Syndicate content

Archive - Nov 23, 2014


Four Gene Loci Newly Identified for Severe Food Allergy

Scientists have identified four gene loci newly associated with the severe food allergy eosinophilic esophagitis (EoE). Because the genes appear to have roles in other allergic diseases and in inflammation, the findings may point toward potential new treatments for EoE. "This research adds to the evidence that genetic factors play key roles in EoE, and broadens our knowledge of biological networks that may offer attractive targets for therapy," said study leader Hakon Hakonarson (image), M.D., Ph.D., director of the Center for Applied Genomics at The Children's Hospital of Philadelphia (CHOP). Dr. Hakonarson and colleagues from other hospitals and academic centers published the study online on November 19, 2014 in Nature Communications. The research builds on a 2010 study by Dr. Hakonarson and colleagues that identified TSLP (thymic stromal lymphopoietin ) as the first major gene associated with EoE. Only recently recognized as a distinct condition, EoE has been rapidly increasing in prevalence over the past 20 years. Its hallmark is inflammation and painful swelling in the esophagus, along with high levels of immune cells called eosinophils. It can affect people of any age, but is more common among young men who have a history of other allergic diseases such as asthma and eczema. EoE is often first discovered in children with feeding difficulties and failure to thrive. Because children with EoE are often allergic to many foods, they may be placed on a highly-restricted diet containing no large food proteins, to allow time for their symptoms to resolve. Physicians then perform tests to determine which foods a child can or cannot eat.

Winners of the 2014 Life Science Industry Awards Announced

On Tuesday, November 18, winners of the 2014 Life Science Industry Awards® were formally announced at the Grand Hyatt Washington in Washington, D.C. The Life Science Industry Awards recognize those life science suppliers that are best-in-class in 28 product and service categories. The awards were presented by BioInformatics LLC, considered by many to be the premier market research and advisory firm serving the life science industry. The event was attended by industry executives and product and marketing professionals from 41 life science companies Using industry best-practices market research methodologies, almost 6,000 scientists were surveyed to reveal preferred suppliers in 28 product, communications, and support categories. These scientists were drawn from BioInformatics LLC’s online panel of scientists, The Science Advisory Board®. From the data collected, BioInformatics LLC analysts calculated an overall score for each nominated company based on the number of nominations received, as well as key measurements of customer satisfaction and loyalty. “The vision and foresight of the companies we honored last night have made possible many of the scientific advances of the past decade,” said Jennifer Cotteleer, CEO of BioInformatics LLC.

Histone Variant H3.3 and Its Clipped Version (H3.3cs1) May Promote Senescence and Limit Abnormal Cell Growth in Tumors

Changes to the structure of the histone variant H3.3 may play a key role in silencing genes that regulate cancer cell growth, according to a study led by researchers from the Icahn School of Medicine, Mount Sinai Hospital, in New York City. The results were published online on November 14, 2014 in Nature Communications. According to the authors, this is the first study to identify H3.3 as a key regulator in cellular senescence, a process in which cells stop multiplying. Cellular senescence has garnered significant scientific interest lately because it may be one key to prevent the initiation of cancer. However, little is known about this process and how genes that enable cells to divide and multiply (the cell cycle) are turned off. A growing body of evidence suggests that the process of cellular senescence is driven by changes in the protein complexes called chromatin in the nuclei of cells. Using models of senescence, researchers found that histone variant H3.3, a protein that works closely with chromatin to package and regulate genetic material within cells, and, in particular, the clipped form of this protein, H3.3cs1, help to silence target genes that regulate the cell cycle. Could the presence of this protein stop cells from dividing? Indeed, using genome-wide transcriptional profiling, the researchers discovered that expression of clipped H3.3 (i.e., 3.3cs1) silences genes that regulate the division and duplication of a cell. "Cellular senescence creates a chromatin environment that represses cell multiplication, and thus cell or tumor growth, but how this happens molecularly is what we sought to discover," said lead investigator Emily Bernstein, Ph.D., Department of Oncological Sciences, Icahn School of Medicine, Mount Sinai Hospital.