson Cancer Center, Department of Genitourinary Medical Oncology, 1515 Holcombe Blvd., Houston, TX 77030, USA

64 Departments of Epidemiology & Population Health and of Medicine, Division of Oncology, Stanford Cancer Institute, Stanford University School of Medicine, Stanford, CA 94304 USA

65 Department of Genetics, Portuguese Oncology Institute of Porto (IPO-Porto), 4200072 Porto, Portugal

66 Biomedical Sciences Institute (ICBAS), University of Porto, 4050313 Porto, Portugal

67 Cancer Genetics Group, IPO-Porto Research Center (CI-IPOP), Portuguese Oncology Institute of Porto (IPO-Porto), 4200072 Porto, Portugal

68 Department of Population Sciences, Beckman Research Institute of the City of Hope, 1500 East Duarte Road, Duarte, CA 91010, 626-256-HOPE (4673)

69 Ghent University, Faculty of Medicine and Health Sciences, Basic Medical Sciences, Proeftuinstraat 86, B-9000 Gent

70 Department of Surgery, Faculty of Medicine, University of Malaya, 50603 Kuala Lumpur, Malaysia

71 Department of Urology, University of Washington, 1959 NE Pacific Street, Box 356510, Seattle, WA 98195, USA

72 Institute of Human Genetics, University Medical Center Hamburg-Eppendorf, D-20246 Hamburg, Germany

73 Molecular Medicine Center, Department of Medical Chemistry and Biochemistry, Medical University of Sofia, Sofia, 2 Zdrave Str., 1431 Sofia, Bulgaria

74 Department of Oncology, Cross Cancer Institute, University of Alberta, 11560 University Avenue, Edmonton, Alberta, Canada T6G 1Z2

75 Division of Radiation Oncology, Cross Cancer Institute, 11560 University Avenue, Edmonton, Alberta, Canada T6G 1Z2

76 Molecular Endocrinology Laboratory, Department of Cellular and Molecular Medicine, KU Leuven, BE-3000, Belgium

77 Division of Cancer Sciences, Manchester Cancer Research Centre, Faculty of Biology, Medicine and Health, Manchester Academic Health Science Centre, NIHR Manchester Biomedical Research Centre, Health Innovation Manchester, Univeristy of Manchester, M13 9WL

78 The University of Surrey, Guildford, Surrey, GU2 7XH, UK

79 Genetic Oncology Unit, CHUVI Hospital, Complexo Hospitalario Universitario de Vigo, Instituto de Investigacin Biomdica Galicia Sur (IISGS), 36204, Vigo (Pontevedra), Spain

80 Department of Urology, Erasmus University Medical Center, 3015 CE Rotterdam, The Netherlands

81 "Exposome and Heredity", CESP (UMR 1018), Facult de Mdecine, Universit Paris-Saclay, Inserm, Gustave Roussy, Villejuif

82 Clinical Gerontology Unit, University of Cambridge, Cambridge, CB2 2QQ, UK

83 Division of Epidemiology, Department of Internal Medicine, University of Utah School of Medicine, Salt Lake City, Utah 84132, USA

84 George E. Wahlen Department of Veterans Affairs Medical Center, Salt Lake City, Utah 84148, USA

85 Department of Laboratory Medicine and Pathology, Mayo Clinic, Rochester, MN 55905, USA

86 Nuffield Department of Population Health, University of Oxford, United Kingdom

87 Program in Genetic Epidemiology and Statistical Genetics, Department of Epidemiology, Harvard School of Public Health, Boston, MA, USA

88 Division of Epidemiology, Department of Medicine, Vanderbilt University Medical Center, 2525 West End Avenue, Suite 800, Nashville, TN 37232 USA

