Exploring the Role of Candida spp. in Oral Potentially Malignant Lesions and Carcinogenesis
admin-cespu
Principal Investigator:
Luís Miguel Moutinho da Silva Monteiro
Leader Institution:
UNIPRO, U.CESPU
Research Team:
Leonor Delgado, Sara Ferreira, Cristina Coelho, Filomena Salazar, José Júlio Pacheco, Saman Warnakulasuriya, Fernanda Garcez
Funding entity:
CESPU
Budget:
4590,16
Period covered:
01/09/2026-2027
Abstract:
This project investigates how Candida drives the progression of oral potentially malignant disorders (30 oral leukoplakias, 30 oral lichen planus) into oral squamous cell carcinoma (30 OSCC) against 30 healthy controls (N = 120). Combining retrospective archives and prospective real-time sampling of whole saliva, lesional swabs for microbiologic cultures, and 90 tissue biopsies will undergo precise species identification via MALDI-TOF MS. Fungal tissue invasion and active virulence (Candidalysin/Ece1, Als3) will be mapped via GMS/PAS histochemistry and immunohistochemistry alongside a host microenvironment panel (IL-17, COX-2, IL-1β, CD68/163, CD8). We expect to demonstrate that physical invasion depth and fungal virulence expression directly correlate with dysplasia severity or pro-tumorigenic host tissue reprogramming. Ultimately, this work will provide a validated dual-system predictive model to improve clinical risk stratification and reveal novel targeted therapeutic strategies.
This project investigates how Candida drives the progression of oral potentially malignant disorders (30 oral leukoplakias, 30 oral lichen planus) into oral squamous cell carcinoma (30 OSCC) against 30 healthy controls (N = 120). Combining retrospective archives and prospective real-time sampling of whole saliva, lesional swabs for microbiologic cultures, and 90 tissue biopsies will undergo precise species identification via MALDI-TOF MS. Fungal tissue invasion and active virulence (Candidalysin/Ece1, Als3) will be mapped via GMS/PAS histochemistry and immunohistochemistry alongside a host microenvironment panel (IL-17, COX-2, IL-1β, CD68/163, CD8). We expect to demonstrate that physical invasion depth and fungal virulence expression directly correlate with dysplasia severity or pro-tumorigenic host tissue reprogramming. Ultimately, this work will provide a validated dual-system predictive model to improve clinical risk stratification and reveal novel targeted therapeutic strategies.