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Monoclonal and Polyclonal Antibodies Research / HER2/EGFR in Cancer Research · Journal article
Cancer Biome and Targeted Therapy · August 12, 2026
A consensus or society position rather than new primary data.
This narrative review integrates current understanding of oncogenic KRAS as both an oncogenic driver and regulator of the tumor-immune microenvironment across non-small cell lung cancer, colorectal cancer, and pancreatic cancer. It synthesizes emerging evidence on KRAS-derived neoantigens, direct KRAS inhibitors (sotorasib, adagrasib), and adaptive resistance mechanisms, and proposes that combination strategies integrating KRAS-targeted therapy with immune checkpoint blockade and immunomodulatory approaches may be necessary to overcome resistance.
Journal article. Patients with KRAS-mutant non-small cell lung cancer, colorectal cancer, and pancreatic ductal adenocarcinoma.
KRAS mutations regulate antigen presentation, inflammatory signaling, metabolic adaptation, stromal remodeling, and responsiveness to immunotherapy. KRAS-derived neoantigens can be targeted through T-cell receptor-engineered therapies, bispecific antibodies, and therapeutic vaccines. Direct KRAS inhibitors sotorasib and adagrasib have demonstrated meaningful antitumor activity but are limited by adaptive resistance mechanisms.
No primary efficacy or safety data provided; specific response rates, survival outcomes, or hazard ratios not stated.
Clinicians should consider combination approaches pairing KRAS inhibitors with immunotherapy or immune checkpoint blockade in KRAS-mutant cancers; the review supports a shift from single-agent KRAS targeting to multi-modal strategies guided by biomarkers and immune profiling.
A narrative review synthesizing current knowledge on KRAS biology, immunology, and therapeutic strategies across cancer types, offering a conceptual framework and recommendations for future combination approaches rather than reporting new empirical data.
Clinicians should consider combination approaches pairing KRAS inhibitors with immunotherapy or immune checkpoint blockade in KRAS-mutant cancers; the review supports a shift from single-agent KRAS targeting to multi-modal strategies guided by biomarkers and immune profiling.
Graded across the dimensions that decide whether you should act, each from what the source actually supports. There is no single score, and where a dimension was not assessed it says so.
What is missing. This record has no reported figures. That is a gap in the analysis, not a judgement about the study.
KRAS mutations are among the most prevalent oncogenic drivers in human malignancies and are increasingly recognized as critical determinants of tumor progression, immune evasion, and therapeutic resistance. Beyond its canonical role in promoting oncogenic signaling, accumulating evidence indicates that KRAS functions as a regulator of the tumor immune microenvironment, influencing antigen presentation, inflammatory signaling, metabolic adaptation, stromal remodeling, and responsiveness to immunotherapy. This review synthesizes current knowledge regarding the biological and immunological consequences of oncogenic KRAS across major cancer types, including non-small cell lung cancer, colorectal cancer, and pancreatic ductal adenocarcinoma, with emphasis on the mechanisms by which KRAS-driven tumors establish and maintain immunosuppressive microenvironments. Recent advances in immunopeptidomics and precision immuno-oncology have identified KRAS-derived neoantigens that can be targeted through T-cell receptor-engineered therapies, bispecific antibodies, and therapeutic vaccines. Concurrently, the clinical development of direct KRAS inhibitors, including sotorasib and adagrasib, has demonstrated meaningful antitumor activity while revealing adaptive resistance mechanisms that frequently limit durable responses. Emerging evidence suggests that effective therapeutic strategies will require integrating KRAS-targeted therapies with immune checkpoint blockade and other immunomodulatory approaches to overcome tumor-intrinsic and microenvironment-mediated resistance. Collectively, current evidence supports a paradigm in which KRAS functions not only as an oncogenic driver but also as a regulator of tumor-immune interactions, shaping therapeutic responsiveness and providing opportunities for biomarker-guided and combination-based immunotherapy in KRAS-mutant cancers.
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