Clinical OMICS

JAN-FEB 2018

Healthcare magazine for research scientists, labs, pathologists, hospitals, cancer centers, physicians and biopharma companies providing news articles, expert interviews and videos about molecular diagnostics in precision medicine

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8 Clinical OMICs January/February 2018 News Five Join Strata Precision Oncology Network Precision oncology company Strata On- cology announced the addition of five healthcare systems to the Strata Preci- sion Oncology Network. The network, launched early last year, aims to provide patients with advanced cancer routine tumor profiling with the goal of matching them to active clinical trials. New networks members are University of Wisconsin Carbone Cancer Center, Chris- tiana Care's Helen F. Graham Cancer Center & Research Institute, Kaiser Permanen- te-Northern California, Kettering Health Network, and Ochsner Health System. "With the addition of new partners to the network, we are well on our way to our goal of providing tumor profiling to 25,000 advanced cancer patients annually," said Dan Rhodes, Ph.D., CEO of Strata On- cology. "We are proud to work with these forward-thinking centers to institutionalize tumor profiling and dramatically expand patient access to precision oncology." Network members provide no-cost test- ing to patients using the StrataNGS test, an 87-gene assay that allows for the sequenc- ing of both DNA and RNA. The testing is part of the Strata Trial, a nationwide obser- vational study providing tumor sequencing for 100,000 patients with advanced cancer. "This clinical trial will allow us to offer rou- tine, no-cost tumor sequencing to patients with advanced cancer," said Mark E. Burkard, M.D., Ph.D., associate professor at Universi- ty of Wisconsin. "By addressing key barriers to patient participation, we hope to enable increased access to precision medicine clinical trials." Crick Researchers: Ras Mutations also Boost Tumor Immunoresistance Researchers at the Francis Crick Institute have released new findings to show that Ras genes are not only the driver muta- tion for roughly 25% of all human can- cers, but they also suppress the immune sysem's anticancer response, helping to cloak cancer cells by boosting the expres- sion of the protein programmed death-li- gand 1 (PD-L1). PD-L1, which is ordinarily expressed in small amounts in the body, serves to prevent the immune system from attack- ing healthy cells. But PD-L1 can also be expressed by cancer cells, which use the protein, a so-called checkpoint inhibitor, to avoid coming to the immune system's attention. By revealing the causal link between Ras ROGER HARRIS/SCIENCE PHOTO LIBRARY / Getty Images Caris IDs Mechanism of Aptamer with Potential for Treating Non-Hodgkin Lymphoma Caris Life Sciences reported at the Ameri- can Society of Hematology (ASH) Annual Meeting & Exposition in December that it has identified a new mechanism of ac- tion for an aptamer with potential to treat non-Hodgkin lymphoma (NHL), using the company's proprietary ADAPT Biotarget- ing System. In it research, Caris scientists reported that the single-stranded DNA aptamer C10.36 specifically binds to heterogeneous nuclear ribonucleoprotein U (hnRNP U), a protein that controls pre-mRNA splicing. "The present study identifies cell surface hnRNP U and its ribonucleoprotein interac- tion partners as potential therapeutic tar- gets for NHL and highlights the potential for the development of C10.36 as a novel anti-B cell lymphoma targeted therapy," research- ers from Caris and the University of Bonn, led by Caris' Sonal S. Tonapi, Ph.D., concluded in the study. Study results also showed that C10.36 binding to cell-surface hnRNP U resulted in internalization of the complex, disruption of pre-mRNA splicing and cell death in a subset of NHL cell lines in vitro. The au- thors concluded that the aptamer binds to hnRNP U and kills NHL cells via a novel mechanism of inter- fering with pre-mR- NA splicing. PASIEKA / Getty Images Colin Anderson / Getty Images

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