A Common Gut Yeast Can Travel Into Prostate Tumors and Speed Their Growth

If you or someone you love is fighting prostate cancer that has stopped responding to hormone therapy, part of the reason may not be inside the tumor at all. A new study in Nature Cancer found that a common gut yeast can slip out of the intestines, travel through the bloodstream, and set up inside prostate tumors, where it appears to actively help the cancer resist treatment. The finding adds a surprising fungal layer to a disease already known to interact with gut microbes, and it comes with a mouse experiment that traces the entire chain of cause and effect, from a leaky gut to a specific immune cell to faster tumor growth.

Key Takeaways

• A gut-dwelling yeast called Nakaseomyces glabratus (formerly known as Candida glabrata) was found in the blood and tumors of men with castration-resistant prostate cancer (CRPC, prostate cancer that keeps growing despite hormone-blocking treatment), and its presence in stool tracked with worse survival.
• In mice, oral doses of the yeast sped up tumor growth and shortened survival, but only after castration (the mouse equivalent of hormone therapy), never in intact mice.
• The mechanism runs through a specific immune cell called a PMN-MDSC and a hormone-like protein called activin A that directly helps tumor cells keep growing without testosterone.
• The human findings rest on modest sample sizes and the causal steps were worked out mainly in mice, so this is not yet a reason to change any current treatment.

Gut Yeast Nakaseomyces glabratus Traced to Prostate Tumors

Researchers identified Nakaseomyces glabratus (an opportunistic yeast, formerly classified as Candida glabrata, that normally lives harmlessly in the gut) inside the feces, blood, and tumor tissue of men with prostate cancer. Using ITS sequencing (a genetic method that identifies fungal species from stool samples), the team compared 10 men with hormone-sensitive prostate cancer to 21 men with castration-resistant disease and found N. glabratus enriched in the CRPC group while it was undetectable in the hormone-sensitive group. When they tested blood from 102 prostate cancer patients against 31 healthy donors using PCR (a technique that detects fungal DNA), N. glabratus DNA showed up more often in patients. It also turned up directly inside 2 of 14 tumor biopsies tested, and Sanger sequencing (a method that reads the exact DNA sequence) confirmed those were genuine patient-derived signatures, not lab contamination.

Most tellingly, among every fungal species detected, N. glabratus was the only one significantly tied to survival. Men whose stool tested positive for it had roughly 2.6 times the risk of dying during follow-up (a hazard ratio of 2.6, statistically significant at P = 0.042), a relationship that held up even after the researchers adjusted for age, prior treatments, and standard prostate cancer risk markers like PSA level and Gleason score (a tumor aggressiveness grade).

Castration-Resistant Prostate Cancer Patients Are the Group at Stake

This finding is specific to men whose prostate cancer has progressed to the castration-resistant stage, meaning the cancer keeps growing even though androgen deprivation therapy (ADT, hormone treatment that lowers or blocks testosterone) has cut off its main fuel source. CRPC is the point in prostate cancer where treatment options narrow and outcomes worsen, so anything that explains why some tumors escape hormone therapy is directly relevant to how doctors eventually manage resistant disease, building on an earlier study linking gut bacteria to hormone-therapy resistance in the same cancer. The study does not suggest this fungus plays a role in early, hormone-sensitive prostate cancer, since it was undetectable in that group's stool samples.

Human Samples, Mouse Genetics, and Receptor Knockouts Built the Case

To move from correlation to mechanism, the researchers turned to mice, drawing on the same broader research into how hormone therapy reshapes the gut microbiome. They gave live N. glabratus by mouth to castrated mice carrying prostate tumors, using two separate models: one called TRAMP-C1 that mimics human prostate cancer, and a genetically engineered model that develops tumors similar to human disease. The yeast sped up tumor growth and shortened survival only in castrated mice, never in non-castrated (sham-operated) mice, and a related, common fungus, Candida albicans, given the same way had no effect at all, showing the response is specific to this one species.

The team then traced the mechanism step by step. The fungus recruits and activates immune cells called PMN-MDSCs (polymorphonuclear myeloid-derived suppressor cells, a type of white blood cell that suppresses the immune system's ability to attack tumors). When the researchers used an antibody to deplete these cells in mice given the fungus, the tumor-accelerating effect disappeared, confirming these cells drive the effect rather than just accompanying it. Those immune cells sense the fungus through a surface receptor called Dectin-2 (encoded by a gene named Clec4n); mice engineered to lack this receptor were protected from the fungus's tumor-promoting effect. Once activated, the immune cells pump out a hormone-like signaling protein called activin A, which directly switches on the tumor cells' androgen receptor pathway (the hormone-sensing machinery ADT is designed to shut down), letting the cancer keep growing its own way around the treatment. Mice bred to lack activin A specifically in these immune cells were also protected.

