Table 2.

The association between C. albicans and cancer.

Cancer Type	Findings	Methods	Refs.
Oral cancer	C. albicans enhances the proliferation, migratory processes, as well as invasion of oral squamous cell carcinoma cells in laboratory conditions and also promotes tumor growth and metastases in test animals.	Modulation of tumor cell behavior and the host immune response by upregulating oncogenes and potentiating a premalignant phenotype.	[20]
	C. albicans infection enhances the expression of interleukin-17A(IL-17A) and its receptor (IL-17RA) in oral cancer cells and macrophages.	The increased IL-17A/IL-17RA signaling activates macrophages and promotes the release of inflammatory cytokines, which in turn enhances the proliferation, migration, and invasion of oral cancer cells.	[21]
	Immune cell infiltration was observed in carcinogenesis prompted by C. albicans infection.	Single-cell expression profiling	[22]
	Upregulation in programmed death-ligand 1 (PD-L1) expression in oral cancer cells.	Inhibition of T cell activation and proliferation by upregulation of programmed death-ligand 1 (PD-L1) expression in vivo and in vitro.	[23]
	C. albicans biofilm may contribute to the development and progression of oral cancer.	Induction of lipid droplet formation and decreasing the efficacy of chemotherapy drugs	[24]
	Genetic mutations and chromosomal abnormalities can be associated with the development of cancer.	DNA damage and inhibition of DNA repair mechanisms cause by acetaldehyde.	[25]
	Genetic mutations and chromosomal abnormalities can be associated with the development of cancer.	Reactive oxygen species promote chronic inflammation and cause mitochondrial damage.	[26]
Esophageal cancer	Development of epidermoid esophageal cancer.	Treatment-resistant esophageal candidiasis.	[27]
	Chronic mucocutaneous candidiasis leads to squamous cell carcinoma.	Mutation in STAT1 protein	[28,29]
Gastric cancer	An imbalance in fungal communities with changes in fungal composition and a large increase in the abundance of C. albicans leads to gastric cancer.	The increase in C. albicans is involved in the decrease in the abundance and diversity of other gastric fungi.	[30]
	Deletion of the Dectin-3 gene led to a substantial increase in colorectal cancer development, with fungal burden in the feces of knockout mice.	The deletion of the Dectin-3 gene led to a significantly increased abundance/proportion of C. albicans in knockout mice.	[31]
	Differences in the composition of the feces and abundance of C. albicans could promote the process of colorectal carcinogenesis.	Transplantation of feces from knockout, cancer-bearing mice into other mice confirmed that the feces and C. albicans could promote the process of colorectal carcinogenesis.	[31]
Skin cancer	Compared with the control group, patients with Candida infection had a significantly higher risk for overall skin cancer.	A case-control study enrolled 34,829 patients with Candida infection and an equal number of controls.	[32]
	Progression of verrucous candidiasis of lip to SCC after 12 months of follow-up.	A case report	[33]