StemCell Therapy

The Department of Neurology at the Wayne State University School of Medicine, partnered with Department of Psychiatry and Behavioral Sciences, has an endowment from the Albert and Goldye J. Nelson Fund to support scientific research in the detection, pathogenesis, molecular genetics, neurobiology and therapeutic development to cure Alzheimers disease and related disorders. Available funds for the coming fiscal year are between $50,000 and $100,000.

The Neurology Department is accepting proposals for FY 2021.Interested applicants must submit a proposal that consists of:

1. Specific aim (one page)

2. Research plan (six pages)

3. Human subjects if applicable (two pages)

4. Vertebral animals if applicable (two pages)

5. Biosketch (National Institutes of Health format) for all personnel involved in the study

6. Budget with budget justification

7. Resource

8. Support letters

Funds may not be used to cover the principal investigators salary. Proposals are for two to three years. Applicants must have at least a .25 FTE faculty appointment at the School of Medicine.

The deadline for submission is Jan. 31, 2021. The grant will begin Aug. 1, 2021.

Submit proposals to Carla Santiago, research administrator, WSU Department of Neurology - 8D UHC, 4201 St. Antoine, Detroit, MI 48201. E-mail:csantiago@med.wayne.edu.

Please note that the grant submissions must follow grant guidelines. Please click here for the guidelines.

Link:
Neurology Department calls for grant proposals to support Alzheimer's disease and related research - The South End

Newswise A $53.6 million grant from the National Institutes of Health will aid brain scientists, including a researcher from The University of Texas Health Science Center at Houston (UTHealth), in studying the role of incidental white matter lesions, or WMLs, in dementia among diverse people with cognitive complaints.

The study is led by UC Davis School of Medicine in partnership with UTHealth. It is a new and critical part of the NIHsVascular Contributions to Cognitive Impairment and Dementia(VCID) research program.

Co-principal investigator isMyriam Fornage, PhD, professor of genetics at theBrown Foundation Institute of Molecular Medicine for the Prevention of Human Diseasesat McGovern Medical School at UTHealth. Fornage is a leading researcher on the molecular genetics of cerebrovascular disease.

Our team has been at the forefront of genetic studies of WMLs for two decades, Fornage said. Through the genetic risk profiles we will develop, we will have an opportunity to apply what we have discovered and improve the precision with which we identify patients with a higher prior probability of cognitive impairment and dementia. At the same time, we will be contributing new resources for dementia research everywhere.

The principal investigator isCharles DeCarli, MD, professor of neurology, director of theUC Davis Alzheimers Disease Centerand the nations foremost expert on the role of subcortical cerebrovascular disease in cognitive decline. In the last few years, DeCarli has been awarded national and state research grants exceeding $33 million.

The magnitude of this NIH grant underscores UC Davis Alzheimers Disease Centers national prominence and research leadership, said UC Davis School of Medicine Dean Allison Brashear,MD, a neurologist nationally known for her groundbreaking research in movement disorders. This multiyear research award will enable us to make game-changing advancements in our understanding and treatment of dementia.

WMLs occur when tissue deep in the brain becomes injured, often due to changes in small blood vessels. They are common and often found on brain MRIs of people who have concerns about their brain health.

Why or how WMLs are associated with cognitive decline is not known. Questions surround whether certain WML characteristics, such as size and location, make them greater risk factors for dementia. It also isnt clear how comorbidities additional health conditions such as heart disease or diabetes together with WMLs increase risk for cognitive decline. Defining these connections is essential to improving outcomes for the 5.7 million people in the U.S. affected by cognitive impairment and dementia.

DeCarli and Fornages landmark research is expected to answer these questions and lead to standards for assessing, diagnosing, and treating individuals with WML-related cognitive problems.

This grant gives us the chance to study WMLs from every angle and definitively understand their roles in age- and disease-related cognitive decline and risk for future dementia, DeCarli said. Its the culmination of our three decades of research that has given us great directions, but no final answers yet.

DeCarli and Fornage will conduct a study of patients with WMLs on their MRIs and concerns about cognitive symptoms, but no dementia diagnosis. It will be the first large study of a diverse population on the long-term effects of these lesions on thinking and dementia risk.

Beginning September 2021, study participants will be recruited at UC Davis Health and at least 10 other locations throughout the U.S. They will be from a variety of backgrounds, so the researchers can identify how WML outcomes differ by race, ethnicity, and sex, better representing those at risk for dementia.

Our ultimate goals are to develop a risk profile that identifies the likelihood of WML-related cognitive impairment and dementia over the course of five to 10 years and to identify clear targets for interventional trials, DeCarli said.

Resources to advance all dementia research

Another exciting part of the grant, according to the researchers, is the chance to fund additional studies aimed at refining diagnostic and predictive tools and methods for dementia. The outcomes will enhance dementia research and clinical care worldwide.

Data and samples from these studies will be shared with the wider research community via theNational Alzheimers Coordinating Center at the University of Washingtonand theNational Centralized Repository for Alzheimers Disease and Related Dementias at Indiana University. Images will be shared through theLaboratory of Neuro Imaging at the University of Southern California.

DeCarli and Fornage also participate in theMarkVCID Consortium, supported by the NIHsNational Institute of Neurological Disorders and Stroke. The consortium was established in 2016 to identify biological markers of vascular cognitive impairment and dementia.

This award is co-sponsored by the NIHs National Institute of Neurological Disorders and Stroke andNational Institute on Agingthrough grant 1U19NS120384.

The Brown Foundation Institute of Molecular Medicine (IMM) for the Prevention of Human Diseases is part of McGovern Medical School at The University of Texas Health Science Center at Houston (UTHealth). The IMM is focused on studying and preventing diseases at the genetic, cellular, and molecular levels using DNA and protein technologies and animal models. The IMM is part of the Texas Therapeutics Institute, a multi-institutional collaboration encouraging drug discovery. For more information, visitwww.uth.edu/imm/mission.htm.

The UC Davis Alzheimers Disease Research Center is one of only31 research centers designated and funded by the NIHs National Institute on Aging. The center's goal is to translate research advances into improved diagnosis and treatment for patients while focusing on the long-term goal of finding a way to prevent or cure Alzheimers disease and other dementias. The center also allows researchers to study the effects of the disease on a uniquely diverse population. For more information, visithealth.ucdavis.edu/alzheimers.

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Researchers receive more than $53 million to study role of white matter lesions in dementia - Newswise

Joseph Duffy PhD brings 20+ years of small molecule discovery chemistry and operations to his role as SVP Chemistry of Skyhawk Therapeutics, Elliot Ehrich MD brings 20+ years of clinical development for novel pharmaceuticals to his role as Chief Medical Officer of Skyhawk Therapeutics,and Rob Hershberg MD-PhD with 25+ years of biotech and pharma experience has joined Skyhawk's Scientific Advisory Board.

WALTHAM, Mass., Oct. 5, 2020 /PRNewswire/ -- Skyhawk Therapeutics today announced that Dr. Elliot Ehrich has joined the Company as Chief Medical Officer and Dr. Joseph Duffy has joined as Senior Vice President of Chemistry. The Company also strengthened its Scientific Advisory Board with the addition of Dr. Rob Hershberg.

"We are delighted that Joe and Elliot have come on board at Skyhawk," said Bill Haney, co-founder and CEO of Skyhawk Therapeutics. "Their combined scientific and clinical accomplishments will be invaluable in shepherding our novel RNA-targeting small molecule drug candidates successfully into the clinic. We are also excited to welcome Rob to our Scientific Advisory Board. His clinical and scientific insight and deep experience as a drug developer will be a tremendous addition to Skyhawk."

Elliot Ehrich, MD most recently served as a Venture Partner at 5AM Ventures and Chief Medical Officer (CMO) at Expansion Therapeutics, a 5AM Ventures portfolio company. Previously, Dr. Ehrich spent 17 years at Alkermes ultimately as Executive Vice President of R&D and CMO. At Alkermes he led the development and successful FDA registration of multiple new medicines. Dr. Ehrich has also worked in clinical pharmacology and clinical research at Merck &Co, Inc..

Dr. Ehrich received a BA in biochemistry from Princeton University and an MD from Columbia University. He completed a residency in internal medicine and a fellowship in immunology and rheumatology at Stanford University Medical School followed by postdoctoral research the Department of Microbiology and Immunology.

Over the past four years, Joseph Duffy PhD, served as Executive Director of Discovery Chemistry atMerckResearch Laboratories in Rahway and Kenilworth, New Jersey, where he oversaw multiple preclinical drug discovery teams. Dr. Duffy's contributions over 24 years at Merck included all phases of drug discovery, from lead identification through clinical phase candidate development. He directed successful lead optimization efforts for multiple indications, resulting in clinical candidates and Investigational New Drug (IND) applications from both internal projects and international collaborative research with biotech organizations. Dr. Duffy received his B.Sc. in Chemistry from Kent State University and his Ph.D. from Harvard University.

