Amsterdam, the Netherlands, and Holzgerlingen, Germany, October 30, 2019, 10:00 am CET - Curetis N.V. (the "Company" and, together with its subsidiaries, "Curetis"), a developer of next-level molecular diagnostic solutions, today announced that the Curetis Group Companies will be attending several key conferences in the fourth quarter of 2019.

November 2019

EIT Health German-French Bilateral Meeting, November 4-5 2019 Mannheim, Germany (Ares Genetics GmbH) 54th Annual Northeast Branch American Society for Microbiology, November 7-8, 2019 Randolph, MA, USA (Curetis USA Inc.)DICON/DASON Fall 2019 Symposium (Duke Infection Control Outreach Network / Duke Antimicrobial Stewardship Outreach Network), November 8, 2019 Raleigh, NC, USA (Curetis USA Inc.)Southeastern Association of Clinical Microbiology (SEACM) Annual Fall Meeting, November 14-16, 2019 Myrtle Beach, SC, USA (Curetis USA Inc.)DxPx - Diagnostics and Research Tools Partnering Conference, November 18, 2019 Dsseldorf, Germany (Ares Genetics & Curetis GmbH)European Summit of Industrial Biotechnology, November 18-20, 2019 Graz, Austria (Ares Genetics GmbH)Emerging Antimicrobials and Diagnostics in AMR 2019, November 19-20, 2019 Amsterdam, The Netherlands (Ares Genetics GmbH & Curetis GmbH)EPAASM 49th Annual Symposium (Eastern Pennsylvania Branch of the American Society for Microbiology), November 22, 2019 Philadelphia, PA, USA (Curetis USA Inc.)

December 2019

3rd Congress Immunotherapies & Innovations for Infectious Diseases, December 3-4, 2019 Lyon, France (Ares Genetics GmbH)

ASPH Midyear Clinical Meeting (American Society of Health-System Pharmacists), December 8-12, 2019 Las Vegas, NV, USA (Curetis USA Inc., booth #773)

13. Nationaler Qualittskongress Gesundheit, December 12-13, 2019 Berlin, Germany (Ares Genetics GmbH)

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About Curetis

Curetis N.V.s (CURE.NX) goal is to become a leading provider of innovative solutions for molecular microbiology diagnostics designed to address the global challenge of detecting severe infectious diseases and identifying antibiotic resistances in hospitalized patients.

Curetis Unyvero System is a versatile, fast and highly automated molecular diagnostic platform for easy-to-use, cartridge-based solutions for the comprehensive and rapid detection of pathogens and antimicrobial resistance markers in a range of severe infectious disease indications. Results are available within hours, a process that can take days or even weeks if performed with standard diagnostic procedures, thereby facilitating improved patient outcomes, stringent antibiotic stewardship and health-economic benefits. Unyvero in vitro diagnostic (IVD) products are marketed in Europe, the Middle East, Asia and the U.S.

Curetis wholly owned subsidiary Ares Genetics GmbH offers next-generation solutions for infectious disease diagnostics and therapeutics. The ARES Technology Platform combines what the Company believes to be the most comprehensive database worldwide on the genetics of antimicrobial resistances, ARESdb, with advanced bioinformatics and artificial intelligence.

For further information, please visit http://www.curetis.com and http://www.ares-genetics.com.

Legal Disclaimer

This document constitutes neither an offer to buy nor an offer to subscribe for securities and neither this document nor any part of it should form the basis of any investment decision in Curetis.

The information contained in this press release has been carefully prepared. However, Curetis bears and assumes no liability of whatever kind for the correctness and completeness of the information provided herein. Curetis does not assume an obligation of whatever kind to update or correct information contained in this press release whether as a result of new information, future events or for other reasons.

This press release includes statements that are, or may be deemed to be, forward-looking statements. These forward-looking statements can be identified by the use of forward-looking terminology, including the terms believes, estimates, anticipates, expects, intends, targets, may, will, or should and include statements Curetis makes concerning the intended results of its strategy. By their nature, forward-looking statements involve risks and uncertainties and readers are cautioned that any such forward-looking statements are not guarantees of future performance. Curetis actual results may differ materially from those predicted by the forward-looking statements. Curetis undertakes no obligation to publicly update or revise forward-looking statements, except as may be required by law.