89 International Epidemiology Institute, Rockville, MD 20850, USA

90 Department of Epidemiology and Biostatistics, School of Public Health, Imperial College London, SW7 2AZ, UK

Rainer Malik 1, Ganesh Chauhan 2, Matthew Traylor 3, Muralidharan Sargurupremraj 4,5, Yukinori Okada 6,7,8, Aniket Mishra 4,5, Loes Rutten-Jacobs 3, Anne-Katrin Giese 9, Sander W van der Laan 10, Solveig Gretarsdottir 11, Christopher D Anderson 12,13,14,14, Michael Chong 15, Hieab HH Adams 16,17, Tetsuro Ago 18, Peter Almgren 19, Philippe Amouyel 20,21, Hakan Ay 22,13, Traci M Bartz 23, Oscar R Benavente 24, Steve Bevan 25, Giorgio B Boncoraglio 26, Robert D Brown, Jr. 27, Adam S Butterworth 28,29, Caty Carrera 30,31, Cara L Carty 32,33, Daniel I Chasman 34,35, Wei-Min Chen 36, John W Cole 37, Adolfo Correa 38, Ioana Cotlarciuc 39, Carlos Cruchaga 40,41, John Danesh 28,42,43,44, Paul IW de Bakker 45,46, Anita L DeStefano 47,48, Marcel den Hoed 49, Qing Duan 50, Stefan T Engelter 51,52, Guido J Falcone 53,54, Rebecca F Gottesman 55, Raji P Grewal 56, Vilmundur Gudnason 57,58, Stefan Gustafsson 59, Jeffrey Haessler 60, Tamara B Harris 61, Ahamad Hassan 62, Aki S Havulinna 63,64, Susan R Heckbert 65, Elizabeth G Holliday 66,67, George Howard 68, Fang-Chi Hsu 69, Hyacinth I Hyacinth 70, M Arfan Ikram 16, Erik Ingelsson 71,72, Marguerite R Irvin 73, Xueqiu Jian 74, Jordi Jimnez-Conde 75, Julie A Johnson 76,77, J Wouter Jukema 78, Masahiro Kanai 6,7,79, Keith L Keene 80,81, Brett M Kissela 82, Dawn O Kleindorfer 82, Charles Kooperberg 60, Michiaki Kubo 83, Leslie A Lange 84, Carl D Langefeld 85, Claudia Langenberg 86, Lenore J Launer 87, Jin-Moo Lee 88, Robin Lemmens 89,90, Didier Leys 91, Cathryn M Lewis 92,93, Wei-Yu Lin 28,94, Arne G Lindgren 95,96, Erik Lorentzen 97, Patrik K Magnusson 98, Jane Maguire 99, Ani Manichaikul 36, Patrick F McArdle 100, James F Meschia 101, Braxton D Mitchell 100,102, Thomas H Mosley 103,104, Michael A Nalls 105,106, Toshiharu Ninomiya 107, Martin J ODonnell 15,108, Bruce M Psaty 109,110,111,112, Sara L Pulit 113,45, Kristiina Rannikme 114,115, Alexander P Reiner 65,116, Kathryn M Rexrode 117, Kenneth Rice 118, Stephen S Rich 36, Paul M Ridker 34,35, Natalia S Rost 9,13, Peter M Rothwell 119, Jerome I Rotter 120,121, Tatjana Rundek 122, Ralph L Sacco 122, Saori Sakaue 7,123, Michele M Sale 124, Veikko Salomaa 63, Bishwa R Sapkota 125, Reinhold Schmidt 126, Carsten O Schmidt 127, Ulf Schminke 128, Pankaj Sharma 39, Agnieszka Slowik 129, Cathie LM Sudlow 114,115, Christian Tanislav 130, Turgut Tatlisumak 131,132, Kent D Taylor 120,121, Vincent NS Thijs 133,134, Gudmar Thorleifsson 11, Unnur Thorsteinsdottir 11, Steffen Tiedt 1, Stella Trompet 135, Christophe Tzourio 5,136,137, Cornelia M van Duijn 138,139, Matthew Walters 140, Nicholas J Wareham 86, Sylvia Wassertheil-Smoller 141, James G Wilson 142, Kerri L Wiggins 109, Qiong Yang 47, Salim Yusuf 15, Najaf Amin 16, Hugo S Aparicio 185,48, Donna K Arnett 186, John Attia 187, Alexa S Beiser 47,48, Claudine Berr 188, Julie E Buring 34,35, Mariana Bustamante 189, Valeria Caso 190, Yu-Ching Cheng 191, Seung