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Culprits of PDAC resistance to gemcitabine and immune checkpoint inhibitor: Tumour microenvironment components

Sheng-Kai Hsu1,2, Mahendra Jadhao3,4, Wei-Ting Liao1

  • 1Department of Biotechnology, Kaohsiung Medical University, Kaohsiung, Taiwan.

Frontiers in Molecular Biosciences
|October 27, 2022
PubMed

Insights

Pancreatic ductal adenocarcinoma (PDAC) treatment resistance is driven by its complex tumor microenvironment (TME). Understanding TME crosstalk offers new strategies for personalized medicine and drug delivery in PDAC therapy.

Area of Science:

  • Oncology
  • Cancer Biology
  • Immunology

Background:

  • Pancreatic ductal adenocarcinoma (PDAC) has a poor prognosis with a 5-year survival rate of 11%.
  • PDAC exhibits significant resistance to current cancer therapeutics.
  • Key pathological features include a desmoplastic reaction and an immunosuppressive tumor microenvironment (TME).

Purpose of the Study:

  • To review the mechanisms by which the complex PDAC TME influences drug resistance.
  • To summarize current clinical trials targeting PDAC.
  • To explore novel applications of TME and exosome analysis in PDAC treatment.

Main Methods:

  • Literature review of PDAC pathology and treatment resistance.
  • Analysis of the interplay between cellular and noncellular components of the TME.
  • Review of clinical trials and emerging TME-based therapeutic strategies.

Main Results:

  • The PDAC TME, comprising diverse cells and extracellular matrix, creates a complex barrier to treatment.
  • Crosstalk between TME components significantly modulates resistance to chemotherapy and immune checkpoint inhibitors.
  • Exosome analysis presents potential for disease monitoring and drug delivery.

Conclusions:

  • Targeting the PDAC TME is crucial for overcoming treatment resistance.
  • TME exploration and exosome analysis offer promising avenues for personalized PDAC medicine.
  • Further research into TME modulation could improve therapeutic outcomes for PDAC patients.
Keywords:
ICI resistancechemoresistancedesmoplasiaimmunomodulationpancreatic ductal adenocarcinomatumour microenvironment

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