biostudies-literatureUnknown51(6)Jawert FDepartment of Research and Development, NU Hospital GroupSveriges Tandläkarförbund<h4>Background</h4>A major challenge in the management of patients with oral leukoplakia is the difficulty to identify patients at high risk of developing oral squamous cell carcinoma. Our knowledge about genomic alterations in oral leukoplakia, and in particular those that progress to oral squamous cell carcinoma, is scarce and there are no useful biomarkers that can predict the risk of malignant transformation.<h4>Methods</h4>Using a novel, custom-made tissue microarray including 28 high-risk oral leukoplakias and the corresponding oral squamous cell carcinomas from 14 cases that progressed to cancer, we assayed copy number alterations involving the oral squamous cell carcinoma driver genes CDKN2A, CCND1, EGFR, and MYC by fluorescence in situ hybridization. The copy number alterationss wJournal of oral pathology & medicine : official publication of the International Association of Oral Pathologists and the American Academy of Oral Pathology546-552https://www.ebi.ac.uk/biostudies/studies/S-EPMC9546103biostudies-literatureRecurrent copy number alterations involving EGFR, CDKN2A, and CCND1 in oral premalignant lesions.PMC9546103Kjeller GJawert FStenman GFehr AOhman JfalseRecurrent copy number alterations involving EGFR, CDKN2A, and CCND1 in oral premalignant lesions.<h4>Background</h4>A major challenge in the management of patients with oral leukoplakia is the difficulty to identify patients at high risk of developing oral squamous cell carcinoma. Our knowledge about genomic alterations in oral leukoplakia, and in particular those that progress to oral squamous cell carcinoma, is scarce and there are no useful biomarkers that can predict the risk of malignant transformation.<h4>Methods</h4>Using a novel, custom-made tissue microarray including 28 high-risk oral leukoplakias and the corresponding oral squamous cell carcinomas from 14 cases that progressed to cancer, we assayed copy number alterations involving the oral squamous cell carcinoma driver genes CDKN2A, CCND1, EGFR, and MYC by fluorescence in situ hybridization. The copy number alterationss w2022-01-01T00:00:00Z2022 Jul2025-04-05T20:11:45.678Z2025-04-05T20:11:45.678ZS-EPMC95461033548877710.1111/jop.13303