Rob Hershberg MD-PhD began his career as an Assistant Professor at Harvard Medical School and an Associate Physician at Brigham and Women's Hospital in Boston. Later, Dr. Hershberg co-founded VentiRx Pharmaceuticals and, as President and Chief Executive Officer, led the company through its transformational partnership with Celgene. Dr. Hershberg joined Celgene in 2014 to lead their efforts in Immuno-Oncology, was promoted to Chief Scientific Officer in 2016, and was subsequently Executive Vice President and Head of Business Development & Global Alliances and served as a member of the Executive Committee until the acquisition of Celgene by Bristol-Myers Squibb in 2019. Rob is currently a Venture Partner on the Frazier Life Sciences team. He completed his undergraduate and medical degrees at the University of California, Los Angeles and received his Ph.D. at the Salk Institute for Biological Studies.

Dr Hershberg joins Skyhawk's distinguished Scientific Advisory Board which includes:

Skyhawk Therapeutics is committed to discovering, developing and commercializing therapies that use its novel SkySTARTM (Skyhawk Small molecule Therapeutics for Alternative splicing of RNA) platform to build small molecule drugs that bring breakthrough treatments to patients.

For more information visit: http://www.skyhawktx.com, https://twitter.com/Skyhawk_Tx, https://www.linkedin.com/company/skyhawk-therapeutics/

SKYHAWK MEDIA CONTACT:Anne Deconinck[emailprotected]

SOURCE Skyhawk Therapeutics

http://www.skyhawktx.com

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Skyhawk Therapeutics Expands Leadership Team with Chief Medical Officer and Head of Chemistry, and adds to its Scientific Advisory Board - PRNewswire

Ohio State students with disabilities are adjusting to new accommodations for virtual learning. Credit: Mackenzie Shanklin | Assistant Photo Editor

Online classes are decreasing commute times, allowing students to rewatch live lectures and keeping the university community safe from COVID-19; however, for students with disabilities, the technological interface and isolation pose difficulties they dont face in a typical semester.

As a majority of Ohio State courses have moved to distance learning, Scott Lissner, the universitys Americans with Disabilities Act coordinator, said his office is working to provide students with disabilities a comprehensive education while also keeping them safe during the pandemic. For some of those accommodations, online learning is making the process easier.

If everybody is [taking classes] online, it removes a lot of challenges and simplifies things. We know how to integrate captioning in Zoom. We know how to integrate ASL interpreting into Zoom, Lissner said.

CarmenZoom offers captioning of class and lecture recordings, but did not offer live, automated captioning until recently.

Amy Shuman, a professor in the Department of English and former director of disability studies in the department, said although she records all her classes and uploads the videos with transcripts to make them more accessible, she hasnt seen a widespread shift toward the practice.

Ive talked to some of the older faculty who have hearing aids, and theyre frustrated by the lack of the closed captioning, Shuman said.

Lissner said in an email that Zoom tested live, automated captioning over the summer and Ohio State evaluated the system before releasing it Friday. A Friday press release from Ohio States IT department stated that live captioning is a setting Zoom meeting hosts must manually enable for their classes.

Lindsay Rogers, a first-year in molecular genetics who is hearing impaired, said online classes are easier for her than in-person classes because professors can talk directly into her hearing implants via Bluetooth, but shes had difficulty getting accommodations she typically gets each semester.

I requested [note taking assistance] for this semester, and no one contacted me about getting any sort of note taking assistance, Rogers said.

Lissner said students who do not have proper technology for their classes such as small monitors or devices that cannot connect to hearing aids via Bluetooth are sometimes able to borrow devices from the university. The university has screen-reader compatible monitors, for example, and high-quality speakers that can play sound at higher volumes.

Lissner said these loans are offered on a case-by-case basis depending on students specific disabilities. Students with disabilities are encouraged to participate in live class sessions and are provided with the materials necessary to successfully take part, he said.

We work with faculty and students to make sure accessible versions of whatever is being presented on the shared screen are distributed to students who need them prior to class. So they can either open it up in another window or have a dual monitor setup, Lissner said.

Hybrid courses and discussion-based courses can be difficult to replicate for students who require accommodations, but the ADA office tries to make students feel included while working virtually, Lissner said.

For example, if a student needs ADA accommodations in a hybrid class and is unable to attend in-person sessions, monitors can be set up in a circle around the student, with a wide angle camera used in the physical classroom. This creates an environment closer to that of an in-person class.

Isaac Meisner, a second-year in environmental policy and decision making, said having mostly online courses presents challenges with their mental illnesses.

When youre having classes that are completely online, it makes my mental disorders more difficult to handle just because I need that interaction with other people, and Im not really getting it outside of where I live, Meisner said.

Kayden Gill, a third-year in health sciences and co-president of Buckeyes for Accessibility, said as a wheelchair user and someone with a visual impairment, online courses present both positives and negatives. One of the main cons, Gill said, is it is harder to find ways to exercise without traveling across campus.

From a visual disability standpoint, its a lot easier not to have to worry about finding the place in the lecture hall that you can see, or just always having something as large as your screen can make it is nice, Gill said.

Students can register for accommodations on the Student Life Disability Services website.

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Students with disabilities, university accommodations adapt to virtual learning - OSU - The Lantern

It was Saturday, February 22, 1997, and Scottish researchers Ian Wilmut and Keith Campbell were expecting a final moment of calm before the results of their unprecedented scientific experiment were announced to the world.

The team had kept the breakthrough under wraps for seven months while they waited for their paper to be published in the prestigious journal Nature. Confidential press releases had gone out to journalists with the strict instruction not to leak the news before February 27.

But that night, the team was tipped off that journalist Robin McKie was going to break the story the very next day in the British newspaper The Observer.

Wilmut and Campbell raced to the lab at the Roslin Institute on Sunday morning as McKie's story hit the media like a thunderbolt. International news outlets had already started swarming at the institute for access to Wilmut and Campbell's creation: Dolly the sheep, the world's first mammal successfully cloned from a single adult cell. Shielded from the general public, she stuck her nose through the fence and munched calmly on the hay in her pen, unperturbed by the horde of news photographers. Dolly, a woolly, bleating scientific miracle, looked much like other sheep, but with a remarkable genetic difference.

By the end of that Sunday, February 23, nearly every major newspaper in the world carried headlines about Dolly the sheep.

Born on July 5, 1996, Dolly was cloned by Wilmut and Campbell's team at the Roslin Institute, a part of the University of Edinburgh, and Scottish biotechnology company PPL Therapeutics. The scientists cloned Dolly by inserting DNA from a single sheep mammary gland cell into an egg of another sheep, and then implanting it into a surrogate mother sheep. Dolly thus had three mothersone that provided the DNA from the cell, the second that provided the egg, and the third that carried the cloned embryo to term. Technically, though, Dolly was an exact genetic replica of only the sheep from which the cell was taken.

Following the announcement, the Roslin Institute received 3000 phone calls from around the world. Dolly's birth was heralded as one of the most important scientific advances of the decade.

But Dolly wasn't science's first attempt at cloning. Researchers had been exploring the intricacies of cloning for almost a century. In 1902, German embryologists Hans Spemann and Hilda Mangold, his student, successfully grew two salamanders from a single embryo split with a noose made up of a strand of hair. Since then, cloning experiments continued to become more sophisticated and nuanced. Several laboratory animal clones, including frogs and cows, were created before Dolly. But all of them had been cloned from embryos. Dolly was the first mammal to be cloned from a specialized adult cell.

Embryonic stem cells, which form right after fertilization, can turn into any kind of cell in the body. After they modify into specific types of cells, like neurons or blood cells, they're call specialized cells. Since the cell that gave rise to Dolly was already specialized for its role as a mammary gland cell, most scientists thought it would be impossible to clone anything from it but other mammary gland cells. Dolly proved them wrong.

Many scientists in the '90s were flabbergasted. Dollys advent showed that specialized cells could be used to create an exact replica of the animal they came from. It means all science fiction is true, biology professor Lee Silver of Princeton University told The New York Times in 1997.

The Washington Post reported that "Dolly, depending on which commentator you read, is the biggest story of the year, the decade, even the century. Wilmut has seen himself compared with Galileo, with Copernicus, with Einstein, and at least once with Dr. Frankenstein."

Scientists, lawmakers, and the public quickly imagined a future shaped by unethical human cloning. President Bill Clinton called for review of the bioethics of cloning and proposed legislation that would ban cloning meant ''for the purposes of creating a child (it didn't pass). The World Health Organization concluded that human cloning was "ethically unacceptable and contrary to human integrity and morality" [PDF]. A Vatican newspaper editorial urged governments to bar human cloning, saying every human has "the right to be born in a human way and not in a laboratory."

Meanwhile, some scientists remained unconvinced about the authenticity of Wilmut and Campbells experiment. Norton Zinder, a molecular genetics professor at Rockefeller University, called the study published in Nature "a bad paper" because Dolly's genetic ancestry was not conclusive without testing her mitochondriaDNA that is passed down through mothers. That would have confirmed whether Dolly was the daughter of the sheep that gave birth to her. In The New York Times, Zinder called the Scottish pair's work ''just lousy science, incomplete science." But NIH director Harold Varmus toldthe Times that he had no doubt that Dolly was a clone of an adult sheep.

