Abstract
Background: Efforts to characterize the mutational landscape in pancreatic cancer have revealed almost ubiquitous activating mutation of KRAS, high incidence of inactivation of TP53, SMAD4, CDKN2A and KDM6A but a very low prevalence of currently actionable targets. However, patients with high genomic instability suggesting defective DNA maintenance (up to 20%) show high response rate to platinum agents with or without PARP inhibition. While no more than 5% of patients harbor germline BRCA1/2 inactivation, molecular alterations in other genes related to homologous recombination are also found in these pancreatic tumors. These observations support the concept of BRCAness in pancreatic cancer, where tumors showing traits of defective homologous recombination (HR) even in the absence of BRCA1/2 deficiency are associated with exquisite sensitivity to DNA-damaging agents. This study seeks to identify new molecular determinants of BRCAness in Pancreatic cancer and what assay constitutes the best predicator of a favorable response to therapeutic targeting HR defects.
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