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The role of the tumor microenvironment and inflammatory pathways in driving drug resistance in gastric cancer: A

Francesco Albano1, Francesca Lospinoso Severini2, Giovanni Calice2

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Biochimica Et Biophysica Acta. Molecular Basis of Disease
|April 9, 2025
PubMed
Summary

The tumor microenvironment (TME) in gastric cancer (GC) promotes chemoresistance and progression. Targeting inflammatory pathways and specific immune cells like TAMs and Tregs offers strategies to improve chemotherapy response.

Keywords:
CytokinesDrug resistanceGastric cancerImmune cellsInflammationTumor microenvironment

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Area of Science:

  • Oncology
  • Immunology
  • Cancer Biology

Background:

  • The tumor microenvironment (TME) is crucial in gastric cancer (GC) progression and chemotherapy resistance.
  • Chronic inflammatory pathway activation is a key event in gastric tumorigenesis.
  • Immune cells within the TME interact with cancer cells, creating an immunosuppressive environment that impacts treatment efficacy.

Purpose of the Study:

  • To explore the role of the TME and inflammatory pathways in gastric cancer.
  • To identify strategies for enhancing patient response to chemotherapy.
  • To provide insights into TME cytotypes and their impact on GC chemoresistance.

Main Methods:

  • Systematic review and discussion of existing literature on TME, inflammation, and GC.
  • Analysis of immune cell infiltration and their interactions within the GC TME.
  • Examination of molecular signatures associated with TME components.

Main Results:

  • The TME significantly influences GC progression and reduces chemotherapy responsiveness.
  • Sustained inflammatory pathway activation is integral to gastric tumorigenesis.
  • Tumor-associated macrophages (TAMs) and regulatory T cells (Tregs) play critical roles in promoting GC chemoresistance.

Conclusions:

  • Understanding the TME and its inflammatory components is essential for improving GC treatment outcomes.
  • Targeting specific TME cytotypes, particularly TAMs and Tregs, presents a promising therapeutic strategy.
  • Modulating the inflammatory status of the TME could overcome chemoresistance in gastric cancer.