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

Author:

Jamison Jacob K1ORCID,May Michael S2ORCID,Raufi Alexander G3,Luk Lyndon4,Wong Winston5,Mundi Prabhjot S4,Manji Gulam A24

Affiliation:

1. Weill Cornell Medical College , New York, NY , USA

2. Department of Medicine, Vagelos College of Physicians and Surgeons, Columbia University , New York, NY , USA

3. Division of Hematology/Oncology, Department of Medicine, Lifespan Health System and Brown University , Providence, RI , USA

4. Herbert Irving Comprehensive Cancer Center, Vagelos College of Physicians and Surgeons, Columbia University , New York, NY , USA

5. Memorial Sloan Kettering Cancer Center , New York, NY , USA

Abstract

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.

Funder

National Cancer Institute

National Institutes of Health

Publisher

Oxford University Press (OUP)

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5. Core signaling pathways in human pancreatic cancers revealed by global genomic analyses;Jones,2008

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