Because she was cloned from a mammary gland cell, Dolly was nameddad joke alertafter buxom country music superstar Dolly Parton. (Parton didnt mind the attribution.) Like her namesake, Dolly the sheep was a bona fide celebrity: She posed for magazines, including People; became the subject of books, journal articles, and editorials; had an opera written about her; starred in commercials; and served as a metaphor in an electoral campaign.

And that wasn't all: New York Times reporter Gina Kolata, one of the first journalists to give readers an in-depth look at Dolly, wroteClone: The Road to Dolly, and the Path Ahead and contrasted the animal's creation with the archetypes in Frankenstein and The Island of Dr. Moreau. American composer Steve Reich was so affected by Dolly's story that he featured it in Three Tales, a video-opera exploring the dangers of technology.

The sheep also became an inadvertent political player when the Scottish National Party used her image on posters to suggest that candidates of other parties were all clones of one another. Appliance manufacturer Zanussi used her likeness for a poster with her name and the provocative caption "The Misappliance of Science" (the poster was later withdrawn after scientists complained). In fact, so widespread was the (mis)use of her name that her makers eventually trademarked it to stop the practice.

Following Dolly, many larger mammals were cloned, including horses and bulls. Roslin Biomed, set up by the Roslin Institute to focus on cloning technology, was later sold to the U.S.-based Geron Corporation, which combined cloning technology with stem cell research. But despite her popularityand widespread fearDolly's birth didn't lead to an explosion in cloning: Human cloning was deemed too dangerous and unethical, while animal cloning was only minimally useful for agricultural purposes. The sheep'sreal legacy is considered to be the advancement in stem cell research.

Dollys existence showed it was possible to change one cells gene expression by swapping its nucleus for another. Stem cell biologist Shinya Yamanaka told Scientific American that Dollys cloning motivated him to successfully develop stem cells from adult cells. He later won a Nobel Prize for his results, called induced pluripotent stem cells (iPS) because they're artificially created and can have a variety of uses. They reduced the need for embryonic stem cells in research, and today, iPS cells form the basis for most stem cell research and therapies, including regenerative medicine.

Dolly had sixoffspring, and led a productive, sociable life with many human fans coming to visit her. In 2003, a veterinary examination showed that Dolly had a progressive lung disease, and she was put down. But four clonescreated from the same cell line in 2007 faced no such health issues and aged normally.

Dolly is still a spectacle, though, nearly 25 years after her creation: Her body was taxidermied and puton display at the National Museum of Scotland in Edinburgh.

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Dolly the Sheep: '90s Media Sensation - Mental Floss

Genetic scissors: a tool for rewriting the code of life: The Nobel Prize in Chemistry 2020

The Royal Swedish Academy of Sciences has decided to award the Nobel Prize in Chemistry 2020 toEmmanuelle CharpentierMax Planck Unit for the Science of Pathogens, Berlin, Germany ANDJennifer A. Doudna University of California, Berkeley, USA

for the development of a method for genome editing

Emmanuelle Charpentier and Jennifer A. Doudna have discovered one of gene technologys sharpest tools: the CRISPR/Cas9 genetic scissors. Using these, researchers can change the DNA of animals, plants and microorganisms with extremely high precision. This technology has had a revolutionary impact on the life sciences, is contributing to new cancer therapies and may make the dream of curing inherited diseases come true.

Researchers need to modify genes in cells if they are to find out about lifes inner workings. This used to be time-consuming, difficult and sometimes impossible work. Using the CRISPR/Cas9 genetic scissors, it is now possible to change the code of life over the course of a few weeks.

There is enormous power in this genetic tool, which affects us all. It has not only revolutionised basic science, but also resulted in innovative crops and will lead to ground-breaking new medical treatments, says Claes Gustafsson, chair of the Nobel Committee for Chemistry.

As so often in science, the discovery of these genetic scissors was unexpected. During Emmanuelle Charpentiers studies of Streptococcus pyogenes, one of the bacteria that cause the most harm to humanity, she discovered a previously unknown molecule, tracrRNA. Her work showed that tracrRNA is part of bacterias ancient immune system, CRISPR/Cas, that disarms viruses by cleaving their DNA.

Charpentier published her discovery in 2011. The same year, she initiated a collaboration with Jennifer Doudna, an experienced biochemist with vast knowledge of RNA. Together, they succeeded in recreating the bacterias genetic scissors in a test tube and simplifying the scissors molecular components so they were easier to use.

In an epoch-making experiment, they then reprogrammed the genetic scissors. In their natural form, the scissors recognise DNA from viruses, but Charpentier and Doudna proved that they could be controlled so that they can cut any DNA molecule at a predetermined site. Where the DNA is cut it is then easy to rewrite the code of life.

Since Charpentier and Doudna discovered the CRISPR/Cas9 genetic scissors in 2012 their use has exploded. This tool has contributed to many important discoveries in basic research, and plant researchers have been able to develop crops that withstand mould, pests and drought. In medicine, clinical trials of new cancer therapies are underway, and the dream of being able to cure inherited diseases is about to come true. These genetic scissors have taken the life sciences into a new epoch and, in many ways, are bringing the greatest benefit to humankind.

Source: https://www.nobelprize.org/prizes/chemistry/2020/press-release/

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Genetic scissors: a tool for rewriting the code of life - The Hippocratic Post

Intersexuality in female moles

Female moles are intersexual and develop masculinizing ovotestes, a distinctive trait among mammals. Real et al. investigated the origin of this trait by sequencing the Iberian mole genome and applying comparative strategies that integrate transcriptomic, epigenetic, and chromatin interaction data. They identified mole-specific genomic rearrangements that alter the three-dimensional regulatory landscape of the androgen-converting gene CYP17A1 and the pro-testicular factor gene FGF9, both of which show distinct expression patterns in mole gonads. The use of transgenic mice confirms the capability of these factors to increase circulating testosterone levels and to induce gonadal masculinization. This study highlights how integrative approaches can reveal the phenotypic impact of genomic variation.

Science, this issue p. 208

Linking genomic variation to phenotypical traits remains a major challenge in evolutionary genetics. In this study, we use phylogenomic strategies to investigate a distinctive trait among mammals: the development of masculinizing ovotestes in female moles. By combining a chromosome-scale genome assembly of the Iberian mole, Talpa occidentalis, with transcriptomic, epigenetic, and chromatin interaction datasets, we identify rearrangements altering the regulatory landscape of genes with distinct gonadal expression patterns. These include a tandem triplication involving CYP17A1, a gene controlling androgen synthesis, and an intrachromosomal inversion involving the pro-testicular growth factor gene FGF9, which is heterochronically expressed in mole ovotestes. Transgenic mice with a knock-in mole CYP17A1 enhancer or overexpressing FGF9 showed phenotypes recapitulating mole sexual features. Our results highlight how integrative genomic approaches can reveal the phenotypic impact of noncoding sequence changes.

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The mole genome reveals regulatory rearrangements associated with adaptive intersexuality - Science Magazine

Fluorescent image shows chromosomes (green) segregating in two developing eggs. In each egg, one chromosome (the largest green one) has too many crossovers and is having problems segregating. The image was taken on a deconvolution fluorescent microscope. Credit: Image courtesy of Diana Libuda

University of Oregon and Northwestern University biologists show that too many crossover events can increase infertility.

The exchange of DNA between chromosomes during the early formation of sperm and egg cells normally is limited to assure fertility.

But when there are too many of these genetic exchanges, called crossover events, the segregation of chromosomes into eggs is flawed, biologists have learned in a project done across three labs at the University of Oregon and Northwestern University.

In a paper published online in September 2020 in the journal PLOS Genetics, researchers documented how the disruptions, as seen in basic research with microscopic roundworms (Caenorhabditis elegans), lead to a range of meiotic defects as the chromosomes are subjected to improper spindle forces.

Inaccurate chromosome segregation in humans is associated with Down syndrome and miscarriages. Such segregation defects as seen in the research can result in increased infertility, said UO biologist Diana E. Libuda, the studys principal investigator.

Over the past century, research has focused on making sure enough crossovers are made during sperm and egg development, said Libuda, a professor in the UOs Department of Biology and Institute of Molecular Biology. It was known that developing sperm and eggs had ways to make sure that not too many crossovers are made, but it was unclear why.

The research team identified two mechanisms that help counteract defects triggered by excess crossover activity in developing eggs and, thus, assist the coordination of the process that helps assure genomic integrity in new generations.

Libuda had reported in the October 9, 2013, issue of Nature the discovery of a mechanism that inhibits the overproduction of crossovers in roundworms. However, Libuda said, it was not possible at that time to study the downstream effects in cases where too many crossovers did occur. Since then, her lab developed a way to generate extra crossovers on a single chromosome.

