Fig. 5

Tumor-associated mycobiome and cancer therapy. (a) The fungus can interact with chemotherapy. Elevated fungal diversity in patients who responded to chemotherapy compared to non-responders. However, high-intensity chemotherapy can reduce alpha diversity and fungal abundance, e.g., Malassezia. A bidirectional effect may exist between cancer therapies and human-mycobiome. For example, antifungals may kill pathogenic fungi but may also lead to microbiome dysbiosis, favoring the invasion and colonization of other opportunistic pathogenic fungi. (b) Fungal-bacterial interactions may affect the efficacy of radiotherapy. Fungal ablation induces an increase in CD8 T cells, which increases the RT efficacy, whereas bacterial ablation induces an increase in M2 macrophages, which decreases the RT efficacy. (c) Components of fungi, such as β-glucan, can enhance the efficacy of immunotherapy. β-glucan can promote the conversion of M2-type macrophages to M1-type, secrete cytokines and chemokines such as INF-γ, TNF-α, IL-12, CXCL9 and CXCL10, and increase the expression of PD-L1, which promotes anti-tumour therapeutic effects. Systemic administration of β-glucan induces T-lymphocyte activation, secretes INF-γ, and promotes anti-tumour immunity. (d) Gut mycobiome can influence the therapeutic efficacy of FMT. High Candida abundance pre-FMT is associated with clinical response and increased bacterial diversity post-FMT. (e) S. boulardii, a probiotic, inhibits EGF-induced proliferation, reduces colony formation, and promotes apoptosis