DNA repair deficiency association with prognosis in pancreatic cancer: A single-institution experience.

Abstract

e15798 Background: Understanding survival outcomes of various pathogenic mutations helps guide treatment decision making for patients. Classic pancreatic cancer mutations such as KRAS and TP53 have well documented survival outcomes while other mutations leading to DNA repair deficiency do not have well understood survival outcomes. Methods: We retrospectively evaluated survival outcomes of 70 pancreatic cancer patients who had their cancers genetically profiled by NGS methods. Patients with DNA repair deficiency harbored mutations in genes such as BRCA1 (1 Pts), BRCA2 (8 Pts), ATM (5 Pts), NBN (1 Pt), and BRIP1 (1 Pt). We compared baseline characteristics, tumor stage and clinical outcomes between patients with DNA repair deficiency versus DNA repair proficient cancer patients. Comparative survival analysis between the two groups was performed using Kaplan-Meir methods. Results: Baseline characteristics for all patients are recorded in (Table). Median OS is 24 months for DNA repair proficient group and 20 months for DNA repair deficient group. A comparison of Kaplan-Meir survival curves between the two groups yielded a p-value of 0.72. This is most likely due to sample size and different chemotherapy regimens which make it hard to retrospectively compare patient groups. Conclusions: Patients with mutated DNA repair genes did not have significantly worse survival. We are designing a clinical trial utilizing a PARP inhibitor, for these patients in order to better control for all factors in order to better ascertain any survival differences between the two groups. PARP inhibitor will create multiple single strand breaks which cancer cells deficient in DNA repair genes cannot repair and thus trigger cancer cell death[Table: see text]