That ability led to a National Institutes of Health-funded collaboration with Sadie Wignall of Northwestern University, an expert on high-resolution imaging of structures involved in segregation of chromosomes into developing eggs. What Wignall found led Libuda back to Bruce Bowermans UO lab to take a look at chromosome segregation in live developing eggs.

Overall, it was a great joining of scientific strengths to take a multipronged approach to answer this important question, Libuda said.

The research provides fundamental insights that can guide research in other organisms to better understand the mechanisms and, eventually, lead to potential clinical applications.

The same proteins that we are studying in C. elegans are also in humans, Libuda said. In fact, most proteins required for fertility are used across organisms that include yeast, fruit flies, nematodes, zebrafish, mice and humans. Research using these microscopic worms has been shown in numerous contexts to have relevance in human health.

Reference: Excess crossovers impede faithful meiotic chromosome segregation in C. elegans by Jeremy A. Hollis, Marissa L. Glover, Aleesa J. Schlientz, Cori K. Cahoon, Bruce Bowerman, Sarah M. Wignall and Diana E. Libuda, 4 September 2020, PLOS Genetics.DOI: 10.1371/journal.pgen.1009001

Co-authors with Libuda, Bowerman and Wignall on the paper were: Jeremy A. Hollis, a technician in Wignalls lab; former UO biology undergraduate student Marissa L. Glover, now a doctoral student at the University of California, Santa Cruz; Aleesa J. Schlientz, who earned a doctorate from the UO this year; and Cori K. Cahoon, a postdoctoral researcher working in Libudas lab under a fellowship from the Jane Coffin Childs Memorial Fund for Medical Research.

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Over-Exchange of DNA in Sperm and Eggs Results in Chromosome Defects That Can Increase Infertility - SciTechDaily

Aim:Colorectal cancer (CRC) is the third most common cancer in Australia, and survival after diagnosis of metastatic disease is improving. Our aim was to assess trends in epidemiology, treatment, molecular testing and survival in patients with metastatic CRC (mCRC).

Methods:Clinical data from February 2013 to December 2018 was recorded in a prospective, observational, multicenter cohort study conducted in Queensland, Australia, examining clinical and molecular biomarkers in cases of mCRC.

Results:A total of 159 patients who had metastasis diagnosed after February 2013 were included in survival analysis. Median age at diagnosis was 63.9 years, but 29% had early-onset disease (diagnosis aged <50 years). Median overall survival was 2.5 years (95% confidence interval [CI], 2.2-3.0) for the 159 patients included in survival analysis. Independent factors correlated with poor prognosis included right-sided primary tumor, neutrophil-lymphocyte ratio >5, increased alkaline phosphatase level (ALP) and an increasing number of sites of metastatic disease. In contrast, metastasectomy was associated with improved overall survival (adjusted HR = 0.29 95% CI, 0.16-0.54), with similar survival between patients who had liver and non-liver metastasectomy sites. Half (10/20) of the BRAF mutant CRC were also microsatellite unstable. The proportion of detected mutations amongst tested samples increased over time for Kirsten Rat Sarcoma (KRAS; OR [per year] = 1.19; 95% CI, 1.01-1.39). Concurrently, the methods of molecular genetics testing employed in routine clinical practice changed towards the adoption of next-generation sequencing.

Conclusions:Metastasectomy in mCRC may be beneficial regardless of the anatomical site of metastasis. The adoption of next-generation sequencing techniques for molecular genetics testing coincided with a slightly increased rate of detection of KRAS and BRAF mutations, potentially reflecting greater test sensitivity. Further translational research is required in mCRC to define novel targets for treatment.

Keywords:cancer epidemiology; cancer genetics; colorectal; medical oncology; registry.

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Trends in epidemiology, treatment and molecular testing of metastatic colorectal cancer in a real-world multi-institution cohort study - DocWire News

https://research-highlights.keio.ac.jp/

On 21 May, 2020, the Joint Research Coronavirus Task Force was launched in Japan to promote the development of a mucosal vaccine for COVID-19 based on advanced genomic analysis.

"We will analyze 600 blood samples taken from Japanese COVID-19 patients located in approximately 100 hospitals throughout Japan," explains Takanori Kanai of the Keio University School of Medicine, who leads the task force. "One of the goals of the research is to try to understand why the mortality rate due to COVID-19 has remained significantly lower in Japan than the United States and European countries. We think it may be related to genetic differences. We want to resolve this issue and share our results with our colleagues around the world."

Background and goals

This research is being undertaken by experts affiliated with Keio University, Tokyo Medical and Dental University, Osaka University, the Institute of Medical Science at the University of Tokyo, the National Center for Global Health and Medicine, the Tokyo Institute of Technology, Kitasato University, and Kyoto University.

"Our research team includes specialists in infectious diseases as well as other fields such as molecular genetics, computational science, and gastroenterology, which is my area of expertise, and is not directly related to epidemiology or infectious diseases," says Kanai. "This project was conceived by a small group of medical doctors and researchers without experience of handling infectious diseases. But the actual project is interdisciplinary, with members including ICU and medical care staff at university hospitals, community healthcare practitioners, immunologists, and even members of the general public. Ultimately, we want to contribute to society through medicine and science."

Working hypotheses for possible reasons for fewer COVID-19 deaths in Japan and Asia

The members of the task force compiled the following list of potential reasons for the low mortality rate in Japan: Japan's world-class medical system; a history of regular face mask use and attention to hygiene (including hand washing) in daily life; a culture of avoiding physical contact akin to social distancing; low expression of virus receptors; BCG vaccination; and differences in immune response due to differences in racial HLA and other polymorphisms.

Gathering samples and genetic information

The task force's goals are to establish a medical response system to predict who is at risk of contracting severe COVID-19 and develop a vaccine using proprietary technology. Genomic analysis technology is being employed to elucidate the genetic basis of the mechanisms that trigger COVID-19 infections to worsen, and thereby develop methods to fight the disease and develop a mucosal vaccine.

The team is focusing on the fact that the number of COVID-19 deaths per capita is far smaller in the Japanese population than it is in Western countries. The 600 blood samples are being studied by methods including high-resolution HLA analysis, SNP array and whole-genome sequence analysis, and T-cell repertoire analysis.

"Our analysis is being used to compare severe cases with mild and asymptomatic cases to identify genes that may be responsible for the exacerbation of COVID-19 in Japanese patients," explains Kanai. "Regarding vaccine development, predicting the target epitope is a major challenge. We are planning to use supercomputer simulations to identify potential antigens for SARS-CoV-2 based on our results for determining the genes that lead to severe cases of COVID-19 in Japanese patients."

Initial findings will be announced in September 2020

The task force plans to announce the initial findings of their research in September 2020. This will include the identities of the genes associated with triggering severe cases of COVID-19 among Japanese people that could be used to predict potential severity during early diagnostics.

"We want to use our results to produce guidelines to mitigate the dangers of overloading the medical care system during potential second or possibly third waves of COVID-19," says Kanai. "Furthermore, our immunological genetic information will be valuable for designing potential vaccines for SARS-CoV-2 for many Japanese people. We will share our results with colleagues in other countries so that they can use them to develop strategies to combat COVID-19 for their own populations."

About the researcher

Takanori Kanai Professor

Department of Gastroenterology and Hepatology, School of Medicine

Takanori Kanai graduated from the Keio University School of Medicine in 1988. Between 1989 and 2003 he held teaching positions at the Keio University School of Medicine, Keio Cancer Center, and Tokyo Medical and Dental University (TMDU). He has also held distinguished positions including as a committee member of the Harvard Medical Institute Educational Program at TMDU; Section Editor of the journal Inflammatory Bowel Diseases; Associate Editor of Journal of Gastroenterology; Editorial Board Member, American Journal of Physiology and Gastrointestinal and Liver Physiology; and Clinical Professor of Medicine (Visiting), TMDU. At the Keio University School of Medicine, he was appointed as an associate professor in 2007 and a professor in 2013, and he has been serving as a vice dean since 2017.

Links

COVID-19 taskforce https://www.covid19-taskforce.jp/en/home/

Takanori Kanai informationhttps://k-ris.keio.ac.jp/html/100002919_en.html

Further informationKeio UniversityOffice of Research Development and Sponsored Projects2-15-45 Mita, Minato-ku, Tokyo 108-8345 JapanE-mail: [emailprotected]

WebsitesKeio Universityhttps://www.keio.ac.jp/en/

Keio Research Highlightshttps://research-highlights.keio.ac.jp/

About Keio University

Keio University is a private, comprehensive university with six major campuses in the Greater Tokyo area along with a number of affiliated academic institutions. Keio prides itself on educational and research excellence in a wide range of fields and its state-of-the-art university hospital.

Keio was founded in 1858, and it is Japan's first modern institution of higher learning. Over the last century and a half, it has evolved into and continues to maintain its status as a leading university in Japan through its ongoing commitment to producing leaders of the future. Founder Yukichi Fukuzawa, a highly respected educator and one of the most important intellectuals of modern Japan, aspired for Keio to be a pioneer of new discoveries and contribute to society through learning.

