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Stress Signature Score and Molecular Subtypes in Bulk Tumor Samples

Abstract

Viola Paulus*

Pancreatic ductal adenocarcinoma (PDAC), the more common form of pancreatic cancer (PC), is dominated by mutations in four well-known cancer genes (KRAS, TP53, CDKN2A, and SMAD4). Pancreatic cancer (PC) has recently overtaken breast cancer to become the third leading cause of cancer death in the United States1, and it is predicted to become the second leading cause within a decade. Biomarkers that predict response to novel and established treatments are urgently needed and must extend beyond the detection of point mutations in coding genes and low-prevalence actionable genomic events in order to better select patients for clinical trials. This diversity may explain the lack of progress with targeted therapies because actionable genomic events being targeted therapeutically are present in only a small proportion of unselected participants in clinical trials. To better select patients for clinical trials, biomarkers that predict response to novel and established treatments must extend beyond the detection of point mutation

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