Syndicate content

Archive - 2019

December 17th

Bio-Techne's Exosome Diagnostics Lab Receives Accreditation from College of American Pathologists (CAP); Recognition Builds on Recent Achievements of Company’s ExoDx™ Prostate (IntelliScore) (EPI) Exosome-Based Liquid Biopsy Test

In a December17, 2019 press release, Bio-Techne Corporation (NASDAQ:TECH) announced that the Accreditation Committee of the College of American Pathologists (CAP) has awarded accreditation to its Exosome Diagnostics (ExosomeDx) laboratory based on results of a recent on-site inspection as part of the CAP's Accreditation Program. ExosomeDx was advised of this national recognition and congratulated for the excellence of services being provided. ExosomeDx is now one of more than 8,000 CAP-accredited facilities worldwide. "Receipt of CAP Accreditation represents another milestone in a banner year for our ExosomeDx platform and team," commented Chuck Kummeth, President and Chief Executive Officer of Bio-Techne. "This accreditation, combined with the CLIA, ISO 13485 and New York certifications already awarded to our laboratory, serve as a testament to the high-quality standards at our Waltham, Massachusetts facility. This recognition builds on the recent achievements of our ExoDx™ Prostate (IntelliScore) (EPI) test, including NCCN guideline inclusion, attaining FDA Breakthrough Device Designation, as well as the recently effective Medicare reimbursement determination issued by Medicare Administrative Contractor (MAC) National Government Services, Inc. All of these achievements position Bio-Techne to scale our EPI test and enable men to make more informed decisions on whether to proceed with an initial prostate biopsy.” Johan Skog (, PhD, CSO of Exosome Diagnostics, willbe giving a presentation at the upcoming Precision Medicine World Conference (PMWC 2020) in Santa Clara, California (January 21-January 24) (

December 17th

Brain Protein (CD33) Regulates Microglia Cells and May Protect Against Alzheimer’s

Research shows that white blood cells in the human brain are regulated by a protein called CD33 (image)--a finding with important implications in the fight against Alzheimer's disease, according to a new study by University of Alberta chemists. "Immune cells in the brain, called microglia, play a critical role in Alzheimer's disease," explained Matthew Macauley, PhD, Assistant Professor in the Department of Chemistry and co-author on the paper. "They can be harmful or protective. Swaying microglia from a harmful to protective state could be the key to treating the disease." Scientists have identified the CD33 protein as a factor that may decrease a person's likelihood of Alzheimer's disease. Less than 10 percent of the population have a version of CD33 that makes them less likely to get Alzheimer's disease. "The fact that CD33 is found on microglia suggests that immune cells can protect the brain from Alzheimer's disease under the right circumstances," said Abhishek Bhattacherjee, PhD, first author and postdoctoral fellow in the Macauley lab. Now, Dr. Macauley's research shows that the most common type of CD33 protein plays a crucial role in modulating the function of microglia."These findings set the stage for future testing of a causal relationship between CD33 and Alzheimer's Disease, as well as testing therapeutic strategies to sway microglia from harmful to protecting against the disease--by targeting CD33," said Dr. Macauley.

Extrachomosomal Circular DNA Drives Oncogenic Remodeling in Childhood Cancer; First Detailed Map of Circular DNA in Neuroblastoma Yields Unanticipated Insights