SOURCE Keio University

Link:
Keio University Research: Combating COVID-19: Nationwide genomic analysis to study possible reasons for the low COVID-19 mortality rate in Japan -...

Toronto scientists have mapped the genes allowing cancer cells to avoid getting killed by the immune system in a finding that paves the way for the development of immunotherapies that would be effective for larger patient populations and across different tumour types.

"Over the last decade, different forms of immunotherapy have emerged as really potent cancer treatments but the reality is that they only generate durable responses in a fraction of patients and not for all tumour types," says Jason Moffat, a professor of molecular genetics in the Donnelly Centre for Cellular and Biomolecular Research at the University of Toronto who led the work.

The study also revealed the need for new therapy to take into account the genetic composition of tumours because of mutations in the cancer cells that can potentially make the disease worse in response to treatment, often referred to as cancer resistance mutations.

"It's very important to understand at the molecular level how cancer develops resistance to immunotherapies in order to make them more broadly available. Advances in systematic genetic approaches have let us key in on genes and molecular pathways that are commonly involved in resistance to therapy," says Moffat, who holds Canada Research Chair in Functional Genomics of Cancer.

In immunotherapy, a patient's own immune cells, known as T killer cells, are engineered to find and destroy cancer. But treatment resistance has precluded its use in most patients, especially those with solid tumours.

"It's an ongoing battle between the immune system and cancer, where the immune system is trying to find and kill the cancer whereas the cancer's job is to evade that killing," says Keith Lawson, a co-lead author completing a PhD in Moffat's lab as part of his medical training in the Surgeon-Scientist Program at U of T's Faculty of Medicine.

Tumour heterogeneity--genetic variation in tumour cells within and across individuals that can impact therapy response--further complicates things.

"It's important to not just find genes that can regulate immune evasion in one model of cancer, but what you really want are to find those genes that you can manipulate in cancer cells across many models because those are going to make the best therapeutic targets," says Lawson.

The team, including collaborators from Agios Pharmaceuticals in Cambridge, Massachusetts, looked for genes that regulate immune evasion across six genetically diverse tumor models derived from breast, colon, kidney and skin cancer. The cancer cells were placed in a dish alongside the T cells engineered to kill them, where the ensuing onslaught served as a baseline. The researchers next deployed the gene editing tool CRISPR to switch off one-by-one every gene in the cancer cells and measured the resulting deviations from the killing baseline.

They identified 182 "core cancer intrinsic immune evasion genes" whose deletion makes the cells either more sensitive or more resistant to T cell attack. Among the resisters were all the genes known to develop mutations in patients who stopped responding to immunotherapy, giving the researchers confidence that their approach worked.

Many of the found genes had no previous links to immune evasion.

"That was really exciting to see, because it means that our dataset was very rich in new biological information", says Lawson.

Genes involved in autophagy, a process when cells ramp up recycling their components to mitigate damage following stress, came up as key for immune evasion. This raises a possibility that cancer's susceptibility to immunotherapy could be boosted by targeting its autophagy genes.

But as the researchers delved deeper, they found that deleting certain autophagy genes in pairs rendered the cells resistant to T cell killing. It means that if a tumour already harbors a mutation in one autophagy gene, a treatment that combines immunotherapy with a drug targeting another autophagy gene could make the disease worse in that patient.

"We found this complete inversion of gene dependency", says Moffat. "We did not anticipate this at all. What it shows us is that genetic context, what mutations are present, very much dictates whether the introduction of the second mutations will cause no effect, resistance or sensitivity to therapy".

As more research explores combinatorial effects of mutations across different types of cancer cells, it should become possible to predict from a tumour's DNA what type of therapy will be most effective.

Reference: Lawson KA, Sousa CM, Zhang X, et al.Functional genomic landscape of cancer-intrinsic evasion of killing by T cells. Nature, 2020. doi:10.1038/s41586-020-2746-2

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

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182 Genes Identified That Regulate Interactions Between Cancer Cells and T Cells - Technology Networks

Molecular Biomarkers Market Overview 2020 2025

This has brought along several changes in This report also covers the impact of COVID-19 on the global market.

The risingtechnology in Molecular Biomarkers Marketis also depicted in thisresearchreport. Factors that are boosting the growth of the market, and giving a positive push to thrive in the global market is explained in detail.

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Key Competitors of the Global Molecular Biomarkers Market are: , Alere, Atossa Genetics, Biophysical, Abbott, BioCept, BioTheranostics, DiagnoCure, GenomeDx, Genomic Health, Gen-Probe, Life Technologies, 20/20 GeneSystems, Cynvenio, Dako (Agilent), Epic Sciences, Foundation Medicine, Genomic Health, Molecular Response, Nodality, PGD

Historical data available in the report elaborates on the development of the Molecular Biomarkers on national, regional and international levels. Molecular Biomarkers Market Research Report presents a detailed analysis based on the thorough research of the overall market, particularly on questions that border on the market size, growth scenario, potential opportunities, operation landscape, trend analysis, and competitive analysis.

Major Product Types covered are:GenomicsProteomicsOthers

Major Applications of Molecular Biomarkers covered are:MedicineBiologyOthers

This study report on global Molecular Biomarkers market throws light on the crucial trends and dynamics impacting the development of the market, including the restraints, drivers, and opportunities.

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The fundamental purpose of Molecular Biomarkers Market report is to provide a correct and strategic analysis of the Molecular Biomarkers industry. The report scrutinizes each segment and sub-segments presents before you a 360-degree view of the said market.

Market Scenario:

The report further highlights the development trends in the global Molecular Biomarkers market. Factors that are driving the market growth and fueling its segments are also analyzed in the report. The report also highlights on its applications, types, deployments, components, developments of this market.

Highlights following key factors:

:-Business descriptionA detailed description of the companys operations and business divisions.:-Corporate strategyAnalysts summarization of the companys business strategy.:-SWOT AnalysisA detailed analysis of the companys strengths, weakness, opportunities and threats.:-Company historyProgression of key events associated with the company.:-Major products and servicesA list of major products, services and brands of the company.:-Key competitorsA list of key competitors to the company.:-Important locations and subsidiariesA list and contact details of key locations and subsidiaries of the company.:-Detailed financial ratios for the past five yearsThe latest financial ratios derived from the annual financial statements published by the company with 5 years history.

Our report offers:

Market share assessments for the regional and country level segments. Market share analysis of the top industry players. Strategic recommendations for the new entrants. Market forecasts for a minimum of 9 years of all the mentioned segments, sub segments and the regional markets. Market Trends (Drivers, Constraints, Opportunities, Threats, Challenges, Investment Opportunities, and recommendations). Strategic recommendations in key business segments based on the market estimations. Competitive landscaping mapping the key common trends. Company profiling with detailed strategies, financials, and recent developments. Supply chain trends mapping the latest technological advancements.

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Molecular Biomarkers Market Incredible Possibilities, Growth Analysis and Forecast To 2026 |112233 - The Daily Chronicle

LA JOLLA, Calif., Sept. 29, 2020 (GLOBE NEWSWIRE) -- Artelo Biosciences, Inc. (NASDAQ: ARTL), a clinical stage biopharmaceutical company focused on the development of therapeutics that modulate the endocannabinoid system, todayannounced the receipt of Ethics Committee approval in the U.K. for the Companys Cancer Appetite Recovery Study (CAReS) entitled A Phase 1/2 Trial of the Synthetic Cannabinoid ART27.13 in Patients with Cancer Anorexia and Weight Loss. Barry J. A. Laird, M.D. of the Institute of Genetics and Molecular Medicine at the University of Edinburgh and St. Columbias Hospice Reader in Palliative Medicine, will serve as the coordinating investigator. ART27.13 is a highly potent, peripherally restricted synthetic, dual cannabinoid agonist believed to target peripheral CB1/CB2 receptors, and has the potential to increase appetite and food intake. Artelo intends to initially develop ART27.13 as a supportive care therapy for cancer patients suffering from anorexia and weight loss.

Receiving Ethics Committee approval is an essential step towards commencing our CAReS trial in the UK, stated Steven D. Reich, M.D., Artelos Chief Medical Officer. We are very pleased to have Dr. Laird as our Coordinating Investigator as we believe that his extensive knowledge of and focus on palliative medicine as well as his direct expertise in clinical trials evaluating treatments for anorexia will be invaluable as we evaluate ART27.13. We are working diligently on securing the additional regulatory requisite approvals which will enable us to open our clinical sites and initiate patient enrollment later this year.

"As an academic clinician, I am passionate about improving symptoms in people with life-limiting illness and I am honored to be working with Artelo on this exciting program and the CAReS clinical trial, stated Dr. Laird. My teams overarching goal is to help find therapies which improve the care of patients with cancer and I look forward to evaluating the potential of ART27.13 to reduce the devastating symptoms and improve quality of life of those suffering from this disease."