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Contact details

Curetis Contact DetailsCuretis N.V.Max-Eyth-Str. 4271088 Holzgerlingen, GermanyTel. +49 7031 49195-10pr@curetis.com or ir@curetis.comwww.curetis.com - http://www.unyvero.com

International Media & Investor InquiriesakampionDr. Ludger Wess / Ines-Regina Buth Managing Partnersinfo@akampion.comTel. +49 40 88 16 59 64Tel. +49 30 23 63 27 68

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Originally posted here:
Curetis To Attend Key Conferences in the Fourth Quarter of 2019 - Yahoo Finance

More than 150 New Zealand scientists under 30 have signed a letter to the Green Party urging a rethink of its stance on the regulation of genetic modification. The full text of the letter follows.

To the members and supporters of the Green Party of Aotearoa New Zealand and their representatives in government

Climate change is one of the greatest crises in human history, and our current law severely restricts the development of technologies that could make a vital difference. In 2003 the 1996 Hazardous Substances and New Organisms Act was modified to tightly regulate research into genetic modification (GM). This legislation and the surrounding public debate was driven by uncertainty about the risks that these new technologies posed to biodiversity and human health, and resulted in creating one of the toughest regulatory environments in the world for this field of research.

We, an emerging generation of New Zealand scientists with expertise in and/or undertaking research in the biological sciences*, are writing to request that the Green Party reconsider its position on the regulation of these technologies. We are addressing this letter to the Greens because of a history of leading in science-based policy such as climate action, even when that path is difficult. We believe that GM based research could be decisive in our efforts to reduce New Zealand and global climate emissions as well as partially mitigating some of the impacts of climate change. At the same time, we emphasise that potential reduction of impact is not a substitute for emission reduction.

The period since the introduction of the 2003 legislation has seen important GM related research in the areas of agricultural efficiency, carbon sequestration, and alternative protein production. The existing regulation in New Zealand inhibits application of advances such as these, blocking not only the development of green technology, but the potential for a just transition away from extractive and polluting industries. New Zealand has the opportunity to be a world leader in such a transition: for example, the development and demonstration of effective technologies to reduce agricultural emissions could have an international impact and set an example for other countries.

While such a powerful technology as targeted genetic modification certainly requires controls, existing frameworks do not enable public and environmental benefits from these technologies to be realised. The gene editing expert advice panel supported by The Royal Society Te Aprangi, the Prime Ministers Chief Science Advisor, and the interim climate change committee have recently called for public discussion on potential reform of New Zealands laws around modern gene editing techniques.

As a confidence and supply member of the current government the Greens have the ability to drive this reform: the members can persuade the party to reconsider its policy position, and the Members of Parliament can influence the government it supports to revise the legislation. The Greens have been strong advocates of both climate action and evidence based policy informed by science. In this light we call upon its members, supporters, ministers, and MPs to add their voices to the cause of a science-based approach to climate, on behalf of the people and environment of both Aotearoa and the world.

Ng mihi

PhD

Kyle Webster, University of Auckland, Bio-nanotechnology

Luke Stevenson, Victoria University of Wellington, Biotechnology

Emilie Gios, University of Auckland, Microbial ecology

Morgane Merien, University of Auckland, Biological Sciences Entomology

Lucie Jiraska, University of Auckland, Environmental Microbiology

Victor Yim, University of Auckland, Peptide chemistry

Zach McLean, University of Auckland, Genetic engineering

Declan Lafferty, Plant and FoodResearch/University of Auckland, Genetics and Molecular Biology

