Cancer is among the leading causes of death globally. Despite advances in cancer research, a full understanding of the exact cause has not been established. Recent data have shown that the microbiome has an important relationship with cancer on various levels, including cancer pathogenesis, diagnosis and prognosis, and treatment. Since most studies have focused only on the role of bacteria in this process, in this article we review the role of fungi—another important group of the microbiome, the totality of which is referred to as the “mycobiome”—in the development of cancer and how it can impact responses to anticancer medications. Furthermore, we provide recent evidence that shows how the different microbial communities interact and affect each other at gastrointestinal and non-gastrointestinal sites, including the skin, thereby emphasizing the importance of investigating the microbiome beyond bacteria.

Non-Saccharomyces yeasts are of growing interest as probiotic candidates, but strain-level charac-terization remains limited. We characterized Pichia kluyveri PK88™, isolated from coffee beans (NRRL deposit # 68561), using phenotypic assays, whole-genome sequencing, and in silico screen-ing. PK88™ was non-hemolytic and produced no detectable patulin, ochratoxin A, or aflatoxins. Genome analysis confirmed species identity (98.5–98.8% average nucleotide identity) and identi-fied no acquired antimicrobial-resistance genes, canonical virulence factors, or decarboxylases for harmful biogenic amines. By high-inoculum broth microdilution, MICs were low for echi-nocandins and amphotericin B and higher for fluconazole and posaconazole. Measured survival after acid, bile and anaerobic exposure was retained (93% at pH 2; 82–84% in bile), although sur-vival at pH 1 and under anaerobiosis was lower; hydrophobicity fell from 91% to 73–77% and auto-aggregation rose to 98–100%. PK88 supernatant inhibited Escherichia coli and Candida albi-cans in preliminary assays. In two independent experiments, Caco-2 cells exposed to PK88™ showed cytotoxicity ≤20% in every replicate up to 6 × 104 organisms/well and variable increases at higher doses. These preliminary data support further evaluation.

Superficial mycoses, encompassing a range of fungal infections affecting the outer layers of the skin, hair, and nails, have become increasingly prevalent in recent years. While these infections are generally non-life-threatening, the emergence of antifungal resistance poses a growing threat to effective treatment strategies. In this article we explore the escalating specter of antifungal resistance in superficial mycoses, focusing on the underlying mechanisms driving resistance, the clinical implications, and potential avenues for mitigation. The rise of antifungal resistance in superficial mycoses is multifactorial. Consequently, the efficacy of conventional treatments is diminishing, leading to persistent or recurrent infections. Understanding the molecular mechanisms underlying antifungal resistance is crucial for developing targeted therapeutic approaches. Research efforts aimed at unraveling these mechanisms are essential for identifying new drug targets and designing innovative treatment strategies to combat resistant strains. In response to the escalating threat of antifungal resistance, a multifaceted approach is required. This includes enhanced surveillance of antifungal susceptibility patterns, the development of novel antifungal agents, and the implementation of stringent guidelines for antifungal use. Additionally, educational initiatives targeting healthcare professionals and the public are essential to promote responsible antifungal use, reduce the risk of resistance emergence, and improve treatment outcomes.