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Peer-reviewedCC BY-NC-ND 4.0BMC Medicine

Current and emerging strategies to enhance chemotherapeutic efficacy in pancreatic ductal adenocarcinoma

  • David Hackett1,2
  • Laura E. Kane1,2
  • Adriele Prina-Mello2,3
  • Stephen G. Maher1,2
  1. 1Discipline of Surgery, School of Medicine, Trinity Translational Medicine Institute, Trinity College Dublin, Dublin, Ireland
  2. 2Trinity St. James’s Cancer Institute, Trinity College Dublin, Dublin, Ireland
  3. 3Nanomedicine Group and Laboratory for Biological Characterisation of Advanced Materials (LBCAM), Department of Clinical Medicine, Trinity Translational Medicine Institute, Trinity College Dublin, Dublin, Ireland
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Abstract

Background: Pancreatic cancer remains one of the most aggressive solid malignancies. The majority of patients present with locally advanced or metastatic disease, limiting treatment options to systemic chemotherapy. Conventional chemotherapy forms the backbone of the standard-of-care regimen and offers modest but significant survival benefits.

Main body: This review discusses currently established standard-of-care regimens and cutting edge clinical trials which aim to enhance chemotherapy efficacy in pancreatic cancer. Pancreatic cancer’s distinct pathological features—including its high metastatic potential, inherent chemoresistance, dense desmoplastic stroma, and profoundly immunosuppressive tumour microenvironment—underscore the rationale for the clinical development of chemosensitizing agents. As mechanisms of chemoresistance continue to be uncovered, new therapeutic avenues are emerging that aim to enhance the efficacy of chemotherapy. Emerging targets including KRAS, MTAP, EGFR, Claudin 18.2, and WEE1, which present unique vulnerabilities for rational combination therapies, are discussed.

Conclusion: Given the central role of chemotherapy in pancreatic cancer treatment, ongoing clinical strategies that improve its efficacy are essential to achieving better outcomes for patients.

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Cite

BibTeXRIS
BibTeX
@article{hackett2026current,
  title = {{Current and emerging strategies to enhance chemotherapeutic efficacy in pancreatic ductal adenocarcinoma}},
  author = {David Hackett and Laura E. Kane and Adriele Prina-Mello and Stephen G. Maher},
  journal = {BMC Medicine},
  year = {2026},
  month = aug,
  doi = {10.1186/s12916-026-05134-x},
  url = {https://doi.org/10.1186/s12916-026-05134-x},
  note = {CC BY-NC-ND 4.0},
}
RIS
TY  - JOUR
TI  - Current and emerging strategies to enhance chemotherapeutic efficacy in pancreatic ductal adenocarcinoma
AU  - David Hackett
AU  - Laura E. Kane
AU  - Adriele Prina-Mello
AU  - Stephen G. Maher
PY  - 2026
DA  - 2026/08/11
JO  - BMC Medicine
DO  - 10.1186/s12916-026-05134-x
UR  - https://doi.org/10.1186/s12916-026-05134-x
AB  - Background: Pancreatic cancer remains one of the most aggressive solid malignancies. The majority of patients present with locally advanced or metastatic disease, limiting treatment options to systemic chemotherapy. Conventional chemotherapy forms the backbone of the standard-of-care regimen and offers modest but significant survival benefits.  Main body: This review discusses currently established standard-of-care regimens and cutting edge clinical trials which aim to enhance chemotherapy efficacy in pancreatic cancer. Pancreatic cancer’s distinct pathological features—including its high metastatic potential, inherent chemoresistance, dense desmoplastic stroma, and profoundly immunosuppressive tumour microenvironment—underscore the rationale for the clinical development of chemosensitizing agents. As mechanisms of chemoresistance continue to be uncovered, new therapeutic avenues are emerging that aim to enhance the efficacy of chemotherapy. Emerging targets including KRAS, MTAP, EGFR, Claudin 18.2, and WEE1, which present unique vulnerabilities for rational combination therapies, are discussed.  Conclusion: Given the central role of chemotherapy in pancreatic cancer treatment, ongoing clinical strategies that improve its efficacy are essential to achieving better outcomes for patients.
SN  - 1741-7015
ER  -