Macrophages and therapeutic resistance in cancer

Brian Ruffell1, Lisa M Coussens1

  • 1Department of Cell, Developmental, and Cancer Biology and Knight Cancer Institute, Oregon Health and Science University, Portland, OR 97034.

Cancer Cell
|April 11, 2015
PubMed

Insights

Tumor microenvironment, not just genetics, affects cancer therapy response. Targeting macrophages, key immune regulators, shows promise for improving cancer treatment efficacy and patient survival.

Area of Science:

  • Immunology
  • Oncology
  • Cell Biology

Background:

  • Neoplastic cell response to therapy is influenced by tumor microenvironment dynamics, not solely genomic complexity.
  • Tumor microenvironment plays a critical role in regulating therapeutic efficacy and patient survival.
  • Macrophages are central regulators of tissue homeostasis and tumor microenvironments.

Purpose of the Study:

  • To review molecular and cellular pathways through which macrophages mediate therapeutic responses.
  • To highlight the potential of targeting macrophage pathways to enhance anti-tumor immunity and improve cancer treatment outcomes.
  • To discuss the clinical evaluation of therapeutics that modulate macrophage presence and bioactivity.

Main Methods:

  • Literature review of preclinical and clinical studies.
  • Analysis of molecular and cellular mechanisms involving macrophages in cancer therapy.
  • Synthesis of current research on macrophage-mediated therapeutic responses.

Main Results:

  • Macrophages significantly influence the efficacy of cancer therapies.
  • Targeting macrophage pathways can bolster anti-tumor immune responses.
  • Therapeutics modulating macrophage activity show promise in preclinical models and are under clinical investigation.

Conclusions:

  • Macrophages are critical mediators of therapeutic response in cancer.
  • Modulating macrophage function presents a promising strategy for improving cancer treatment.
  • Further research into macrophage-centric pathways is essential for advancing cancer therapy.

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