Samarth Samarth, University of Canterbury, Plant Biology

Juliane Gaviraghi Mussoi, University of Auckland, Avian Behaviour

Alex Noble, University of Canterbury, Biology

Kelsey Burborough, University of Auckland, Genetics

Matthew Mayo-Smith, University of Auckland, Plant Molecular Biology

Moritz Miebach, University of Canterbury, Plant-microbe interactions

Olivia Ogilvie, University of Auckland, Food Biotech / Biochemistry

Rachel Bennie, University of Canterbury, Human Toxicology

Sean Mackay, University of Otago, Chemistry and Nanotechnology

Georgia Carson, Victoria University of Wellington, Cell and Molecular Biology

Ruby Roach, Massey University

Jeremy Stephens, Massey University, Biology

Zidong (Andy) Li, Massey University, Molecular Cancer Biology

Aqfan Jamaluddin, University of Auckland, Molecular Pharmacology

Michael Fairhurst, Victoria University of Wellington, Microbiology

Nikolai Kondratev, Massey University, Plant Biology

Mariana Tarallo, Massey University, Plant pathology

Ellie Bradley, Massey University, Plant pathology

Mercedes Rocafort Ferrer, Massey University, Plant pathology

Yi-Hsuan Tu, Massey University, Biochemistry & Microbiology

Sean Bisset, Massey University, Biochemistry

Patrick Main, Massey University, Biological sciences

Abigail Sharrock, Victoria University of Wellington, Biotechnology

Alvey Little, Victoria University of Wellington, Molecular Microbiology

William Odey, Victoria University of Wellington, Biotechnology

Gabrielle Greig, Victoria University of Wellington, Molecular Microbiology

Melanie Olds, Victoria University of Wellington, Biotechnology

Jennifer Soundy, Victoria University of Wellington, Biological Sciences

Matire Ward, Victoria University of Wellington, Cell and molecular bioscience

Tom Dawes, Victoria University of Wellington, Plant Ecology

Hamish Dunham, Victoria University of Wellington, Biomedical science

Amy Alder, Victoria University of Wellington, Neuroscience

Caitlin Harris, University of Otago, Plant genetics

Lucy Gorman, Victoria University of Wellington, Coral reef biology

Vincent Nowak, Victoria University of Wellington, Biotechnology

Brandon Wright, University of Otago, Biochemistry

Anna Tribe, Victoria University of Wellington, Cancer cell biology

Conor McGuinness, University of Otago, Breast Cancer

Genomics/Immunology Kelsi Hall, Victoria University of Wellington, Biotechnology

Andrew Howard, University of Waikato, Biochemistry

Mitch Ganley, Victoria University of Wellington, Biotechnology/vaccines

Matt Munro, Victoria University of Wellington, Biomedical Science

Prashath Karunaraj, University of Otago, Genetics

Pascale Lubbe, University of Otago, Evolutionary genetics

Mackenzie Lovegrove, University of Otago, Genetics, Insect evolution

Nicholas Foster, University of Otago, Ecology

Taylor Hamlin, University of Otago, Antarctic Marine Ecosystem & Movement Ecology

