Gut Fungus Found Lurking in Prostate Tumors Speeds Cancer Growth in Mice

A fungus long considered a quiet, harmless resident of the human body may play a far more sinister role in one of the most difficult cancers to treat. New research published in Nature Cancer reports that Nakaseomyces glabratus, a commensal yeast closely related to Candida, is enriched in both fecal and tumor samples from patients with castration-resistant prostate cancer, the lethal stage of the disease that no longer responds to hormone deprivation therapy. Strikingly, when the researchers administered the fungus to castrated mice bearing prostate tumors, cancer progression accelerated, suggesting that this microscopic hitchhiker is not merely a passive bystander in the tumor environment but may be an active participant in the disease’s most dangerous phase.

The finding lands at the intersection of two of the most rapidly evolving fields in cancer biology: the tumor microbiome and the study of fungi as overlooked members of our resident microbial communities. For decades, research into the microbiome concentrated overwhelmingly on bacteria, and rightly so, given their staggering abundance. But fungi, though numerically minor, possess qualities that make them uniquely capable of influencing their hosts. They have robust cell walls built from beta-glucans and other sugar polymers, they can switch between morphological forms, and they are armed with molecules that interact directly with the innate immune system. In recent years, fungal DNA and even intact fungal cells have been detected inside tumors ranging from pancreatic cancer to melanoma, prompting an urgent question: are these organisms contaminants, opportunists exploiting a weakened tissue, or drivers of malignant progression?

The new study, led by Lai and colleagues, adds substantial weight to the third possibility, at least in the context of advanced prostate cancer. By analyzing fecal samples and tumor tissue from patients with castration-resistant prostate cancer, the team found that Nakaseomyces glabratus was enriched in both compartments relative to comparisons, indicating that the fungus is not only more abundant in the gut of these patients but also physically present within the tumor microenvironment itself. That dual enrichment is important. A microbe found solely in stool could simply reflect a systemic shift in body ecology; a microbe found inside the tumor, in the same patients, raises the possibility of migration — that organisms originating in the intestinal lumen can translocate across epithelial barriers, travel through circulation or adjacent tissues, and colonize tumor sites.

Nakaseomyces glabratus, known in older literature as Candida glabrata, is no exotic pathogen. It is a genuine commensal, carried harmlessly by a large fraction of healthy people on mucosal surfaces of the gut, the genitourinary tract, and elsewhere. In immunocompromised individuals, however, it can become an opportunistic pathogen and is a recognized cause of invasive candidiasis in hospital settings. Its evolutionary kinship with Candida albicans makes the new findings particularly thought-provoking, because C. albicans has already been implicated in other contexts in which commensal fungi appear to reshape host physiology, from inflammatory bowel disease to oral carcinogenesis. The new work extends this emerging paradigm to the prostate, an organ whose tumor microenvironment had not previously been considered a destination for migrating fungi.

The castrated mouse experiments provide the study’s most consequential evidence. Prostate cancers typically depend on androgen receptor signaling, which is why androgen deprivation therapy — surgical or chemical castration — is a mainstay of treatment for advanced disease. Over time, however, tumors adapt and progress despite near-castrate hormone levels, becoming the castration-resistant form that accounts for most prostate cancer deaths. When the researchers gave Nakaseomyces glabratus to castrated mice bearing prostate tumors, the fungus accelerated cancer progression in this precisely defined hormonal context. In other words, the organism’s pro-tumor effect was observed under the very conditions that define the lethal, treatment-resistant stage of human disease, closely mirroring the patient population in which the fungus was found to be enriched.

How might a commensal yeast push a tumor toward faster growth? The authors’ demonstration does not yet fully resolve the mechanism, but the broader literature offers several plausible avenues. Fungal cell wall components, including beta-glucans and mannans, are recognized by innate immune receptors such as Dectin-1 and Toll-like receptors, which can trigger inflammatory programs that tumors frequently exploit for growth, survival, and immune evasion. Chronic low-grade inflammation within the tumor microenvironment can promote angiogenesis, remodel the extracellular matrix, and suppress effective anti-tumor immunity, all of which favor progression. Fungi can also alter the local metabolic landscape, consume nutrients, and engage in cross-kingdom interactions with bacteria that themselves modulate inflammation and therapy response. Disentangling which of these pathways Nakaseomyces glabratus activates in the prostate will be a central task for follow-up research.

