A Somatic BRCA2-Mutated Pancreatic Adenocarcinoma With Sustained Exceptional Response to Modified FOLFIRINOX

Oncologist. 2024 Apr 4;29(4):350-355. doi: 10.1093/oncolo/oyad315.

Abstract

Homologous recombination repair (HRR) pathway deficiency opens multiple therapeutic avenues within pancreatic cancer. Patients with HRR deficiency-associated gene mutations such as BRCA1, BRCA2, and PALB2 are more susceptible to platinum-based chemotherapies and in those with somatic BRCA mutations, PARP inhibitor therapy prolongs progression-free survival. The case discussed herein illustrates the therapeutic opportunities offered through the identification of HRR deficiency in pancreatic cancer, as well as the challenges associated with treatment and prevention of central nervous system metastases in long-term survivors of pancreatic cancer.

Keywords: homologous recombination deficiency; pancreatic cancer; precision medicine.

MeSH terms

  • Adenocarcinoma* / drug therapy
  • Adenocarcinoma* / genetics
  • Antineoplastic Combined Chemotherapy Protocols / therapeutic use
  • BRCA1 Protein / genetics
  • BRCA2 Protein / genetics
  • Cancer Survivors*
  • Fluorouracil
  • Humans
  • Irinotecan
  • Leucovorin
  • Oxaliplatin
  • Pancreatic Neoplasms* / drug therapy
  • Pancreatic Neoplasms* / genetics

Substances

  • folfirinox
  • BRCA2 Protein
  • BRCA1 Protein
  • BRCA2 protein, human
  • Irinotecan
  • Oxaliplatin
  • Leucovorin
  • Fluorouracil