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Peer-reviewedCC BY-NC-ND 4.0Medical Oncology (Northwood, London, England)

Cancer-associated fibroblasts and immune evasion in endometrial cancer: current evidence and therapeutic perspectives

  • Jie Zhan1
  • Zhuqing Yan2
  • Zhu Cao2
  • Fan Wu1
  • Yinfeng Wang2
  • Yaying Zhan2
  1. 1Traditional Chinese Medicine College, Anhui University of Chinese Medicine, Hefei, 230012 China
  2. 2Department of Gynecology, Women’s Hospital, Zhejiang University School of Medicine, Hangzhou, 310006 China
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Abstract

Cancer-associated fibroblasts (CAFs) are potential contributors to tumor progression and immune resistance in endometrial cancer (EC), but the extent of EC-specific mechanistic and therapeutic evidence remains uneven. Studies using EC-derived fibroblasts support tumor-promoting paracrine activity and provide experimental evidence of altered natural killer cell function. Single-cell and spatial analyses further characterize stromal heterogeneity and candidate intercellular interactions. However, many proposed mechanisms of CAF-mediated immune exclusion and most CAF-directed therapeutic strategies are informed by studies in other malignancies. This review distinguishes findings obtained in EC patient samples and experimental models from evidence extrapolated from pancreatic, breast, gastric, and other cancers. We examine CAF heterogeneity, soluble signaling, matrix remodeling, and immune-cell interactions, while identifying where functional validation in EC is still required. Therapeutic approaches, including FAP-directed interventions, stromal reprogramming, and signaling blockade combined with immune checkpoint inhibition, are discussed as candidate research strategies rather than established EC treatments. Priorities include validating CAF-immune mechanisms in EC, developing reproducible stromal biomarkers, and testing treatment combinations in appropriate disease-specific models and clinical studies.

Graphical abstract:

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Cite

BibTeXRIS
BibTeX
@article{zhan2026cancerassociated,
  title = {{Cancer-associated fibroblasts and immune evasion in endometrial cancer: current evidence and therapeutic perspectives}},
  author = {Jie Zhan and Zhuqing Yan and Zhu Cao and Fan Wu and Yinfeng Wang and Yaying Zhan},
  journal = {Medical Oncology (Northwood, London, England)},
  year = {2026},
  month = oct,
  doi = {10.1007/s12032-026-03471-8},
  url = {https://doi.org/10.1007/s12032-026-03471-8},
  note = {CC BY-NC-ND 4.0},
}
RIS
TY  - JOUR
TI  - Cancer-associated fibroblasts and immune evasion in endometrial cancer: current evidence and therapeutic perspectives
AU  - Jie Zhan
AU  - Zhuqing Yan
AU  - Zhu Cao
AU  - Fan Wu
AU  - Yinfeng Wang
AU  - Yaying Zhan
PY  - 2026
DA  - 2026/10/26
JO  - Medical Oncology (Northwood, London, England)
DO  - 10.1007/s12032-026-03471-8
UR  - https://doi.org/10.1007/s12032-026-03471-8
AB  - Cancer-associated fibroblasts (CAFs) are potential contributors to tumor progression and immune resistance in endometrial cancer (EC), but the extent of EC-specific mechanistic and therapeutic evidence remains uneven. Studies using EC-derived fibroblasts support tumor-promoting paracrine activity and provide experimental evidence of altered natural killer cell function. Single-cell and spatial analyses further characterize stromal heterogeneity and candidate intercellular interactions. However, many proposed mechanisms of CAF-mediated immune exclusion and most CAF-directed therapeutic strategies are informed by studies in other malignancies. This review distinguishes findings obtained in EC patient samples and experimental models from evidence extrapolated from pancreatic, breast, gastric, and other cancers. We examine CAF heterogeneity, soluble signaling, matrix remodeling, and immune-cell interactions, while identifying where functional validation in EC is still required. Therapeutic approaches, including FAP-directed interventions, stromal reprogramming, and signaling blockade combined with immune checkpoint inhibition, are discussed as candidate research strategies rather than established EC treatments. Priorities include validating CAF-immune mechanisms in EC, developing reproducible stromal biomarkers, and testing treatment combinations in appropriate disease-specific models and clinical studies.  Graphical abstract:
SN  - 1357-0560
SN  - 1559-131X
ER  -