Abstract

Abstract Increased fungal infection has been reported in oral and esophageal squamous cell carcinomas (SCCs) derived from patients with autoimmune polyendocrinopathy-candidiasis-ectodermal dystrophy, immunodeficient patients, and non-autoimmune patients, as well as patients with other cancer types after radiation and chemotherapy. Thus, it is important to understand the role of increased fungal infection in tumor development. Our lab used several animal models to demonstrate that increased oral infection or colonization with Cladosporium cladosporioide (one of the most common fungi indoor and outdoor) or Candida albicans, which is one of the human commensal yeasts and opportunistic pathogens, promoted SCCs in the oral-esophageal-forestomach organs as well as distal cutaneous carcinogenesis. We revealed the mechanism underlying the relationship of increased fungal colonization with inflammatory pathways, epithelial cancer cell-oncogenic pathways, and bacteria during carcinogenesis. Those fungus-associated pathogenic phenotypes, inflammatory signaling, and epithelial oncogenic pathways observed in mice were also seen in human cancers. Based on these results in mice and human, we speculate that increased oral fungal colonization promotes human carcinogenesis. Citation Format: Yinling Hu. Fungal infection and carcinogenesis [abstract]. In: Proceedings of the AACR Special Conference on the Microbiome, Viruses, and Cancer; 2020 Feb 21-24; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2020;80(8 Suppl):Abstract nr IA19.

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