Hoan Choi 192,48, Ayesha Chowhan 185,48, Natalia Cullell 31, Jean-Franois Dartigues 193,194, Hossein Delavaran 95,96, Pilar Delgado 195, Marcus Drr 196,197, Gunnar Engstrm 19, Ian Ford 198, Wander S Gurpreet 199, Anders Hamsten 200,201, Laura Heitsch 202, Atsushi Hozawa 203, Laura Ibanez 204, Andreea Ilinca 95,96, Martin Ingelsson 205, Motoki Iwasaki 206, Rebecca D Jackson 207, Katarina Jood 208, Pekka Jousilahti 63, Sara Kaffashian 4,5, Lalit Kalra 209, Masahiro Kamouchi 210, Takanari Kitazono 211, Olafur Kjartansson 212, Manja Kloss 213, Peter J Koudstaal 214, Jerzy Krupinski 215, Daniel L Labovitz 216, Cathy C Laurie 118, Christopher R Levi 217, Linxin Li 218, Lars Lind 219, Cecilia M Lindgren 220,221, Vasileios Lioutas 222,48, Yong Mei Liu 223, Oscar L Lopez 224, Hirata Makoto 225, Nicolas Martinez-Majander 172, Koichi Matsuda 225, Naoko Minegishi 203, Joan Montaner 226, Andrew P Morris 227,228, Elena Muio 31, Martina Mller-Nurasyid 229,230,231, Bo Norrving 95,96, Soichi Ogishima 203, Eugenio A Parati 232, Leema Reddy Peddareddygari 56, Nancy L Pedersen 98,233, Joanna Pera 129, Markus Perola 63,234, Alessandro Pezzini 235, Silvana Pileggi 236, Raquel Rabionet 237, Iolanda Riba-Llena 30, Marta Ribass 238, Jose R Romero 185,48, Jaume Roquer 239,240, Anthony G Rudd 241,242, Antti-Pekka Sarin 243,244, Ralhan Sarju 199, Chloe Sarnowski 47,48, Makoto Sasaki 245, Claudia L Satizabal 185,48, Mamoru Satoh 245, Naveed Sattar 246, Norie Sawada 206, Gerli Sibolt 172, sgeir Sigurdsson 247, Albert Smith 248, Kenji Sobue 245, Carolina Soriano-Trraga 240, Tara Stanne 249, O Colin Stine 250, David J Stott 251, Konstantin Strauch 229,252, Takako Takai 203, Hideo Tanaka 253,254, Kozo Tanno 245, Alexander Teumer 255, Liisa Tomppo 172, Nuria P Torres-Aguila 31, Emmanuel Touze 256,257, Shoichiro Tsugane 206, Andre G Uitterlinden 258, Einar M Valdimarsson 259, Sven J van der Lee 16, Henry Vlzke 255, Kenji Wakai 253, David Weir 260, Stephen R Williams 261, Charles DA Wolfe 241,242, Quenna Wong 118, Huichun Xu 191, Taiki Yamaji 206, Dharambir K Sanghera 125,169,170, Olle Melander 19, Christina Jern 171, Daniel Strbian 172,173, Israel Fernandez-Cadenas 31,30, W T Longstreth, Jr 174,65, Arndt Rolfs 175, Jun Hata 107, Daniel Woo 82, Jonathan Rosand 12,13,14, Guillaume Pare 15, Jemma C Hopewell 176, Danish Saleheen 177, Kari Stefansson 11,178, Bradford B Worrall 179, Steven J Kittner 37, Sudha Seshadri 180,48, Myriam Fornage 74,181, Hugh S Markus 3, Joanna MM Howson 28, Yoichiro Kamatani 6,182, Stephanie Debette 4,5, Martin Dichgans 1,183,184.

1 Institute for Stroke and Dementia Research (ISD), University Hospital, LMU Munich, Munich, Germany

2 Centre for Brain Research, Indian Institute of Science, Bangalore, India

3 Stroke Research Group, Division of Clinical Neurosciences, University of Cambridge, UK

4 INSERM U1219 Bordeaux Population Health Research Center, Bordeaux, France

5 University of Bordeaux, Bordeaux, France

6 Laboratory for Statistical Analysis, RIKEN Center for Integrative Medical Sciences, Yokohama, Japan

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