About the CAReS Study CAReS is a Phase 1/2 clinical trial of the synthetic cannabinoid ART27.13 in patients with cancer anorexia and weight loss, which will enroll up to 49 subjects, initially in clinical trial sites located in the U.K. The primary endpoint in Phase 1 of the study is to determine the most effective and safe dose of ART27.13 to be utilized in Phase 2. The primary endpoint in Phase 2 of the study is to determine point estimates of activity of ART27.13 in terms of lean body mass, weight gain, and improvement of anorexia.

About ART27.13ART27.13 is a potent, peripherally restricted dual synthetic agonist of the CB1/CB2 receptors. Existing ART27.13 clinical data suggests meaningful potential for the treatment of cancer-related anorexia and weight loss. In five Phase I clinical studies including over 200 subjects, ART27.13 previously demonstrated a statistically significant and dose-dependent increase in body weight in subjects without cancer. Artelo plans to advance ART27.13 as a supportive care therapy for cancer patients suffering from anorexia and weight loss.

About Artelo Biosciences, Inc. Artelo Biosciences, Inc.is a San Diego-based biopharmaceutical company dedicated to the development and commercialization of proprietary therapeutics targeting the endocannabinoid system. Artelo is rapidly advancing a portfolio of broadly applicable product candidates designed to address significant unmet needs in multiple diseases and conditions, including anorexia, cancer, post-traumatic stress disorder, pain, and inflammation. Led by proven biopharmaceutical executives collaborating with highly respected researchers and medical experts, the company applies leading edge scientific, regulatory, and commercial discipline to develop high-impact therapies. More information is available atwww.artelobio.comand Twitter:@ArteloBio.

Forward Looking Statements

This press release contains certain forward-looking statements within the meaning of Section 27A of the Securities Act of 1933 and Section 21E of the Securities Exchange Act of 1934 and Private Securities Litigation Reform Act, as amended, including those relating to the Companys product development, clinical and regulatory timelines, market opportunity, competitive position, possible or assumed future results of operations, business strategies, potential growth opportunities and other statement that are predictive in nature. These forward-looking statements are based on current expectations, estimates, forecasts and projections about the industry and markets in which we operate and managements current beliefs and assumptions.

These statements may be identified by the use of forward-looking expressions, including, but not limited to, expect, anticipate, intend, plan, believe, estimate, potential, predict, project, should, would and similar expressions and the negatives of those terms. These statements relate to future events or our financial performance and involve known and unknown risks, uncertainties, and other factors which may cause actual results, performance or achievements to be materially different from any future results, performance or achievements expressed or implied by the forward-looking statements. Such factors include those set forth in the Companys filings with the Securities and Exchange Commission, including our ability to raise additional capital in the future. Prospective investors are cautioned not to place undue reliance on such forward-looking statements, which speak only as of the date of this press release. The Company undertakes no obligation to publicly update any forward-looking statement, whether as a result of new information, future events or otherwise, except to the extent required by applicable securities laws.

Investor Relations Contact:Crescendo Communications, LLCTel: 212-671-1020Email:ARTL@crescendo-ir.com

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Artelo Biosciences Receives Ethics Approval to Commence its Cancer Appetite Recovery Phase I/II Clinical Study (CAReS) of ART27.13 for the Treatment...

Dublin, Sept. 29, 2020 (GLOBE NEWSWIRE) -- The "Anal Cancer - Pipeline Review, H2 2020" drug pipelines has been added to ResearchAndMarkets.com's offering.

Anal Cancer - Pipeline Review, H2 2020, provides comprehensive information on the therapeutics under development for Anal Cancer (Oncology), complete with analysis by stage of development, drug target, mechanism of action (MoA), route of administration (RoA) and molecule type. The guide covers the descriptive pharmacological action of the therapeutics, its complete research and development history and latest news and press releases.

The Anal Cancer (Oncology) pipeline guide also reviews the key players involved in therapeutic development for Anal Cancer and features dormant and discontinued projects. The guide covers therapeutics under Development by Companies /Universities /Institutes, the molecules developed by Companies in Phase III, Phase II, Phase I, IND/CTA Filed and Preclinical stages are 1, 19, 18, 2 and 5 respectively. Similarly, the Universities portfolio in Phase I stages comprises 1 molecules, respectively.

Anal Cancer (Oncology) pipeline guide helps in identifying and tracking emerging players in the market and their portfolios, enhances decision making capabilities and helps to create effective counter strategies to gain competitive advantage. The guide is built using data and information sourced from the publisher's proprietary databases, company/university websites, clinical trial registries, conferences, SEC filings, investor presentations and featured press releases from company/university sites and industry-specific third party sources. Additionally, various dynamic tracking processes ensure that the most recent developments are captured on a real time basis.

Scope

Reasons to Buy

Key Topics Covered:

Introduction

Anal Cancer - Therapeutics Assessment

Anal Cancer - Companies Involved in Therapeutics Development

Anal Cancer - Dormant Projects

Appendix

Companies Mentioned

For more information about this drug pipelines report visit https://www.researchandmarkets.com/r/jteb4n

Research and Markets also offers Custom Research services providing focused, comprehensive and tailored research.

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Global Anal Cancer Pipeline Report 2020: Breakdown by Stage of Development, Drug Target, Mechanism of Action, Route of Administration and Molecule...

Urothelial carcinoma of the bladder (UCB) exhibits significant sexual dimorphism in the incidence, etiology, and response to intravesical immunotherapy. Environmental factors such as tobacco use and clinical management issues such as delayed presentation have widely been associated with sex differences in UCB outcomes. Emerging findings from immune checkpoint blockade trials are suggestive of differential outcomes in females compared with males. Sex-specific differences in the way immune system functions and responds to pathogenic insults are well established. As such, an in-depth understanding of the genetic and epigenetic factors contributing to sex-associated differences in response to immunomodulatory therapies is needed urgently for improved management of UCB.

To review the associations between patient sex and clinical outcomes, with a focus on the incidence, host intrinsic features, and response to therapies in UCB.

Using the PubMed database, this narrative review evaluates published findings from mouse model-based and clinical cohort studies to identify factors associated with sex and clinical outcomes in bladder cancer. A scoping review of the key findings on epidemiology, genetic, hormonal, immune physiology, and clinical outcomes was performed to explore potential factors that could have implications in immunomodulatory therapy design.

Sex-associated differences in UCB incidence and clinical outcomes are influenced by sex hormones, local bladder resident immune populations, tumor genetics, and bladder microbiome. In the context of therapeutic outcomes, sex differences are prominent in response to bacillus Calmette-Gurin immunotherapy used in the treatment of non-muscle-invasive bladder cancer. Similarly, with respect to tumor molecular profiles in muscle-invasive bladder cancer, tumors from females show enrichment of the basal subtype.

Among proposed tumor/host intrinsic factors that may influence response to immune-based therapies, patient sex remains a challenging consideration that deserves further attention. Evidence to date supports a multifactorial origin of sexual dimorphism in the incidence and outcomes of UCB.

In this review, we highlight the sex-associated host and tumor intrinsic features that may potentially drive differential disease progression and therapeutic response in urothelial carcinoma of the bladder.

European urology oncology. 2020 Sep 20 [Epub ahead of print]

Madhuri Koti, Molly A Ingersoll, Shilpa Gupta, Christa M Lam, Xue Li, Ashish M Kamat, Peter C Black, D Robert Siemens

Department of Biomedical and Molecular Sciences, Queen's University, Kingston, Ontario, Canada; Department of Obstetrics and Gynecology, Queen's University, Kingston, Ontario, Canada; Cancer Biology and Genetics Division, Queen's Cancer Research Institute, Queen's University, Kingston, Ontario, Canada; Department of Urology, Queen's University, Kingston, Ontario, Canada. Electronic address: ., Department of Immunology, Institut Pasteur, Paris, France., Department of Hematology and Oncology, Taussig Cancer Institute, Cleveland Clinic Foundation, Cleveland, OH, USA., Department of Urology and Surgery, Boston Children's Hospital, Harvard Medical School, Boston, MA, USA., Department of Urology, Division of Surgery, The University of Texas, MD Anderson Cancer Center, Houston, TX, USA., Department of Urologic Sciences, University of British Columbia, Vancouver, BC, Canada., Department of Urology, Queen's University, Kingston, Ontario, Canada.

PubMed http://www.ncbi.nlm.nih.gov/pubmed/32967818

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Sex Differences in Bladder Cancer Immunobiology and Outcomes: A Collaborative Review with Implications for Treatment. - UroToday

Pune, Sept. 29, 2020 (GLOBE NEWSWIRE) -- The global genomics market size is projected to reach USD 82.60 billion by the end of 2027. The massive investments in the research and development of efficient products will have a massive impact on the growth of the market in the coming years.

According to a report published by Fortune Business Insights, titled Genomics Market Size, Share & COVID-19 Impact Analysis, By Type (Products (Instruments & Software and Consumables) and Services), By Technology (Polymerase Chain Reaction (PCR), Next Generation Sequencing (NGS), Microarray, Sanger Sequencing, and Others), By Application (Diagnostics, Research, and Others), By End User (Research Institutes, Healthcare Facilities & Diagnostic Centers, Pharmaceutical & Biotechnological Companies, Contract Research Organization (CROs)), and Regional Forecast, 2020-2027, the market was worth USD 18.85 billion in 2019 and will exhibit a CAGR of 19.5% during the forecast period 2020-2027.

