Two Malassezia Species Promote Cell Multiplication in Culture

Two Malassezia fungal species promoted cell multiplication in cultured epithelial cells—the cells that form tissue surfaces—after 12 hours. This laboratory result does not establish that the fungi cause basal cell carcinoma, a type of skin cancer.

Evidence

The Malassezia study examined archived basal cell carcinoma specimens from 50 patients and paired fresh tumor and adjacent tissue from three patients. Researchers screened archived tissue using reverse-transcription quantitative polymerase chain reaction, a targeted method for detecting genetic material. They used metagenomic sequencing to characterize fungal communities in the fresh pairs. Malassezia globosa was the most abundant species in archived specimens and was also detectable in fresh tissue.

The laboratory experiments used HaCaT keratinocytes, a skin epithelial cell line, and A-431 epidermoid carcinoma cells. Neither model was specific to basal cell carcinoma. After 12 hours, Malassezia globosa at 12 million colony-forming units per milliliter and Malassezia yamatoensis at 16 million significantly promoted proliferation, meaning cell multiplication. Colony-forming units measure viable fungal concentration. Both strains also increased activity of genes associated with inflammation and responses to oxidative stress, a form of chemical stress on cells.

The breast-tumor study used RNA sequencing, which measures gene transcripts as indicators of gene activity, in 270 tumors from Peruvian women with invasive breast cancer. In HER2-enriched tumors—a subtype classified by its gene-expression pattern—the rs140068132-G allele, a particular version of a genetic variant, was associated with higher expression of nearby genes ARMT1 and RMND1. The association with CCDC170 expression was borderline.

The genetic models accounted for age at diagnosis, Indigenous American genetic ancestry, tumor subtype, and whether the genotype association differed by subtype. Both studies were published October 1, 2026.

Analysis

Interpretation: Both studies connect observations in cancer tissue with bounded biological signals. The fungal experiment shows a short-term cellular response under specified laboratory conditions. The genetic study identifies associations with gene activity within a particular tumor subtype.

These are different lines of inquiry, not independent confirmation of one another or evidence for a common cancer mechanism. Finding fungi in a tumor does not establish their role in its development; linking a genetic variant to gene activity does not demonstrate the molecular steps connecting that variant to cancer risk.

Limitations

The skin study was retrospective and enrolled only people with confirmed basal cell carcinoma. Preservation and storage can degrade DNA in archived tissue. Only three fresh tissue pairs were available, leaving insufficient matched material for systematic culture-based validation. The non-basal-cell-carcinoma cell models further limit interpretation. The available results provide neither numerical proliferation effect sizes nor patient outcomes tied to fungal measurements.

The genetic analysis was exploratory. Its genotype distribution included 66 carriers with one copy of the G allele and only two with two copies, limiting statistical power for subtype-specific comparisons. Numerical effect estimates and uncertainty ranges are unavailable for the gene-expression associations. The borderline CCDC170 result particularly requires independent replication.

What to watch

An independent HER2-enriched tumor series with more G-allele carriers could test the ARMT1 and RMND1 associations, quantify their size, and determine whether the borderline CCDC170 association persists.

Confidence in the fungal hypothesis would increase if basal-cell-carcinoma-specific models reproduced the proliferation response at fungal concentrations measured in patient tissue, with quantified effect sizes and uncertainty ranges.