Clinical OMICS

SEP-OCT 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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www.clinicalomics.com September/October 2018 Clinical OMICs 5 Game Theory Can Improve Outcomes for Cancer Patients Physicians wanting to improve patient outcomes beyond tra- ditional standard of care ought to view treating people with cancer as a game, say researchers from Moffitt Cancer Center and Maastricht University. Oncol- ogists stand a better chance against cancer by developing flexible strategic treatment plans rather than relying on standard of care. "Physicians can exploit the advantages inherent in the asymmetries of the can- cer treatment game, and likely improve outcomes, by adopting more dynam- ic treatment protocols that integrate eco-evolutionary dynamics and mod- ulate therapy accordingly," Robert A. Gatenby, M.D., of Moffitt Cancer Center, concluded. Specifically, doctors can pinpoint po- tential flaws in current cancer treatment approaches, by developing new strategies to improve outcomes in patients with metastatic cancer. n Konica Minolta adds Niederhuber as Chair of SAB Konica Minolta Precision Medicine, a new company division formed recently with the acquisitions of Ambry Genetics and Invicro, has named John E. Niederhuber, M.D., as the chairman of their Scientific Advisory Board. Since 2010, Neiderhuber has been ex- ecutive vice president and CEO of Inova Translational Medi- cine Institute (TMI) and was recently named President and CEO of the newly formed Ge- nomics and Bioin- formatics Research Institute (GBRI), a joint venture between Inova Health System and the University of Virginia. Previously he served as director of the National Cancer Institute, National In- stitutes of Health. n Reputed Oncogene May Act as a Tumor Suppressor PLK1, or polo-like kinase 1, has long been implicated as an on- cogene. But now, according to researchers from the Spanish Na- tional Cancer Research Centre (CNIO) and the German Cancer Re- search Centre (DKFZ), PLK1 may function not as an oncogene, but as the exact opposite: a tumor suppressor. Initially, the researchers sought to confirm PLK1's oncogen- ic nature. They modified the genome of a mouse so that it was possible to overexpress the PLK1 gene at will. The first thing they noticed was that mice in which PLK1 was overexpressed did not develop any more tumors than did normal mice. The researchers also crossed their mice with others that ex- pressed the oncogenes H-Ras or HER2, oncogenes associated with very aggressive breast tumors. The researchers expected a much greater incidence of can- cer, but the result was unexpected: by overexpressing PLK1 together with the oncogenes, the incidence of tumors was re- duced drastically. If PLK1 can act as a tumor suppressor, does that call into ques- tion therapeutic strategies that are based on the inhibition of Plk1? Not necessarily, concludes the CNIO/DKFZ team. "Many essential components of cell proliferation may be used as cancer targets despite having no oncogenic activity," they explained in their paper which appeared in Nature Communications, "owing to the non-oncogene addiction of cancer cells for specific cellular processes such as cell division. n Andrey Danilovich / Getty Images Tetra Imagesy / Getty Images Wikimedia Commons

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