VCU Massey study identifies genetic driver of pancreatic cancer

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New research out of VCU Massey Cancer Center suggests that the inactivation of NF1—a gene known as Neurofibromin-1 that holds natural tumor-suppressing functions—could be instrumental in the onset of pancreatic cancer, either in tandem with KRAS mutations, which occur in 85-90% of all pancreatic tumors, or even before any mutations occur in the KRAS gene, in partnership with TP53, the most inactivated tumor suppressor gene in human malignancies.

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In a phase II clinical trial, a research team led by Nilofer Azad, professor of oncology and co-leader of the Kimmel Cancer Center’s Cancer Genetics and Epigenetics Program, and Marina Baretti, the Jiasheng Chair in Hepato-Biliary Cancer at the Kimmel Cancer Center, tested the safety and efficacy of the combination of two drugs: an immunotherapy, nivolumab, and an epigenetic drug, entinostat—a histone deacetylase inhibitor. 

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