Homologous recombination-DNA damage response defects increase TMB and neoantigen load, but not effector T cell density and clonal diversity in pancreatic cancer

Homologous recombination-DNA damage response defects increase TMB and neoantigen load, but not effector T cell density and clonal diversity in pancreatic cancer

Abstract Pancreatic ductal adenocarcinoma (PDAC) is highly resistant to chemotherapy. However, PDAC with germline BRCA mutations, which lead to homologous recombination (HR) deficiency (HRD), demonstrated an increased sensitivity to platinum-based chemotherapy regimens. This increased chemosensitivi...

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Bibliographic Details
Main Authors: Mengyue Lei, Jessica Gai, Thomas J. McPhaul, Huijuan Luo, Penghui Lin, Dongbing Liu, Michael Pishvaian, Nicholas J. Roberts, Kui Wu, Jin He, Lei Zheng
Format: Article
Language:English
Published: BMC 2025-06-01
Series:Experimental Hematology & Oncology
Subjects:
Pancreatic ductal adenocarcinoma (PDAC)
Homologous recombination-DNA damage response defects
Tumor mutation burden (TMB)
T cell infiltration
T cell clonal diversity
Immune checkpoint inhibitors
Online Access:https://doi.org/10.1186/s40164-025-00673-0
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https://doi.org/10.1186/s40164-025-00673-0

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