Re: Human Papillomavirus DNA and p53 Polymorphisms in Squamous Cell Carcinomas From Fanconi Anemia Patients

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Kutler et al. ( 1 ) recently reported that human papillomavirus (HPV) DNA is frequently detected in squamous cell carcinomas (SCCs) of Fanconi anemia patients, who are predisposed to develop cancer at an early age, particularly acute myeloid leukemia and SCCs of the head and neck (HNSCCs) and the anogenital region. Kutler et al. speculated that HPV infection might be critically involved in the pathogenesis of SCC in Fanconi anemia patients, which raises hope that vaccination against HPV might prevent such tumors. HPV is known to be etiologically involved in SCCs that arise in the anogenital region (cervix) and in a minority of HNSCCs, particularly those in the oropharynx ( 2 , 3 ) . Inhibitory oncoproteins expressed by HPV cause inactivation of the p53 and pRb pathways. HNSCCs that contain transcriptionally active HPV DNA typically lack mutations in TP53, the gene encoding p53, whereas 50%–60% of HNSCCs that do not contain HPV DNA have mutations in TP53 ( 2 ) .