Genomics is a concept that involves the human gene and sequencing for treatment and study of several diseases or potential diseases. The study of human genetics helps identify and track critical diseases, with equal focus on the qualities and behaviour of a specific individual. In the past few years, genomics has contributed to the growth of numerous similar branches including the popular precision medicine.

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The massive investments in the research and development of genomics and genomic sequencing will have a positive impact on the growth of the overall market in the coming years. The presence of several large scale companies has had a massive impact on the growth of the market in recent years and the influx of start-ups will create opportunities for growth in the foreseeable future.

Recent Clinical Studies have Indicated the Potential of Genomics to Tracking Patterns of Covid-19 Spread

The recent coronavirus outbreak has created a sense of panic among businesses across the world. Although healthcare industry has witnessed a contrasting impact, as compared to a few other sectors, there has been a recent surge in the need for healthcare professionals. The lack of skilled labour is consequential to the hesitancy among workers due to the severity of the disease. Although there are several ongoing research activities associated with the treatment of the coronavirus, there has been little success in this field.

Accounting to increasing cases of Covid-19 across the world, researchers are focusing on implementing preventive and precautionary measures through newer concepts. The excessive research associated with the use of genomics in Covid-19 pandemic has yielded a few successful measures. As a result, genomics has recently attracted attention from across the world.

The whole world is fighting the novel coronavirus. Sectors and industries are devasted due to the major loss caused by COVID-19 in business. The authorities of several countries have initiated lockdown to prevent the spread of this deadly virus. Such plans have caused disturbances in the production and supply chain. But, with time and resolution, we will be able to combat this stern time and get back to normality. Our well-revised reports will help companies to receive in-depth information about the present scenario of every market so that you can adopt the necessary strategies accordingly.

To get to know more about the short-term and long-term impacts of COVID-19 on this market, please visit: https://www.fortunebusinessinsights.com/industry-reports/genomics-market-100941

Constant Product Innovations are Consequential to Increasing R&D Efforts

The report encompasses several factors that have contributed to the growth of the overall market in recent years. Among all factors, the increasing number of product innovations, driven by rising investments in the research and development of the product, has made the highest impact on the growth of the market. In April 2020, Eurofins announced the launch of a new product in the genome sequencing space.

The company introduced SARS-CoV 2 full length genome sequencing, a product that is categorized under the next-generation (NGS) sequencing category. Increasing number of such product innovations will have a positive impact on the growth of the overall market in the coming years.

North America to Emerge Dominant; Increasing Activities associated with Whole-genome Sequencing will Emerge in Favor of Market Growth

The report analyses the ongoing market trends across five major regions, including North America, Latin America, Europe, Asia Pacific, and the Middle East and Africa. Among all regions, the market in North America is projected to emerge dominant in the coming years. The increasing research activities associated with whole-genome sequencing by private companies as well as government organizations will contribute to the growth of the regional market.

As of 2019, the market in North America was worth USD 8.27 billion and this value is projected to rise at a considerable pace in the coming years. The market in Asia Pacific will derive growth form the efforts put in towards genetic sequencing by countries such as China.

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List of companies profiled in the Genomics Market report:

Industry Developments:

February 2020: Nebula Genomic announced the launch of a new product that will offer whole genome sequencing at US$ 299 to its customers.

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TOC Continued.!

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Genomics Market to Rise at 19.5% CAGR and Reach USD 82.60 Billion by 2027; Advances in Diagnostic Applications will Lead to a Wider Product Adoption,...

Media Advisory

Thursday, September 24, 2020

New findings by scientists at the National Institutes of Health and their collaborators help explain why some people with COVID-19 develop severe disease. The findings also may provide the first molecular explanation for why more men than women die from COVID-19.

The researchers found that more than 10% of people who develop severe COVID-19 have misguided antibodiesautoantibodiesthat attack the immune system rather than the virus that causes the disease. Another 3.5% or more of people who develop severe COVID-19 carry a specific kind of genetic mutation that impacts immunity. Consequently, both groups lack effective immune responses that depend on type I interferon, a set of 17 proteins crucial for protecting cells and the body from viruses. Whether these proteins have been neutralized by autoantibodies orbecause of a faulty genewere produced in insufficient amounts or induced an inadequate antiviral response, their absence appears to be a commonality among a subgroup of people who suffer from life-threatening COVID-19 pneumonia.

These findings are the first published results from the COVID Human Genetic Effort, an international project spanning more than 50 genetic sequencing hubs and hundreds of hospitals. The effort is co-led by Helen Su, M.D., Ph.D., a senior investigator at the National Institute of Allergy and Infectious Diseases (NIAID), part of NIH; and Jean-Laurent Casanova, M.D., Ph.D., head of the St. Giles Laboratory of Human Genetics of Infectious Diseases at The Rockefeller University in New York. Major contributions were made by Luigi Notarangelo, M.D., chief of the NIAID Laboratory of Clinical Immunology and Microbiology (LCIM); Steven Holland, M.D., director of the NIAID Division of Intramural Research and senior investigator in the NIAID LCIM; clinicians and investigators in hospitals in the Italian cities of Brescia, Monza and Pavia, which were heavily hit by COVID-19; and researchers at the Uniformed Services University of the Health Sciences in Bethesda, Maryland.

The wide variation in the severity of disease caused by SARS-CoV-2, the virus behind COVID-19, has puzzled scientists and clinicians. SARS-CoV-2 can cause anything from a symptom-free infection to death, with many different outcomes in between. Since February 2020, Drs. Su and Casanova and their collaborators have enrolled thousands of COVID-19 patients to find out whether a genetic factor drives these disparate clinical outcomes.

The researchers discovered that among nearly 660 people with severe COVID-19, a significant number carried rare genetic variants in 13 genes known to be critical in the bodys defense against influenza virus, and more than 3.5% were completely missing a functioning gene. Further experiments showed that immune cells from those 3.5% did not produce any detectable type I interferons in response to SARS-CoV-2.

Examining nearly 1,000 patients with life-threatening COVID-19 pneumonia, the researchers also found that more than 10% had autoantibodies against interferons at the onset of their infection, and 95% of those patients were men. Biochemical experiments confirmed that the autoantibodies block the activity of interferon type I.

Q Zhang et al. Inborn errors of type I IFN immunity in patients with life-threatening COVID-19. Science DOI: 10.1126/science.abd4570 (2020).

P Bastard et al. Auto-antibodies against type I IFNs in patients with life-threatening COVID-19. Science DOI: 10.1126/science.abd4585 (2020).

NIAID Director Anthony S. Fauci, M.D., NIAID Senior Investigator Helen C. Su, M.D., Ph.D., and Luigi Notarangelo, M.D., chief of the NIAID Laboratory of Clinical Immunology and Microbiology, are available for interviews.

To schedule interviews, please contact NIAID Office of Communications, (301) 402-1663, NIAIDNews@niaid.nih.gov.

NIAID conducts and supports research at NIH, throughout the United States, and worldwide to study the causes of infectious and immune-mediated diseases, and to develop better means of preventing, diagnosing and treating these illnesses. News releases, fact sheets and other NIAID-related materials are available on the NIAID website.

About the National Institutes of Health (NIH):NIH, the nation's medical research agency, includes 27 Institutes and Centers and is a component of the U.S. Department of Health and Human Services. NIH is the primary federal agency conducting and supporting basic, clinical, and translational medical research, and is investigating the causes, treatments, and cures for both common and rare diseases. For more information about NIH and its programs, visit http://www.nih.gov.

NIHTurning Discovery Into Health

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Scientists discover genetic and immunologic underpinnings of some cases of severe COVID-19 - National Institutes of Health

Researchers at the University of Toronto have mapped the genes that allow cancer cells to avoid being killed by the immune system a finding that paves the way for the development of immunotherapies that could be effective for large patient populations and across different tumour types.

Over the last decade, different forms of immunotherapy have emerged as really potent cancer treatments, but the reality is that they only generate durable responses in a fraction of patients and not for all tumour types, saysJason Moffat, a professor of molecular genetics at the Donnelly Centre for Cellular and Biomolecular Research who led the work.

The study, published inNature, also revealed the need for new therapy to take into account the genetic composition of tumours because of mutations in the cancer cells that can potentially make the disease worse in response to treatment, often referred to as cancer resistance mutations.

Its very important to understand at the molecular level how cancer develops resistance to immunotherapies in order to make them more broadly available, saysMoffat, who holds a Canada Research Chair in Functional Genomics of Cancer.Advances in systematic genetic approaches have let us key in on genes and molecular pathways that are commonly involved in resistance to therapy.

In immunotherapy, a patients own immune cells, known as T killer cells, are engineered to find and destroy cancer. But treatment resistance has precluded its use in most patients, especially those with solid tumours.