Fionnuala Murphy, Massey University, Proteomics

Amanda Board, University of Canterbury, Protein Biochemistry

Esther Onguta, Massey University, Food Technology

Nomie Petit, University of Auckland, Proteins

Liam Le Lievre, University of Otago, Plant Reproduction

James Hunter, University of Otago, Ecology

Samarth Kulshrestha, University of Canterbury,

Rebecca Clarke, University of Otago, Whole body regeneration

Sarah Killick, University of Auckland, Environmental Science

Stephanie Workman, University of Otago, Developmental Genetics

Erik Johnson, University of Otago, Oceanography

Declan Lafferty, University of Auckland, Molecular Biology

Laurine van Haastrecht, Victoria University of Wellington, Glaciology

Leo Mercer, Victoria University of Wellington, Environmental Studies

Aidan Joblin-Mills, Victoria University of Wellington, Chemical Genetics

Gabrielle Keeler-May, University of Otago, Marine Science

Aqfan Jamaluddin, University of Auckland, Pharmacology

Spencer McIntyre, University of Auckland, Biological Sciences

Sarah Inwood, University of Otago, Genetics

Isabelle Barrett, University of Canterbury, Freshwater ecology

Olivia Angelin-Bonnet, Massey University, Biostatistics

Hannah McCarthy, Massey University, Plant Pathology

Sofie Pearson, Massey University, Plant Science

Zac Beechey-Gradwell, Lincoln University, Plant physiology

Hannah Lee-Harwood, Victoria University of Wellington, Biotechnology

Euan Russell, University of Otago, Microbiology

Masters

Kelly Styles, University of Auckland, Biological Sciences

Merlyn Robson, University of Auckland, Virology

Andra Popa, University of Auckland

James Love, University of Auckland, Bioinformatics

Evie Mansfield, University of Auckland, Molecular Microbiology

Ash Sargent, University of Auckland, Immunology

Sabrina Cuellar, University of Auckland, Plant Genetics

Renji Jiang, University of Canterbury, Plant pathology

Morgan Tracy, University of Canterbury, Ecology

See the original post here:
GM could be decisive: An open letter to the Green Party from young NZ scientists - The Spinoff

Adding carvedilol, the active compound of a blood pressuremedicine, to enzyme replacement therapy (ERT) for Pompe disease can improve its effectiveness in reaching and strengthening skeletal muscles, a study in mice suggests.

This finding, Evaluation of antihypertensive drugs in combination with enzyme replacement therapy in mice with Pompe disease was published in Molecular Genetics and Metabolism.

At present, enzyme replacement therapy (ERT) is the only effective treatment for Pompe disease, a rare genetic disorder caused by the absence or deficiency of the acid alpha-glucosidase (GAA) enzyme.

When GAA activity is low, a sugar molecule called glycogen accumulates inside cells, damaging organs and tissues throughout the body, but primarily skeletal muscle, smooth muscle, and cardiac muscle. If left untreated, the accumulation of glycogen in cardiac and skeletal muscle leads to severe and progressive muscular weakness, risking heart and respiratory failure.

There is, however, a major limitation in ERT. Skeletal muscle is less accessible to it, meaning the therapy has trouble getting into this type of muscle cell. Skeletal muscles poor response to ERT has been attributed to a serious lack of a protein receptor called cation-independent mannose-6-phosphate receptor (CI-MPR) on its cells.

Animal studies suggest that an active compound common to blood pressure medications (with work to control hypertension) could increase the uptake of ERT by muscle cells, by increasing the amount of muscle (muscle hypertrophy), and therefore the amount of CI-MPR.

Investigators atDuke Universityevaluated the effects of ERT with and without three anti-hypertensive agents: carvedilol, losartan, and propranolol. All these compounds have different ways of working, or mechanisms of action, in the body. They experimented using a mouse model of Pompe disease called the GAA knockout (absent) mouse.

Animals were assigned to one of seven groups: no treatment, ERT alone, ERT with carvedilol, ERT with losartan, ERT with propranolol, or to only losartan or carvedilol. Drugs were given to the mice in drinking water, and one week after treatment initiation, recombinant human GAA was given by injection every week for a month. Five days following the last GAA injection, scientists examined the animals cardiac and muscle function.

The team reported that carvedilol uniquely increased muscle strength, while losartan uniquely decreased heart rate. GAA activity was also found to be significantly higher in the heart following either losartan or propranolol being added to enzyme replacement therapy, compared to mice left untreated as a control group.

Both carvedilol or propranolol significantly increased GAA activity in the animals quadriceps, the muscles in the front of the thigh, compared to control mice. However, only carvedilol administration significantly increased GAA activity in quadriceps, in comparison with ERT alone, the scientists wrote.

These findings indicate that the greatest rise in enzymatic activity occurred in response to carvedilol, the active substance in the blood pressure medication Coreg. Carvedilol is a beta-blocker that relaxes the smooth muscle that makes up blood vessels, leading to an overall reduction in blood pressure.

Because more than half (seven of 13) of the mice given losartan, either alone or in combination with ERT, died during the study, researchers thought this active molecule potentially toxic in Pompe, and suggested physicians should be mindful of it when prescribing high blood pressure medications to Pompe patients.

Currently we demonstrated unique toxicity from the administration of losartan in mice with Pompe disease, the researchers wrote.

Because of the benefits seen in diseased micegiven carvedilol during ERT, they recommended the compound be studied in a clinical trial in patients.

