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Cited by 44Pancreatic and Hepatic Oncology ResearchBRCA gene mutations in cancerPARP inhibition in cancer therapy

Pancreas cancer and BRCA : A critical subset of patients with improving therapeutic outcomes

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Momtaz, Parisa, O’Connor, Catherine A., Chou, Joanne F., Capanu, Marinela, Park, Wungki, Bandlamudi, Chaitanya, Berger, Michael F., Kelsen, David P. +16 more·2021·Cancer
DOI 10.1002/cncr.33812PMC PMC9301324
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Abstract

Background: Patients with germline/somatic BRCA1/BRCA2 mutations (g/s BRCA1/2 ) comprise a distinct biologic subgroup of pancreas ductal adenocarcinoma (PDAC). Methods: Institutional databases were queried to identify patients who had PDAC with g/s BRCA1/2 . Demographics, clinicopathologic details, genomic data (annotation s BRCA1/2 according to a precision oncology knowledge base for somatic mutations), zygosity, and outcomes were abstracted. Overall survival (OS) was estimated using the Kaplan‐Meier method. Results: In total, 136 patients with g/s BRCA1/2 were identified between January 2011 and June 2020. Germline BRCA1/2 (g BRCA1/2 ) mutation was identified in 116 patients (85%). Oncogenic somatic BRCA1/2 (s BRCA1/2 ) mutation was present in 20 patients (15%). Seventy‐seven patients had biallelic BRCA1/2 mutations (83%), and 16 (17%) had heterozygous mutations. Sixty‐five patients with stage IV disease received frontline platinum therapy, and 52 (80%) had a partial response. The median OS for entire cohort was 27.6 months (95% CI, 24.9‐34.5 months), and the median OS for patients who had stage IV disease was 23 months (95% CI, 19‐26 months). Seventy‐one patients received a poly(adenosine diphosphate ribose) polymerase (PARP) inhibitor (PARPi), and 52 received PARPi monotherapy. For maintenance PARPi, 10 patients (36%) had a partial response, 12 (43%) had stable disease, and 6 (21%) had progression of disease as their best response. Six patients (21%) received maintenance PARPi for >2 years. For those with stage IV disease who received frontline platinum, the median OS was 26 months (95% CI, 20‐52 months) for biallelic patients (n = 39) and 8.66 months (95% CI, 6.2 months to not reached) for heterozygous patients (n = 4). The median OS for those who received PARPi therapy was 26.5 months (95% CI, 24‐53 months) for biallelic patients (n = 25) and 8.66 months (95% CI, 7.23 months to not reached) for heterozygous patients (n = 2). Conclusions: g/s BRCA1/2 mutations did not appear to have different actionable utility. Platinum and PARPi therapies offer therapeutic benefit, and very durable outcomes are observed in a subset of patients who have g/s BRCA1/2 mutations with biallelic status.

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  • Recent studies show that PDAC patients with de novo somatic BRCA1/2 and PALB2 mutations also benefit from PARP inhibitors if there is bi-allelic loss and established homologous repair deficiency.

    “More recent studies have demonstrated that, in addition to patients with germline mutations, those harboring de novo somatic mutations of BRCA1/2 and PALB2 also show benefit from PARP inhibitors, provided there is bi-allelic loss and established homologous repair deficiency in the tumors89.”

    From Pancreatic cancer: Advances and challenges (2023) · cites this paper as [89]

  • The comparison of outcomes between screen-detected PDAC and PDAC diagnosed after dropping out of surveillance is worthwhile because these groups have similar demographic/risk characteristics, but the number of such cases was small.

    “Comparing outcomes of those diagnosed with a screen-detected PDAC to those whose PDAC was diagnosed after dropping out of surveillance is worthwhile because these groups have similar demographic/risk characteristics, and for whom data on pancreatic cancer outcomes is limited,41-43 but the number of such cases was small.”

    From The Multicenter Cancer of Pancreas Screening Study: Impact on Stage and Survival (2022) · cites this paper as [41]

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Authors
Momtaz, P., O’Connor, C. A., Chou, J. F., Capanu, M., Park, W., Bandlamudi, C., Berger, M. F., Kelsen, D. P., Suehnholz, S. P., Chakravarty, D., Yu, K. H., Varghese, A. M., Zervoudakis, A., Li, J., Ku, G. Y., Park, J. S., Shcherba, M., Harding, J. J., Goldberg, Z., Abou‐Alfa, G. K., Salo‐Mullen, E. E., Stadler, Z. K., Iacobuzio‐Donahue, C. A., & O’Reilly, E. M.
Affiliations
  • Memorial Sloan Kettering Cancer Center (US)
  • Department of Medicine Memorial Sloan Kettering Cancer Center New York New York
  • Department of Pathology Memorial Sloan Kettering Cancer Center New York New York
ORCID
Venue
Cancer
Publisher
Wiley
Published
2021-08-05
Volume
127
Issue
23
Pages
4393-4402
ISSN
  • 0008-543X (ISSN-L)
  • 1097-0142
DOI
10.1002/cncr.33812
PMC
PMC9301324
OpenAlex
W3192055652
Cited by
44
References
42
Citations by year
2026: 5 · 2025: 8 · 2024: 10 · 2023: 12 · 2022: 9
FWCI
2.82
Type
journal article
Language
en
Open access
Licence
onlinelibrary.wiley.com/termsAndConditions#vor (vor)
Locations
  • Cancer (publishedVersion)
  • PubMed (publishedVersion)
  • PubMed Central (acceptedVersion)
Funders
National Cancer Institute (P30 CA008748)
Topics
  • Health Sciences › Medicine › Oncology › Pancreatic and Hepatic Oncology Research
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › BRCA gene mutations in cancer
  • Health Sciences › Medicine › Oncology › PARP inhibition in cancer therapy
Keywords
pancreatic ductal adenocarcinoma, BRCA mutations, PARP inhibitors, platinum-based chemotherapy, overall survival, stage IV disease, maintenance therapy, zygosity, treatment response, precision oncology, targeted therapy
MeSH terms
Poly(ADP-ribose) Polymerase Inhibitors, Humans, Ovarian Neoplasms, Pancreatic Neoplasms, Treatment Outcome, Germ-Line Mutation, BRCA1 Protein, Carcinoma, Pancreatic Ductal, BRCA2 Protein, Precision Medicine

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