Introduction Since the 1960s has been implicated in the progression of some Candida albicans leukoplakias, the most common of the potentially malignant oral disorders (PMOD), to oral squamous cell carcinoma (OSCC).1,2 The attributes of that may Candida contribute to cancer progression have been extensively reviewed 3,4 but the role of in promoting oral cancer has always been controversial. Major risk factors Candida definitely associated with oral cancer are tobacco smoking and alcohol consumption. Alcohol itself is not carcinogenic but it is the metabolic product, acetaldehyde, that is linked to carcinogenesis.6-10 The enzyme isoforms responsible for the reversible production of acetaldehyde from ethanol are alcohol dehydrogenases encoded by the genes. In seven genes have been annotated in the ADH C. albicans, ADH C. albicans genome database (http://www.candidagenome.org/) by homology to S. cerevisiae genes but little is known about the functions of the alcohol dehydrogenase enzymes in the acetaldehyde metabolism of The expression of and C. albicans. CaADH1 CaADH2 were investigated in this study as they have the highest amino acid sequence homology to genes involved in acetaldehyde metabolism; - the S. cerevisiae ScADH1 major contributor to ethanol production5 and - responsible for acetaldehyde ScADH2 production.6,7 In this study, the presence of and the expression of particular Candida genes in archival biopsies from human oral leukoplakic lesions was C. albicans ADH studied to investigate whether the presence of or gene activity, could Candida, ADH be related to histopathological diagnosis. Histological examination of a lesion with a clinical diagnosis of homogeneous leukoplakia rarely shows infection with Candida8. If was detected, the lesion by definition is not leukoplakia and an alternative Candida clinical and histological diagnosis is chronic hyperplastic candidosis (CHC). CHC has the potential to progress to OSCC.9-11
Introduction Since the 1960s Candida albicans has been implicated in the progression of some leukoplakias, the most common of the potentially malignant oral disorders (PMOD), to oral squamous cell carcinoma (OSCC).1,2 The attributes of Candida that may contribute to cancer progression have been extensively reviewed 3,4 but the role of Candida in promoting oral cancer has always been controversial. Major risk factors definitely associated with oral cancer are tobacco smoking and alcohol consumption. Alcohol itself is not carcinogenic but it is the metabolic product, acetaldehyde, that is linked to carcinogenesis.6-10 The enzyme isoforms responsible for the reversible production of acetaldehyde from ethanol are alcohol dehydrogenases encoded by the ADH genes. In C. albicans, seven ADH genes have been annotated in the C. albicans genome database (http://www.candidagenome.org/) by homology to S. cerevisiae genes but little is known about the functions of the alcohol dehydrogenase enzymes in the acetaldehyde metabolism of C. albicans. The expression of CaADH1 and CaADH2 were investigated in this study as they have the highest amino acid sequence homology to S. cerevisiae genes involved in acetaldehyde metabolism; ScADH1 - the major contributor to ethanol production5 and ScADH2 - responsible for acetaldehyde production.6,7 In this study, the presence of Candida and the expression of particular C. albicans ADH genes in archival biopsies from human oral leukoplakic lesions was studied to investigate whether the presence of Candida, or ADH gene activity, could be related to histopathological diagnosis. Histological examination of a lesion with a clinical diagnosis of homogeneous leukoplakia rarely shows infection with Candida8. If Candida was detected, the lesion by definition is not leukoplakia and an alternative clinical and histological diagnosis is chronic hyperplastic candidosis (CHC). CHC has the potential to progress to OSCC.9-11
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