Carvedilol was well-tolerated, and the ability to use a -blocker [beta-blocker] in patients that will not interfere with ERT would be highly valuable for clinical use in patients with Pompe since they often require a -blocker to mitigate disease-associated hypertension, the investigators concluded.

A clinical trial of carvedilol in patients with Pompe disease should be considered to further evaluate its usefulness.

With over three years of experience in the medical communications business, Catarina holds a BSc. in Biomedical Sciences and a MSc. in Neurosciences. Apart from writing, she has been involved in patient-oriented translational and clinical research.

Total Posts: 3

Margarida graduated with a BS in Health Sciences from the University of Lisbon and a MSc in Biotechnology from Instituto Superior Tcnico (IST-UL). She worked as a molecular biologist research associate at a Cambridge UK-based biotech company that discovers and develops therapeutic, fully human monoclonal antibodies.

Read this article:
ERT to Treat Pompe May Work Better in Combo with Blood Pressure Medication, Study Says - Pompe Disease News

Researchers have identified 57 genetic variations of a gene strongly associated with declines in blood oxygen levels during sleep. Low oxygen levels during sleep are a clinical indicator of the severity of sleep apnea. The study, published today in the American Journal of Human Genetics, was funded by the National Heart, Lung, and Blood Institute (NHLBI), part of the National Institutes of Health.

A persons average blood oxygen levels during sleep are hereditary, and relatively easy to measure, says study author Susan Redline, MD, senior physician in the Division of Sleep and Circadian Disorders at Brigham and Womens Hospital, and professor at Harvard Medical School, in a release. Studying the genetic basis of this trait can help explain why some people are more susceptible to sleep disordered breathing and its related morbidities.

When we sleep, the oxygen level in our blood drops, due to interruptions in breathing. Lung and sleep disorders tend to decrease those levels further, and dangerously so. But the range of those levels during sleep varies widely between individuals and, researchers suspect, is greatly influenced by genetics.

Despite the key role blood oxygen levels play in health outcomes, the influence of genetics on their variability remains understudied. The current findings contribute to a better understanding, particularly because researchers looked at overnight measurements of oxygen levels. Those provide more variability than daytime levels due to the stresses associated with disordered breathing occurring during sleep.

The researchers analyzed whole genome sequence data from the NHLBIs Trans-Omics for Precision Medicine (TOPMed) program. To strengthen the data, they incorporated results of family-based linkage analysis, a method for mapping genes that carry hereditary traits to their location in the genome. The method uses data from families with several members affected by a particular disorder.

This study highlights the advantage of using family data in searching for rare variants, which is often missed in genome-wide association studies, says James Kiley, PhD, director of the Division of Lung Diseases at NHLBI. It showed that, when guided by family linkage data, whole genome sequence analysis can identify rare variants that signal disease risks, even with a small sample. In this case, the initial discovery was done with fewer than 500 samples.

The newly identified 57 variants of the DLC1 gene were clearly associated with the fluctuation in oxygen levels during sleep. In fact, they explained almost 1% of the variability in the oxygen levels in European Americans, which is relatively high for complex genetic phenotypes, or traits, that are influenced by myriad variants.

Notably, 51 of the 57 genetic variants influence and regulate human lung fibroblast cells, a type of cell producing scar tissue in the lungs, says study author Xiaofeng Zhu, PhD, professor at the Case Western Reserve University School of Medicine. This is important, he said, because Mendelian Randomization analysis, a statistical approach for testing causal relationship between an exposure and an outcome, shows a potential causal relationship between how the DLC1 gene modifies fibroblasts cells and the changes in oxygen levels during sleep.

This relationship, Kiley added, suggests that a shared molecular pathway, or a common mechanism, may be influencing a persons susceptibility to the lack of oxygen caused by sleep disordered breathing and other lung illnesses such as emphysema.

Continued here:
Genetic Study: Shared Molecular Pathway Might Influence Susceptibility to Lack of Oxygen Caused by Sleep-disordered Breathing and Other Lung Illnesses...

New research fromNOAA Fisheries, Ocean Associates Inc., Cascadia Research Collective, Tethys Research Institute, and Universidad Autnoma de Baja California Sur, has concluded that fin whales in the northern Pacific Ocean are a separate subspecies. The paper outlines key genetic differences between the fin whales of the Pacific and the Atlantic Oceans.