Cancer development is associated with the gradual accumulation of DNA defects over time. Thus, cancer is considered an age-related disease. But why do children develop cancer? An international team of researchers, led by scientists at Charité-Universitätsmedizin Berlin and the Memorial Sloan Kettering Cancer Center in New York, now reveal that mysterious rings of DNA known as extrachromosomal circular DNA can contribute to cancer development in children. Producing the first detailed map of circular DNA, the scientists have shed new unanticipated insights on long-standing questions in the field of cancer genetics. The work was published online on December 16, 2019 in Nature Genetics. The article is titled “Extrachromosomal Circular DNA Drives Oncogenic Genome Remodeling.” Every year, nearly half a million people in Germany develop cancer. Approximately 2,100 cancer patients are children under the age of 18. The fact that the majority of cancers develop in old adults is due to the mechanisms contributing to cancer development. A range of exogenous factors, including tobacco smoke and radiation, can cause damage to cellular DNA. If this type of DNA damage is left to accumulate over many years, affected cells may lose control over cell division and growth. This results in cancer development. Children, however, are not old enough to be affected by this mechanism of cancer development. What, then, is the reason for childhood cancers? A team of researchers, led by Dr. Anton Henssen of Charité's Department of Pediatrics, Division of Oncology and Hematology and the Experimental and Clinical Research Center (ECRC,) an institution jointly operated by Charité and the Max Delbrück Center for Molecular Medicine (MDC), is now a significant step closer to finding an answer.

December 15th

LAM’s Liquid Biopsy Test of cfDNA Methylation Panel Enables Highly Sensitive and Specific Detection of the Most Common Liver Cancer (Hepatocellular Carcinoma)

Today we discuss the dissemination of DNA-methylation-based tests for non-invasive detection of cancer. BioQuick News recently sat down with Dhruvajyoti Roy (photo), PhD, who is the Director of Technology at the Laboratory for Advanced Medicine Inc. (LAM), an AI-driven healthcare company focused on commercializing early cancer detection tests from a simple blood draw, to learn about the company’s technology and recent advances in the field of DNA methylation analysis. LAM developed a blood-based Liver Cancer Test, which can be used for early detection of liver cancer, as well as for monitoring disease recurrence. Dr. Roy had presented data from a validation study conducted by LAM on the ability of the assay to detect hepatocellular carcinoma (HCC), the most common form of liver cancer (more than 75% of all liver cancers, at The Liver Meeting® 2019 hosted by the American Association for the Study of Liver Diseases (AASLD), which was held in Boston from November 8-12, 2019. AASLD selected LAM's data for its poster presentation as a "Poster of Distinction." Posters of Distinction are classified as being in the top 10% of scored poster abstracts. (Dr. Roy was interviewed by BioQuick News editor Michael D. O'Neill and the text of the interview is provided below). QUESTION: Why did your group decide to focus on methylation status of cfDNA for your test? DR. ROY: Both genetic and epigenetic changes are known to be associated with the development of tumors. Over the last decade, analysis of cell-free DNA (cfDNA) from liquid biopsy samples, has emerged as a promising and potentially transformative, non-invasive diagnostic approach in oncology. cfDNA is composed of fragmented DNA released by cells into the circulation, typically as a result of cell death.

December 13th

DNA Stress Sensed by Mitochondria Can Cause Them to Activate Innate Immune System, Including Interferon-Stimulated Genes (ISGs) That Act to Protect Nuclear DNA and This May Support Development of Resistance to DNA-Damaging Chemotherapy

Mitochondria, tiny structures present in most cells, are known for their energy-generating machinery. Now, Salk researchers have discovered a new function of mitochondria: they set off molecular alarms when cells are exposed to stress or chemicals that can damage DNA, such as chemotherapy. The results, published online in Nature Metabolism on December 9, 2019, could lead to new cancer treatments that prevent tumors from becoming resistant to chemotherapy. The article is titled “Mitochondrial DNA Stress Signalling Protects the Nuclear Genome.” "Mitochondria are acting as a first line of defense in sensing DNA stress. The mitochondria tell the rest of the cell, 'Hey, I'm under attack, you better protect yourself,'" says Gerald Shadel, PhD, a Professor in Salk's Molecular and Cell Biology Laboratory and the Audrey Geisel Chair in Biomedical Science. Most of the DNA that a cell needs to function is found inside the cell's nucleus, packaged in chromosomes and inherited from both parents. But mitochondria each contain their own small circles of DNA (called mitochondrial DNA or mtDNA), passed only from a mother to her offspring. And most cells contain hundreds--or even thousands--of mitochondria. Dr. Shadel's lab group previously showed (in “Mitochondrial DNA Stress Primes the Antiviral Innate Immune Response” at that cells respond to improperly packaged mtDNA similarly to how they would react to an invading virus--by releasing it from mitochondria and launching an immune response that beefs up the cell's defenses.