Finally, the researchers explained how the fungus gets from the gut to the tumor in the first place. Using a dye test (FITC-dextran, a marker that leaks into the blood when the gut lining becomes more porous), they found that castration itself increases intestinal permeability, sometimes called a leaky gut, by reducing proteins that normally seal the gut wall together, including occludin and claudin-1. Giving castrated mice back testosterone restored those sealing proteins, tying the leaky gut directly to loss of the hormone rather than to the tumor itself. Fluorescently tagged fungus tracked from gut to bloodstream to tumor only in castrated mice, clustering close to the implicated immune cells, roughly 19 micrometers away on average, versus about 45 micrometers from T cells, the immune cells that would otherwise attack the tumor.

What This Could Mean If You Or Someone You Know Is on Hormone Therapy

For a reader managing this personally, the study is not yet a green light for any new supplement, probiotic, or antifungal regimen. Nothing here has been tested in a clinical trial, and the researchers themselves frame it as an early mechanistic explanation rather than a ready-made treatment. What may be worth raising with an oncologist, if a patient's disease has become castration-resistant, is that gut and fungal health appear to be one more variable feeding into how well hormone therapy holds up. This study is not evidence that any current antifungal medication should be added to a treatment regimen, and self-medicating with over-the-counter antifungals is not supported by this data.

The Study's Limitations: Small Human Cohorts, Mouse-Based Mechanism

The authors flag several limits directly. The human side of the study rests on modest numbers: ITS sequencing in 10 versus 21 patients, metagenomic confirmation across 91 stool samples, PCR testing in 102 patients' blood, and fungal DNA found directly in just 2 of 14 tumor biopsies. The authors state plainly that the limited sample size prevented a definitive assessment of the fungus's link to disease progression on its own, and that the entire causal chain, from leaky gut to immune activation to tumor growth, was worked out in mice, not confirmed step by step in humans. It also remains unclear whether this fungus plays any role earlier in prostate cancer, before hormone-therapy resistance sets in, since the human samples came only from men already diagnosed with castration-resistant disease.

Next Steps: Bigger Cohorts and a Gut-Sealing Hydrogel

The researchers tested one possible fix in mice: an experimental inflammation-targeting hydrogel (a gel-like material, already explored for inflammatory bowel disease, that preferentially sticks to inflamed intestinal tissue), given by mouth to castrated mice. It sealed the gut barrier, blocked the fungus from reaching tumors, and slowed cancer growth in that model, adding a treatment angle to broader reviews of gut fungi and tumor immunity. The authors are explicit that this hydrogel strategy needs to be confirmed in additional mouse models before it could even be considered for human trials, and they are calling for larger patient cohorts to establish how strongly, and how early, N. glabratus tracks with prostate cancer outcomes. As of this writing the paper is only days old and has not yet drawn mainstream press coverage, so treat it as an early academic finding rather than a settled result.

Common Questions

Is Nakaseomyces glabratus dangerous to have in your gut normally?

No. It is a common, usually harmless yeast that lives in many people's intestines without causing problems; the study found it becomes relevant specifically after prostate tumors form and hormone therapy is underway.

Does this mean antifungal drugs could treat prostate cancer?

Not based on this study alone. The researchers tested an experimental gut-sealing hydrogel, not an antifungal drug, and even that has only been tried in mice so far.

Why does hormone therapy make the gut more permeable?

The study found that testosterone itself helps maintain the proteins that seal the gut lining together; when androgen deprivation therapy lowers testosterone, those sealing proteins decrease, letting gut microbes leak into the bloodstream more easily.

Could this fungus become a useful early warning sign?

Possibly, but not yet. The fungus was linked to worse survival only in a small group of men already diagnosed with castration-resistant disease, so much larger studies are needed before doctors could use it as a biomarker.

References

1. Ping Lai, Lei Liu, Nicolò Pernigoni, et al. (2026). Commensal Nakaseomyces glabratus migrates into prostate tumors to accelerate cancer progression. Nature Cancer. https://doi.org/10.1038/s43018-026-01229-9
2. Nicolò Pernigoni, Elena Zagato, Arianna Calcinotto, et al. (2021). Commensal bacteria promote endocrine resistance in prostate cancer through androgen biosynthesis. Science. https://doi.org/10.1126/science.abf8403
3. Safae Terrisse, Laurence Zitvogel, Guido Kroemer (2022). Effects of the intestinal microbiota on prostate cancer treatment by androgen deprivation therapy. Microbial Cell. https://doi.org/10.15698/mic2022.12.787
4. Natalia Szóstak, Piotr Kozłowski, Tao Zuo, Anna Philips (2025). The role of gut mycobiome in responses to cancer immunotherapy. Gut Microbes. https://doi.org/10.1080/19490976.2025.2571433