The increasing study of cetacean genetics is revealing new diversity among the worlds whales and dolphins that has not been previously recognised, said lead author Eric Archer, a geneticist at NOAA Fisheries Southwest Fisheries Science Center (SWFSC).Theres definitely more diversity out there than has been on the books. There has been a wave of progress in cetacean taxonomy.

Fin whales are the second largest whale on Earth and widely believed to be the fastest whales in the ocean. Not a huge amount is known about this elusive creatures, which tend reside in the open ocean, away from coastlines where they might be seen and studied more easily. Whalers killed approximately 46,000 fin whales in the North Pacific Ocean between 1947 and 1987.

Traditional taxonomy focuses on skeletons to assess biological variation into recognised species and subspecies, butpowerful genetic technologies now allow scientists to compare genes instead of skeletons. They extract DNA from tissue samples the size of a pencil eraser obtained from whales in the field.

Archer and his team made use of the SWFSCsMarine Mammal and Turtle Molecular Research Sample Collection, which is one of the largest collections of marine mammal genetic material in the world. They also used samples from museums and other collections.

By comparing the DNA of fin whales in both the Pacific and Atlantic Oceans, they found that the have been separated for hundreds of thousands of years. To provide further evidence of the two distinct subspecies, the scientistscould also assign individual fin whale samples to their ocean of origin using the genetic data.

There are other new species and subspecies that we are learning about thanks to the technology that has made this possible, Archer added. It is changing the field.

Approximately 14,000 to 18,000 fin whales in the northern Pacific Ocean will be affected by the new subspecies designation.

To read the full paper,Revision of fin whaleBalaenoptera physalus(Linnaeus, 1758) subspecies using genetics, click here.

Photograph courtesy ofPaula Olson/NOAA Fisheries.

For more from our Ocean Newsroom,click hereor on one of the images below:

Read more here:
Pacific subspecies of fin whales has been revealed by new genetic study - Oceanographic - Oceanographic Magazine

Scientists at theHudsonAlpha Institute for Biotechnologyhave pinpointed epigenetic differences in the way lupus affects black women compared to other lupus patients, revealing important mechanics of the puzzling disease. Epidemiologists have identified that lupus impacts black women with greater frequency and severity than other populations. Scientists inDevin Absher's Labat HudsonAlpha published findings in August showing that increased risk and harm to lupus patients can be linked to epigenetic differences--essentially, the degree to which certain genes are functioning.

The finding, published inArthritis & Rheumatology, helps create a more complete understanding of an often misunderstood disease, revealing some of the mechanisms that contribute to it. It also reveals a gap in genetic research, highlighting the lack of information scientists have regarding racial differences on the genetic level.

Devastating Disease

Lupus is an autoimmune disorder, meaning that the immune system attacks healthy cells in the body. It causes symptoms that are often difficult to quantify, including fatigue and extreme joint pain.

Lupus is one of the most historically chronicled diseases, having first been documented by Socrates in 400 BC. The disease gets its name from a common rash that forms on the face which is said to resemble the markings of wolves, hence the latin name "lupus" meaning wolf.

There are more than 200,000 cases of lupus in the US every year, yet there is no universally accepted cause or cure. The disease is chronic, meaning it can last for years or even an entire lifetime.

Megan Breitbach, PhD, is the lead author on the paper. She notes, "The diagnostic process can also prove long and tedious, because the symptoms come and go and often can only be observed through patient description."

"On average," she adds, "it takes six years to diagnose someone with lupus."

While treatment can help manage lupus, the condition cannot be cured. Instead, patients and their physicians try to address symptoms and take the edge off flare-ups.

Molecular Differences

While the disease on the whole remains a mystery, scientists hope to find some answers in the ways that the condition affects different populations. In the United States, lupus has a much higher prevalence in non-white populations. In fact, lupus is the 5th leading cause of death for black women ages 15-24.

Ancestry can dramatically impact disease genetics, so understanding why the disease affects populations differently could go a long way toward telling us what genetic factors play a part in developing the condition.

