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Fungal dysbiosis is associated with altered community structures and immune remodeling in several gastrointestinal cancersFungi may play a role in several types of cancer

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Key Takeaway
Note that fungal dysbiosis is associated with gastrointestinal cancers, but evidence for causality remains limited.

This narrative review examines the role of fungal dysbiosis in colorectal cancer (CRC), gastric cancer (GC), and pancreatic ductal adenocarcinoma (PDAC). The review synthesizes evidence regarding fungal community structures, fungal-bacterial networks, and the impact of fungal sensing on immune remodeling and epithelial injury.

In CRC, human studies provide the broadest ecological evidence, including altered fungal community structures and networks. For GC, evidence is primarily cross-sectional, identifying Candida albicans as a potential tissue-associated signal rather than a proven driver. In PDAC, human tissue studies report fungal signals, but evidence for specific pathways like Malassezia-mannose-binding lectin-complement and fungal IL-33/type 2 immunity is derived primarily from mouse perturbation models.

The authors note several limitations, including low fungal biomass, potential contamination, and the presence of transient dietary or environmental fungi. They also highlight issues with non-standardized sequencing and spatial uncertainty. Clinical translation is currently limited by the need for standardized controls, absolute fungal-load measurements, and longitudinal cohorts to determine if fungal features provide value beyond existing clinical, bacterial, and metabolic markers.

How this fits prior evidence

This narrative review addresses a gap in understanding the role of the mycobiome in gastrointestinal malignancies. It complements existing coverage of colorectal cancer, such as the association between F. nucleatum and colorectal cancer and the use of IVIM MRI parameter D as a marker for rectal cancer cellularity. While the current review identifies fungal dysbiosis as a potential factor in CRC, GC, and PDAC, it notes that fungal detection does not establish viability or tumor causation.

When we think of cancer, we usually think of cells growing out of control. However, researchers are looking closer at the environment surrounding those cells. They are investigating how fungi, the tiny organisms that live in and on our bodies, might interact with tumors in colorectal, gastric, and pancreatic cancers.

In colorectal cancer, studies show clear changes in fungal communities and how they interact with bacteria. For gastric cancer, a specific fungus called Candida albicans is being watched as a potential signal in tissue. In pancreatic cancer, researchers have found fungal signals in human tissue, though some of the strongest evidence for specific immune responses currently comes from mouse models.

It is important to note that finding a fungus in a sample does not mean it is causing the cancer or is even alive. Because of issues like low fungal amounts and potential contamination, the evidence is still early. More research is needed to see if these fungal markers can actually help doctors treat patients better than current methods.

What this means for you:
Fungi are linked to several cancer types, but more research is needed to prove they cause tumors.

Common questions

Does finding fungus in a tumor mean it is causing the cancer?

Not necessarily. Finding a fungus in a tissue sample does not prove that the fungus is alive, that it has colonized the area, or that it is actually causing the tumor to grow. Scientists are still working to determine if these fungi are drivers of the disease or just present in the environment.

What specific types of cancer are linked to fungi?

The research focuses on three main types: colorectal cancer, gastric cancer, and pancreatic ductal adenocarcinoma. Each shows different levels of evidence regarding how fungi interact with the body's tissues and immune systems.

Is this research ready to be used in clinics?

Not yet. To use these findings in a clinic, doctors need more standardized tests, larger groups of patients, and proof that fungal markers provide more information than the tests doctors already use today, such as imaging or metabolic tests.

Study Details

Study typeSystematic review
EvidenceLevel 1
PublishedOct 2026
View Original 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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