Candidal Pathogenesis in Oral Squamous Cell Carcinoma
Summary
Oral squamous cell carcinoma (OSCC) is a globally prevalent malignancy with significant morbidity and mortality. Emerging evidence implicates Candida species, particularly Candida albicans, in both the initiation and progression of OSCC. Candida can shift from a benign commensal state to an opportunistic pathogen under conditions of mucosal injury, immunosuppression or dysbiosis. Filamentous growth and biofilm formation facilitate epithelial adhesion and invasion, while secreted aspartyl proteases and candidalysin damage host tissues and provoke chronic inflammation. Persistent Candida colonisation promotes a pro‐tumour microenvironment by driving cytokine release (for example interleukin 17), recruiting tumour‐associated macrophages skewed towards an immunosuppressive M2 phenotype, and enhancing epithelial–mesenchymal transition in dysplastic cells. Carcinogenic metabolites, notably acetaldehyde produced by Candida metabolism, contribute to DNA damage and mutagenesis. Together, these processes create a feed-forward loop in which fungal invasion amplifies field cancerisation and malignant transformation in the oral mucosa. Understanding the multifaceted roles of Candida in OSCC pathogenesis offers new avenues for early detection, antifungal intervention and immunomodulatory therapy.
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Candidal Pathogenesis in Oral Squamous Cell Carcinoma publication trend
The graph below shows the total number of articles in candidal pathogenesis in oral squamous cell carcinoma across all publications each year (not limited to Nature Index journals).
Technical terms
Biofilm: Structured community of fungal cells adherent to a surface and embedded within an extracellular matrix that enhances survival and antifungal resistance.
Candidalysin: Peptide toxin secreted by Candida albicans hyphae that disrupts epithelial barriers and triggers host immune responses.
Secreted aspartyl proteases (SAP): Family of Candida enzymes that degrade host proteins, facilitating tissue invasion and nutrient acquisition.
Tumour-associated macrophages (TAMs): Macrophages within the tumour microenvironment that often adopt an immunosuppressive phenotype promoting tumour growth.
Epithelial–mesenchymal transition (EMT): Process by which epithelial cells acquire mesenchymal characteristics, enhancing motility and invasiveness.
Dysplasia: Histological alteration of epithelial tissue marked by atypical cell morphology and disordered architecture, representing a precancerous state.
References
- Candida albicans Promotes Oral Cancer via IL-17A/IL-17RA-Macrophage Axis. mBio (2023).
- Candida albicans Enhances the Progression of Oral Squamous Cell Carcinoma In Vitro and In Vivo. mBio (2022).
- Real-Time PCR Detection of Candida Species in Biopsy Samples from Non-Smokers with Oral Dysplasia and Oral Squamous Cell Cancer: A Retrospective Archive Study. Cancers (2023).
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