In the case of lupus, the body's immune B cells function distinctive epigenetic signatures of the disease are found in B cells, which are part of the immune system. The analysis performed by the Absher Lab revealed lupus-specific differences in methylation throughout B cell development between black and white women.

Methylation changes can alter the degree to which a stretch of DNA functions without changing the genetic code itself. This research shows the most significant changes in methylation occur around genes related to Interferons, which are proteins that regulate immune response.

These differences in B cell development could help explain the more severe symptoms and earlier age of onset for lupus in black women.

"What we found," explains Devin Absher, PhD, "was that there are a number of methylation changes we can link to lupus. When you isolate them, you see that the changes are far greater in black women. The population differences could be key to a more complete understanding of the disease on the whole."

Gaps in Understanding

The genetic gap between these two groups of patients with lupus illustrates a broader gap in knowledge. One key limitation of genetics stems from a lack of diverse data, which hurts all populations.

Disease genetics frequently relies on genome-wide association studies (GWAS) to link genes with various health conditions. However the most recent aggregations of GWAS show nearly 88% of participants come from European ancestry. These eurocentric results can make it harder to identify genetic components of diseases that disproportionately affect underrepresented populations.

A lack of diversity in genetic research slows progress across the board. The unique genetic factories of all kinds of ancestry can help us better understand the human genome and even find potential ways to share the benefits of natural resistance. For example, Americans of African descent were found to have mutations on their PCSK9 genes which led to lower levels of cholesterol in their bloodstream. With that information, researchers developed PCSK9 inhibitors to lower cholesterol and heart disease risk across ancestries.

This lupus research from the Devin Absher Lab further illustrates the importance of understanding racial diversity when examining genetic components for diseases.

Absher is involved in a number of efforts to drive greater diversity in genetic research, including the Alabama Genomic Health Initiative, which aims to bring the value of genetic sequencing to diverse populations across the state.

The Way Forward

This lupus research helps open the door for future exploration of methylation around Interferon sites as it relates to the disease. However, the finding is only possible because of an active consideration of the value of diversity in genetic research. HudsonAlpha remains dedicated to bringing the value of genomics to all, as a diverse approach to research opens doors that would otherwise remain closed.

2018 NatureWorldNews.com All rights reserved. Do not reproduce without permission.

Originally posted here:
Lupus Study Illustrates the Importance of Diversity in Genetic Research - Nature World News

PARSIPPANY, NJ, Oct. 29, 2019 (GLOBE NEWSWIRE) -- Interpace (IDXG) announced today that it will be presenting new data on the performance of its molecular thyroid products at the upcoming 89th Annual Meeting of the American Thyroid Association (ATA), being held October 30th to November 3rd, 2019 in Chicago, IL. The ATA meeting is one of the largest gatherings of endocrinologists, ENTs, surgeons and other providers who focus on the diagnosis and treatment of thyroid cancer.

Interpace will be presenting three separate posters focused on the performance of the companys molecular tests for indeterminate thyroid nodules, ThyGeNEXT and ThyraMIR, and are titled:

Together these posters underline the clinical utility of ThyGeNEXT and ThyraMIR in assessing the risk of thyroid nodules with indeterminate cytology results progressing to cancer. They also highlight progress made by the Company to provide quality diagnostic information for the detection of aggressive forms of thyroid cancer.

Jack Stover, CEO of Interpace, stated, We are pleased that our data has been accepted for presentation in this prestigious forum and look forward to sharing our work with such an established group of attendees. Mr. Stover continued, The acceptance of our data supports our belief that our molecular products continue to add value to physicians and patients at risk of thyroid cancer.

About Thyroid Nodules, ThyGeNEXT and ThyraMIR Testing

According to the American Thyroid Association, approximately 20% of the 525,000 thyroid fine needle aspirations (FNAs) performed on an annual basis in the U.S. are indeterminate for malignancy based on standard cytological evaluation, and thus are candidates for ThyGeNEXT and ThyraMIR.

ThyGeNEXT and ThyraMIR reflex testing yields high predictive value in determining the presence and absence of cancer in thyroid nodules. The combination of both tests can improve risk stratification and surgical decision-making when standard cytopathology does not provide a clear diagnosis.