Why Giant Pandas Are Born So Tiny; Short Gestation Period May Be Cause

Born pink, blind, and helpless, giant pandas typically weigh about 100 grams at birth -- the equivalent of a stick of butter. Their mothers are 900 times more massive than that. This unusual size difference has left researchers puzzled for years. With a few exceptions among animals such as echidnas and kangaroos, no other mammal newborns are so tiny relative to their mothers. No one knows why, but a Duke University study of bones across 10 species of bears and other animals finds that some of the current theories don't hold up. Duke biology professor Kathleen Smith, PhD, and her former student Peishu Li published their findings this month in the Journal of Anatomy. The article was published online on December 2, 2019 and is titled "Comparative Skeletal Anatomy of Neonatal Ursids and the Extreme Altriciality of the Giant Panda.” Baby panda skeletons are hard to come by, but the researchers were able to study the preserved remains of baby pandas born at the Smithsonian's National Zoo in Washington, D.C. The National Zoo's first panda couple, Ling-Ling and Hsing-Hsing, had five full-term cubs in the 1980s, but none of them survived long after birth. The researchers took micro-CT scans of two of those cubs, along with newborn grizzlies, sloth bears, polar bears, dogs, a fox, and other closely related animals from the Smithsonian National Museum of Natural History and the North Carolina State College of Veterinary Medicine. They used the scans to create 3-D digital models of each baby's bony interior at birth. As a baby animal grows and develops inside the womb, its bones and teeth do also. The researchers examined the degree of ossification, or how much the skeleton has formed by the time of birth.

Multiple Distinct Psychiatric Diseases Share Common Genetic Structure, According to Large MGH Study Published in Cell; Results May Provide New Clues for Treatment and Prevention of Psychiatric Disorders

Many distinct psychiatric diseases share a common genetic structure, according to new research by scientists at Massachusetts General Hospital (MGH) and the Psychiatric Genomics Consortium, an international team of investigators. Psychiatric disorders affect more than 25 percent of the population in a given year. In the largest-ever study of its kind, published in the December 12, 2019 issue of Cell, researchers identified more than 100 genetic variants that affect the risk for more than one mental health condition. The article is titled “Genomic Relationships, Novel Loci, and Pleiotropic Mechanisms Across Eight Psychiatric Disorders.” A gene is made up of segments of DNA; an alteration in the DNA sequence produces a gene variant, which can increase or decrease the risk for disease. Many individual gene variants that affect the risk for specific psychiatric disorders have been identified. However, genes are often pleiotropic, meaning they produce multiple effects in the body. Identifying gene variants that influence the risk for more than one psychiatric disorder is an important step toward improving the diagnosis and treatment of these conditions, says the study’s senior author, Jordan W. Smoller, MD, ScD, Director of MGH’s Psychiatric and Neurodevelopmental Genetics Unit and a Professor of Psychiatry at Harvard Medical School (HMS). “Understanding how specific genetic variations may contribute to a broad spectrum of illnesses can tell us something about the degree to which these disorders may have a shared biology,” says Dr. Smoller. To identify these multi-purpose gene variants, the researchers used a technique called genome-wide association to analyze genetic data from 494,162 healthy control subjects and 232,964 people diagnosed with at least one of eight common psychiatric disorders.

