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[New Progress in the Relationship between Immune Cells, PD-1 
in Tumor Microenvironment and the Efficacy of EGFR-TKIs]

Shiyang Yuan1, Hui Xu1, Junping Xie1

  • 1Department of Respiratory and Critical Care Medicine, the Second Affiliated Hospital of Nanchang University, 
Nanchang 330006, China.

Zhongguo Fei AI Za Zhi = Chinese Journal of Lung Cancer
|November 24, 2017
PubMed

Insights

Epidermal growth factor receptor-tyrosine kinase inhibitors (EGFR-TKIs) are effective for non-small cell lung cancer (NSCLC) with EGFR mutations, but drug resistance emerges. This review explores how tumor microenvironment immune cells and PD-1 signaling contribute to EGFR-TKI resistance in NSCLC.

Area of Science:

  • Oncology
  • Immunology
  • Pharmacology

Background:

  • Epidermal growth factor receptor-tyrosine kinase inhibitors (EGFR-TKIs) are a primary treatment for advanced non-small cell lung cancer (NSCLC) with EGFR mutations.
  • Acquired resistance to EGFR-TKIs is a significant clinical challenge, limiting long-term patient benefit.
  • The tumor microenvironment, including immune cells and signaling pathways, plays a crucial role in cancer progression and treatment response.

Purpose of the Study:

  • To review the mechanisms by which immune cells within the tumor microenvironment contribute to EGFR-TKI drug resistance in NSCLC.
  • To investigate the potential role of the programmed cell death receptor 1 (PD-1) pathway in mediating resistance to EGFR-TKIs.
  • To identify novel therapeutic targets for overcoming EGFR-TKI resistance and improving anti-tumor efficacy.

Main Methods:

  • Literature review of studies investigating EGFR-TKIs, NSCLC, tumor microenvironment, immune cells, and PD-1/PD-1L signaling.
  • Analysis of preclinical and clinical data on the interplay between immune components and EGFR-TKI efficacy.
  • Synthesis of current understanding regarding resistance mechanisms.

Main Results:

  • The tumor microenvironment harbors various immune cells (e.g., regulatory T cells, dendritic cells, macrophages) that can influence EGFR-TKI sensitivity.
  • Immune checkpoints, such as the PD-1/PD-1L axis, are implicated in the development of resistance to EGFR-TKIs in NSCLC.
  • Cross-talk between immune cells and cancer cells within the tumor microenvironment can promote survival and proliferation despite targeted therapy.

Conclusions:

  • Understanding the complex interactions within the tumor microenvironment is critical for addressing EGFR-TKI resistance in NSCLC.
  • Targeting immune cells and pathways like PD-1/PD-1L may offer new strategies to enhance the effectiveness and duration of EGFR-TKI therapy.
  • Further research into immune-mediated resistance mechanisms could lead to improved treatment outcomes for NSCLC patients.
Keywords:
EGFR-TKIsImmune cellsLung neoplasmsProgramed cell death protein 1Targeted therapyTumor microenvironment

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