ThyGeNEXT utilizes state-of-the-art next-generation sequencing (NGS) to identify more than 100 genetic alterations associated with papillary and follicular thyroid carcinomas, the two most common forms of thyroid cancer, as well as Meduallary Thyroid Carcinoma. ThyraMIR is the first microRNA gene expression classifier. MicroRNAs are small, non-coding RNAs that bind to messenger RNA and regulate expression of genes involved in human cancers, including every subtype of thyroid cancer. ThyraMIR measures the expression of 10 microRNAs. Both ThyGeNEXT and ThyraMIR are covered by both Medicare and Commercial insurers, with more than 280 million patients covered.

About Interpace

Interpace is a leader in enabling personalized medicine, offering specialized services along the therapeutic value chain from early diagnosis and prognostic planning to targeted therapeutic applications.

Interpaces Diagnostic Business is a fully integrated commercial and bioinformatics business unit that provides clinically useful molecular diagnostic tests, bioinformatics and pathology services for evaluating risk of cancer by leveraging the latest technology in personalized medicine for improved patient diagnosis and management. Interpace has four commercialized molecular tests and one test in a clinical evaluation process (CEP): PancraGEN for the diagnosis and prognosis of pancreatic cancer from pancreatic cysts; ThyGeNEXT for the diagnosis of thyroid cancer from thyroid nodules utilizing a next generation sequencing assay; ThyraMIR for the diagnosis of thyroid cancer from thyroid nodules utilizing a proprietary gene expression assay; and RespriDX that differentiates lung cancer of primary vs. metastatic origin. In addition, BarreGEN for Barretts Esophagus, is currently in a clinical evaluation program whereby we gather information from physicians using BarreGEN to assist us in positioning the product for full launch, partnering and potentially supporting reimbursement with payers.

Interpaces Biopharma Business provides pharmacogenomics testing, genotyping, biorepository and other customized services to the pharmaceutical and biotech industries. The Biopharma Business also advances personalized medicine by partnering with pharmaceutical, academic, and technology leaders to effectively integrate pharmacogenomics into their drug development and clinical trial programs with the goals of delivering safer, more effective drugs to market more quickly, and improving patient care.

For more information, please visit Interpaces website at http://www.interpacediagnostics.com.

Forward-looking Statements

This press release contains forward-looking statements within the meaning of Section 27A of the Securities Act of 1933, Section 21E of the Securities Exchange Act of 1934 and the Private Securities Litigation Reform Act of 1995, relating to the Company's future financial and operating performance. The Company has attempted to identify forward looking statements by terminology including "believes," "estimates," "anticipates," "expects," "plans," "projects," "intends," "potential," "may," "could," "might," "will," "should," "approximately" or other words that convey uncertainty of future events or outcomes to identify these forward-looking statements. These statements are based on current expectations, assumptions and uncertainties involving judgments about, among other things, future economic, competitive and market conditions and future business decisions, all of which are difficult or impossible to predict accurately and many of which are beyond the Company's control. These statements also involve known and unknown risks, uncertainties and other factors that may cause the Company's actual results to be materially different from those expressed or implied by any forward-looking statement. Known and unknown risks, uncertainties and other factors include, but are not limited to the fact that there is no assurance the acquisition of the BioPharma business of Cancer Genetics, Inc. will be successfully integrated with the Company, or that the potential benefits of the acquisition, including future revenues, will be successfully realized. Additionally, all forward-looking statements are subject to the Risk Factors detailed from time to time in the Company's most recent Annual Report on Form 10-K, Current Reports on Form 8-K and Quarterly Reports on Form 10-Q. Because of these and other risks, uncertainties and assumptions, undue reliance should not be placed on these forward-looking statements. In addition, these statements speak only as of the date of this press release and, except as may be required by law, the Company undertakes no obligation to revise or update publicly any forward-looking statements for any reason.

CONTACTS:Investor Relations - Edison GroupJoseph Green(646) 653-7030jgreen@edisongroup.com

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Interpace to Present Data at the ATA Annual Meeting - GlobeNewswire