November 26th

Multiple Sclerosis (MS) Linked to HHV-6A Variant of Common Herpes Virus Through New Method

Researchers at Karolinska Institutet in Sweden have developed a new method to distinguish between two different types of a common herpes virus (HHV-6) that has been linked to multiple sclerosis (MS). By analyzing antibodies in the blood against the two most divergent proteins of herpesvirus 6A and 6B, the researchers were able to show that MS patients carry the herpesvirus 6A to a greater extent than healthy individuals. The findings, published online on November 26, 2019 in Frontiers in Immunology, point to a role for HHV-6A in the development of MS, which is an autoimmune disease that affects the central nervous system. The open-access article is titled “Increased Serological Response Against Human Herpesvirus 6A Is Associated with Risk for Multiple Sclerosis.” The cause of MS is unclear, but one plausible explanation is that a virus stimulates the immune system to attack the body's own tissue. Human herpesvirus 6 (HHV-6) has previously been associated with MS, but, in those studies, it wasn't possible to distinguish between 6A and 6B. Through virus isolation from ill individuals, researchers have been able to show that HHV-6B can cause mild conditions such as roseola in children, but it has been unclear if HHV-6A is the cause of any disease. According to estimates, as many as 80 percent of all children are infected with the HHV-6 virus before 2 years of age, and many also carry protection in the form of antibodies against this particular virus for the rest of their lives. But because it hasn't been possible to tell the two variants apart post-infection, it has been difficult to say whether HHV-6A or B is a risk factor for MS.

November 24th

Study in Green Monkeys Suggests That Wound Healing Mechanism in Mucous Tissues Might Help Ward Off Development of AIDS

Wound healing events in mucous tissues during early infection by simian immunodeficiency virus (SIV), guard some primate species against developing AIDS, a recent study has learned. The research looked at why certain species can carry the virus throughout their lives, and still avoid disease progression. SIV is closely related to the human immunodeficiency virus (HIV). It is used as a laboratory model for many studies seeking AIDS and HIV cures and preventions. Despite effective treatments to manage HIV, the virus remains a major global health threat. Approximately 37.9 million people in the world are living with an HIV infection. Each year approximately 770,000 people die of AIDS. As yet, there are no clinically available vaccines against HIV, or cures for the infection. In this latest study, reported online on November 8, 2019 in Nature Communications, scientists sought to uncover, in natural hosts, successful virus-fighting tactics that could inform the design of better antiviral drugs to treat HIV in people. The researchers found that the biological events involved in wound healing of mucosal tissues create an environment inside the body that protects against the destructive consequences of SIV infection. (Mucosal tissues are part of the body's defense against germs.) Aspects of this wound-healing immune response could become targets for developing new therapies to prevent AIDS in people with HIV infections.

November 23rd

Scientists Crack Rabies Virus Weaponry; Elucidate Binding of Virus P-Protein to Host STAT1

Researchers from Monash University and the University of Melbourne, both in Australia, have found a way to stop the rabies virus shutting down the body’s immune defense against it. In doing so, they have solved a key scientific puzzle and have laid the foundation for the development of new anti-rabies vaccines. Rabies kills an estimated 60,000 people a year, most of them in developing countries, overwhelmingly through dog bites. Dr Greg Moseley, from the Monash Biomedicine Discovery Institute (BDI), and Associate Professor Paul Gooley, from the Bio21 Institute were senior authors in the study, published in the November 12, 2019 issue of Cell Reports. The open-access article is titled “Structural Elucidation of Viral Antagonism of Innate Immunity at the STAT1 Interface.” “It’s been known for a long time that many viruses target the human protein STAT1 and related proteins to shut down the host’s immune defences, and it’s also assumed that this is very important for diseases,” Long-term rabies researcher Dr Moseley said. However, it was not known exactly how P-protein ¬– the main ”immune antagonist” of lyssaviruses including the rabies virus – takes hold of STAT1, due to a lack of direct structural data on STAT1 complexes with viral proteins. “The challenge was to produce the key proteins on the viral and host sides in a test tube and keep them stable so we could interrogate the interaction directly; this hadn’t been done before, at least not for the full-size human protein,” Dr Moseley said. The researchers then brought the two proteins together and, using nuclear magnetic resonance spectroscopy, showed the precise regions where the viral protein sticks onto STAT1 and holds onto it to keep it away from locations in the cell where it needs to be to activate the immune response.