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

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.