Myeloid-derived suppressor cells and pancreatic cancer: Implications in novel therapeutic approaches

Anita Thyagarajan, Mamdouh Salman A. Alshehri, Kelly L.R. Miller, Catherine M. Sherwin, Jeffrey B. Travers, Ravi P. Sahu

Research output: Contribution to journalReview article

Abstract

Pancreatic ductal adenocarcinoma (PDAC) remains a devastating human malignancy with poor prognosis and low survival rates. Several cellular mechanisms have been linked with pancreatic carcinogenesis and also implicated in inducing tumor resistance to known therapeutic regimens. Of various factors, immune evasion mechanisms play critical roles in tumor progression and impeding the efficacy of cancer therapies including PDAC. Among immunosuppressive cell types, myeloid-derived suppressor cells (MDSCs) have been extensively studied and demonstrated to not only support PDAC development but also hamper the anti-tumor immune responses elicited by therapeutic agents. Notably, recent efforts have been directed in devising novel approaches to target MDSCs to limit their effects. Multiple strategies including immune-based approaches have been explored either alone or in combination with therapeutic agents to target MDSCs in preclinical and clinical settings of PDAC. The current review highlights the roles and mechanisms of MDSCs as well as the implications of this immunomodulatory cell type as a potential target to improve the efficacy of therapeutic regimens for PDAC.

Original languageEnglish (US)
Article number1627
JournalCancers
Volume11
Issue number11
DOIs
StatePublished - Nov 2019
Externally publishedYes

Keywords

  • Myeloid-derived suppressor cells
  • Pancreatic cancer
  • Pancreatic cancer therapies

ASJC Scopus subject areas

  • Oncology
  • Cancer Research

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    Thyagarajan, A., Alshehri, M. S. A., Miller, K. L. R., Sherwin, C. M., Travers, J. B., & Sahu, R. P. (2019). Myeloid-derived suppressor cells and pancreatic cancer: Implications in novel therapeutic approaches. Cancers, 11(11), [1627]. https://doi.org/10.3390/cancers11111627