Its an ongoing battle between the immune system and cancer, where the immune system is trying to find and kill the cancer whereas the cancers job is to evade that killing, saysKeith Lawson, a co-lead author who iscompleting a PhD in Moffats lab as part of his medical training in the surgeon-scientist program at U of Ts Faculty of Medicine.

Tumour heterogeneity genetic variation in tumour cells within and across individuals that can impact therapy response further complicates treatment.

Its important to not just find genes that can regulate immune evasion in one model of cancer, but what you really want are to find those genes that you can manipulate in cancer cells across many models because those are going to make the best therapeutic targets, Lawson says.

The team, including collaborators from Agios Pharmaceuticals in Cambridge, Mass., looked for genes that regulate immune evasion across six genetically diverse tumor models derived from breast, colon, kidney and skin cancer. The cancer cells were placed in a dish alongside the T cells engineered to kill them, where the ensuing onslaught served as a baseline. The researchers next deployed the gene editing tool CRISPR to switch off one-by-one every gene in the cancer cells and measured the resulting deviations from the killing baseline.

They identified 182 core cancer intrinsic immune evasion genes whose deletion makes the cancer cells either more sensitive or more resistant to T cell attack. Among the resisters were all the genes known to develop mutations in patients who stopped responding to immunotherapy, giving the researchers confidence that their approach worked.

Many of the discovered genes had no previous links to immune evasion.

That was really exciting to see, because it means that our dataset was very rich in new biological information,Lawson says.

Genes involved in autophagy, a process when cells ramp up recycling their components to mitigate damage following stress, came up as key for immune evasion. This raises the possibility that cancers susceptibility to immunotherapy could be boosted by targeting its autophagy genes.

But as the researchers delved deeper, they found that deleting certain autophagy genes in pairs rendered the cells resistant to T cell killing. That means that if a tumour already harbours a mutation in one autophagy gene, a treatment that combines immunotherapy with a drug targeting another autophagy gene could make the disease worse in that patient.

We found this complete inversion of gene dependency,says Moffat. We did not anticipate this at all. What it shows us is that genetic context what mutations are present very much dictates whether the introduction of the second mutationwill cause no effect, resistance or sensitivity to therapy.

As more research explores combinatorial effects of mutations across different types of cancer cells, it should become possible to predict from a tumours DNA what type of therapy will be most effective.

The research was funded by the Canadian Institutes of Health Research, the Ontario Institute for Cancer Research and Agios Pharmaceuticals.

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U of T researchers identify genes that enable cancer to evade the immune system - News@UofT

Virus-fighting viperins, part of the human immune system, turn out to have bacterial counterparts that might boost the fight against human disease.

By tracking the evolution of what may be our oldest means of fighting off viral infection, a group at the Weizmann Institute of Science has uncovered antiviral substances that may lead to the development of highly effective antiviral drugs. These substances are made by virus-fighting enzymes known as viperins, which were previously known to exist only in mammals, and have now been found in bacteria. The molecules produced by the bacterial viperins are currently undergoing testing against human viruses such as the influenza virus and COVID-19. The study was published in Nature.

Studies conducted over the past decade by Prof Rotem Sorek and his group in the Institutes Molecular Genetics Department, as well as those by other scientists, have revealed that bacteria have highly sophisticated immune systems, despite their microscopic size. In particular, they are equipped to fight off phages viruses that infect bacteria. These differ from the kind that infect humans in their choice of targets, but they all consist of genetic material DNA or RNA that hijacks parts of the hosts replication machinery to make copies of themselves and spread.

Prof Sorek has found that some of these bacterial immune responses suggest evolutionary links to our own immune systems, and the present study in his lab shows the strongest evidence yet: They discovered that viperin antiviral enzymes whose function in the human immune system was understood only two years ago play a role in the immune system of bacteria.

In humans, viperin belongs to the innate immune system, the oldest part of the immune system in terms of evolution. It is produced when a signalling substance called interferon alerts the immune system to the presence of pathogenic viruses. The viperin then releases a special molecule that is able to act against a broad range of viruses with one simple rule: The molecule mimics nucleotides, bits of the genetic material needed to replicate their genomes. But the viperin molecule is fake: It is missing a vital piece that enables the next nucleotide in the growing strand to attach. Once the faux-nucleotide is inserted into the replicating viral genome, replication comes to a halt and the virus dies.

This simplicity and broad action against many different viruses suggested viperins had been around for some time, but could they go back as far as our common ancestors with bacteria? Led by former postdoctoral fellow Dr Aude Bernheim in Soreks lab, the group used techniques that had been developed in his lab to detect bacterial sequences encoding possible viperins. They then showed that these viperins did, indeed, protect bacteria against phage infection.

Whereas the human viperin produces a single kind of antiviral molecule, we found that the bacterial ones generate a surprising variety of molecules, each of which can potentially serve as a new antiviral drug, says Sorek.

Based on the genetic sequences, Sorek and his team were able to trace the evolutionary history of viperins: We found that this important component of our own antiviral immune system originated in the bacterial defence against viruses that infect them, says Sorek.

If the bacterial viperins prove effective against human viruses, Sorek thinks it may pave the way for the discovery of further molecules generated by bacterial immune systems that could be adopted as antiviral drugs for human diseases. As we did decades ago with antibiotics antibacterial substances that were first discovered in fungi and bacteria we might learn how to identify and adopt the antiviral strategies of organisms that have been fighting infection for hundreds of millions of years.

The current study was conducted in collaboration with researchers from Pantheon Biosciences, which has licensed the rights through Yeda Research and Development, the technology transfer arm of the Weizmann Institute of Science, to develop anti-viral drugs based on the findings. Further studies are underway to determine which of the bacterial viperins could be best adapted to fighting human viruses, including, COVID-19. Also participating in this research were Adi Millman, Gal Ofir, Gilad Meitav, Carmel Avraham, Sarah Melamed and Dr Gil Amitai, all of Soreks group in the Weizmann Institute of Sciences Molecular Genetics Department.

Prof Rotem Sorek is Head of the Knell Family Center for Microbiology; his research is also supported by the Willner Family Leadership Institute for the Weizmann Institute of Science; the Sagol Weizmann-MIT Bridge Program; the Schwartz/Reisman Collaborative Science Program; the Ben B and Joyce E Eisenberg Foundation; the Yotam Project; and the European Research Council.

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Bacterial viperins prove effective against human viruses: Researchers - Express Pharma

Image: The viperins in bacteria have evolved to fight a variety of viruses (Photo courtesy of Weizmann Institute of Science)

A group of scientists at the Molecular Genetics Department at the Weizmann Institute of Science (Rehovot, Israel) has uncovered a gold mine of antiviral substances made by virus-fighting enzymes known as viperins. The molecules produced by the bacterial viperins are currently undergoing testing against human viruses such as the influenza virus and COVID-19.

Earlier studies conducted by the group as well as other scientists have revealed that bacteria have highly sophisticated immune systems, despite their microscopic size. In particular, they are equipped to fight off phages - viruses that infect bacteria. These differ from the kind that infect humans in their choice of targets, but they all consist of genetic material - DNA or RNA - that hijacks parts of the hosts replication machinery to make copies of themselves and spread.

The group of scientists have now found that some of these bacterial immune responses suggest evolutionary links to our own immune systems, and the present study in their lab shows the strongest evidence yet: They discovered that viperin antiviral enzymes - whose function in the human immune system was understood only two years ago - play a role in the immune system of bacteria.

In humans, viperin belongs to the innate immune system, the oldest part of the immune system in terms of evolution. It is produced when a signaling substance called interferon alerts the immune system to the presence of pathogenic viruses. The viperin then releases a special molecule that is able to act against a broad range of viruses with one simple rule: The molecule mimics nucleotides, bits of genetic material needed to replicate their genomes. But the viperin molecule is fake: It is missing a vital piece that enables the next nucleotide in the growing strand to attach. Once the faux-nucleotide is inserted into the replicating viral genome, replication comes to a halt and the virus dies.

This simplicity and broad action against many different viruses suggested viperins had been around for some time, but could they go back as far as our common ancestors with bacteria? The group used techniques that had been developed in their lab to detect bacterial sequences encoding possible viperins. They then showed that these viperins did, indeed, protect bacteria against phage infection. Based on the genetic sequences, the team was able to trace the evolutionary history of viperins. If the bacterial viperins prove effective against human viruses, then it may pave the way for the discovery of further molecules generated by bacterial immune systems that could be adopted as antiviral drugs for human diseases. Further studies are underway to determine which of the bacterial viperins could be best adapted to fighting human viruses, including, of course, COVID-19.

As we did decades ago with antibiotics - antibacterial substances that were first discovered in fungi and bacteria - we might learn how to identify and adopt the antiviral strategies of organisms that have been fighting infection for hundreds of millions of years, said Prof. Rotem Sorek from the Institutes Molecular Genetics Department.

Related Links:Weizmann Institute of Science

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Virus-Fighting Enzymes in Bacteria Could Lead to Development of Highly Effective Antiviral Drugs Against COVID-19 - HospiMedica