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Updated: Jan 27, 2026

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KRAS mutations reshape the immunosuppressive tumor microenvironment in triple-negative breast cancer: A novel

Yuanhao Lv1, Ziyin Zhao2, Wenyu Di3

  • 1Department of Pathology, The First Affiliated Hospital of Xinxiang Medical University, Xinxiang, China; Department of Pathology, School of Basic Medical Sciences, Xinxiang Medical University, Xinxiang, China.

Critical Reviews in Oncology/Hematology
|January 25, 2026
PubMed

Insights

KRAS mutations in triple-negative breast cancer (TNBC) remodel the tumor microenvironment (TME), promoting immune suppression and therapeutic resistance. Understanding this KRAS-TME axis offers new strategies for aggressive TNBC treatment.

Area of Science:

  • Oncology
  • Cancer Biology
  • Immunology

Background:

  • Triple-negative breast cancer (TNBC) presents a significant clinical challenge due to its aggressive nature and limited targeted therapies.
  • Current research often overlooks the tumor microenvironment (TME) in TNBC, focusing instead on tumor-intrinsic factors.
  • KRAS mutations, though infrequent in TNBC, are linked to worse prognosis and increased tumor aggressiveness.

Purpose of the Study:

  • To explore the novel role of KRAS mutations in shaping the TME of triple-negative breast cancer.
  • To investigate the potential mechanism involving NADPH oxidase 2 (NOX2) and oxidative stress in KRAS-driven TME modulation.
  • To provide a theoretical framework for developing new therapeutic strategies against aggressive TNBC.

Main Methods:

  • Systematic review of existing literature on KRAS mutations in TNBC.
  • Analysis of the proposed mechanistic link between KRAS mutations, NOX2 activity, and oxidative stress in the TME.
  • Evaluation of the impact on immune cell function and therapeutic resistance.

Main Results:

  • KRAS mutations in TNBC are associated with an immunosuppressive TME and poorer clinical outcomes.
  • The KRAS-TME axis may involve the modulation of NADPH oxidase 2 (NOX2) activity, altering oxidative stress dynamics.
  • This remodeling of the TME by KRAS mutations can impair anti-tumor immunity, leading to immune evasion and treatment resistance.

Conclusions:

  • KRAS mutations play a critical role in the progression of aggressive TNBC by remodeling the TME.
  • The proposed KRAS-NOX2-oxidative stress axis offers a new understanding of immune suppression in TNBC.
  • Targeting this axis presents a promising avenue for novel therapeutic interventions in TNBC.
Keywords:
KRAS mutationNOX2ROSTNBCTumor microenvironment

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