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Biomarkers of response to immunotherapy in pancreatic ductal adenocarcinoma (PDAC) with homologous recombination deficiency (HRD)

Background

  • PDAC is associated with a paucity of immune effector cells, low antigenicity, and immunosuppressive factors in the tumor microenvironment (TME). Treatment of unselected PDAC patients with immune checkpoint inhibitors (ICIs) has been ineffective
  • PDAC typically has very low tumor mutation burden levels. When associated with pathogenic BRCA alterations, the TMB levels are almost three-fold higher than in tumors with wild-type BRCA. Thus, the subset of BRCA-mutant PDAC exhibits a molecular profile associated with response to ICI therapy (1,2)
  • Recent data from the TAPUR trial and other retrospective reports show a 14-42% objective response rate to dual PD1/CTLA4 ICI therapy in PDAC patients with pathogenic mutations in HRD genes – Both germline and somatic (3,4)
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