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Peer-reviewedCC BYFrontiers in cellular and infection microbiology

Gut mycobiome dysbiosis in digestive system cancers: immune remodeling and translational implications.

  • LingBo Ma1,2
  • Zhen Wang1,2
  • Jie Mao2
  1. 1Lanzhou University, Lanzhou, China.
  2. 2Department of General Surgery, Lanzhou University Second Hospital, Lanzhou, China.
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Abstract

Fungal dysbiosis has been reported in colorectal cancer (CRC), gastric cancer (GC), and pancreatic ductal adenocarcinoma (PDAC), but evidence strength differs substantially by tumor type and model system. Human CRC studies provide the broadest ecological evidence, including altered fungal community structure and fungal-bacterial networks. Human GC evidence is mainly cross-sectional and identifies Candida albicans as a candidate tissue-associated signal rather than a proven driver. In PDAC, human tissue studies report fungal signals, whereas causal support for Malassezia-mannose-binding lectin (MBL)-complement and fungal IL-33/type 2 immunity derives principally from mouse perturbation models. This narrative review synthesizes cancer-specific observations, fungal sensing, epithelial injury, immune remodeling, cross-kingdom interactions, and translational implications. We emphasize that low fungal biomass, contamination, transient dietary or environmental fungi, non-standardized sequencing, spatial uncertainty, and reverse causation limit interpretation. Fungal detection does not establish viability, colonization, or tumor causation. Clinical translation will require standardized controls, absolute fungal-load measurements, spatial confirmation, longitudinal cohorts, functional validation, and external testing of whether fungal features add value beyond established clinical, bacterial, metabolic, imaging, and immune markers.

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Cite

BibTeXRIS
BibTeX
@article{ma2026mycobiome,
  title = {{Gut mycobiome dysbiosis in digestive system cancers: immune remodeling and translational implications.}},
  author = {LingBo Ma and Zhen Wang and Jie Mao},
  journal = {Frontiers in cellular and infection microbiology},
  year = {2026},
  month = oct,
  doi = {10.3389/fcimb.2026.1902754},
  url = {https://europepmc.org/article/MED/42909229},
  note = {CC BY},
}
RIS
TY  - JOUR
TI  - Gut mycobiome dysbiosis in digestive system cancers: immune remodeling and translational implications.
AU  - LingBo Ma
AU  - Zhen Wang
AU  - Jie Mao
PY  - 2026
DA  - 2026/10/07
JO  - Frontiers in cellular and infection microbiology
DO  - 10.3389/fcimb.2026.1902754
UR  - https://europepmc.org/article/MED/42909229
AB  - Fungal dysbiosis has been reported in colorectal cancer (CRC), gastric cancer (GC), and pancreatic ductal adenocarcinoma (PDAC), but evidence strength differs substantially by tumor type and model system. Human CRC studies provide the broadest ecological evidence, including altered fungal community structure and fungal-bacterial networks. Human GC evidence is mainly cross-sectional and identifies Candida albicans as a candidate tissue-associated signal rather than a proven driver. In PDAC, human tissue studies report fungal signals, whereas causal support for Malassezia-mannose-binding lectin (MBL)-complement and fungal IL-33/type 2 immunity derives principally from mouse perturbation models. This narrative review synthesizes cancer-specific observations, fungal sensing, epithelial injury, immune remodeling, cross-kingdom interactions, and translational implications. We emphasize that low fungal biomass, contamination, transient dietary or environmental fungi, non-standardized sequencing, spatial uncertainty, and reverse causation limit interpretation. Fungal detection does not establish viability, colonization, or tumor causation. Clinical translation will require standardized controls, absolute fungal-load measurements, spatial confirmation, longitudinal cohorts, functional validation, and external testing of whether fungal features add value beyond established clinical, bacterial, metabolic, imaging, and immune markers.
SN  - 2235-2988
ER  -