The translocation question is equally compelling. The intestinal barrier is a heavily policed boundary, and yet a growing body of work shows that microbial migration from gut to distant tissues is far more common than once believed. Bacterial species have been traced from the gut lumen into pancreatic tumors, breast tumors, and lymph nodes, sometimes with measurable functional consequences for disease course. The new study suggests fungi can join this list. If Nakaseomyces glabratus indeed migrates from the gut into prostate tumors, the clinical implications are immediately apparent: the gut mycobiome becomes a potential modifiable risk factor, and strategies to reduce fungal load, alter fungal community composition, or block fungal recognition pathways could, in principle, slow disease progression in affected patients.

Caution is, as always in this field, warranted. Enrichment and acceleration in mice establish association and a causal effect in an animal model, but they do not by themselves prove that the fungus drives progression in every patient, nor that eradicating it would improve outcomes in humans. Tumor-associated microbes can be difficult to distinguish from contaminants, and the field has grappled with reproducibility concerns surrounding low-biomass microbiome sequencing. Moreover, host factors — immune status, diet, prior antifungal or antibiotic exposure, and disease stage — likely shape whether a commensal yeast remains benign or becomes pro-tumorigenic. The most rigorous next steps will include longitudinal studies tracking fungal burden as disease progresses, mechanistic dissection of the immune signaling involved, and intervention experiments in models that test whether reducing the fungus reverses the accelerated growth.

Nevertheless, the conceptual shift is hard to overstate. Prostate cancer research has concentrated on hormones, genetics, and immune checkpoints; the possibility that a common commensal fungus physically resides inside prostate tumors and shapes their trajectory adds an entirely new layer to the disease model. It also resonates with an expanding appreciation that the human body is a multi-kingdom ecosystem, in which fungi, bacteria, viruses, and host cells engage in a continuous negotiation whose outcome can be health or disease. If further work confirms and extends these findings, mycobiome profiling could one day sit alongside PSA testing and genomic analysis in the clinical workup of advanced prostate cancer, and antifungal or microbiome-targeted interventions could emerge as adjuncts to existing therapies.

For now, the study stands as a vivid reminder that the microbes we carry with us every day are not always neutral companions. A yeast that spends most of its existence quietly metabolizing in our intestines can, under the right circumstances, find its way into a tumor and help it grow faster. Understanding when, how, and in whom that happens may open one of the most unexpected new fronts in the fight against castration-resistant prostate cancer — a front that begins not in the prostate at all, but in the gut.

Subject of Research: Enrichment of the commensal fungus Nakaseomyces glabratus in castration-resistant prostate cancer and its acceleration of tumor progression in mice

Article Title: Commensal Nakaseomyces glabratus migrates into prostate tumors to accelerate cancer progression

Article References: Lai, P., Liu, L., Pernigoni, N., Du, Y., Braga, D., Troiani, M., Attanasio, G., Li, Y., Song, P., Pasquini, E., Rezzonico Jost, T., Huang, X., Maddalena, M., Mosole, S., Rinaldi, A., Pecoraro, G., Pedrani, M., Valdata, A., Bancaro, N., … Alimonti, A. (2026). Commensal Nakaseomyces glabratus migrates into prostate tumors to accelerate cancer progression. Nature Cancer. https://doi.org/10.1038/s43018-026-01229-9

Image Credits: AI Generated

DOI: 10.1038/s43018-026-01229-9

Keywords: Nakaseomyces glabratus, prostate cancer, castration-resistant prostate cancer, tumor microbiome, mycobiome, fungal translocation, commensal fungi, tumor microenvironment, androgen deprivation, cancer progression, Nature Cancer, Commensal