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[Cancer Research 63, 1188-1191, March 15, 2003]
© 2003 American Association for Cancer Research

Advances in Brief

Is the p53 Inactivation Frequency in Squamous Cell Carcinomas of the Head and Neck Underestimated? Analysis of p53 Exons 2–11 and Human Papillomavirus 16/18 E6 Transcripts in 123 Unselected Tumor Specimens

Vera Balz1, Kathrin Scheckenbach1, Karl Götte, Ulrike Bockmühl, Iver Petersen and Henning Bier2

Departments of Otorhinolaryngology/Head and Neck Surgery, Heinrich-Heine-University, D-40225 Düsseldorf [V. B., K. S., H. B.]; University Hospital, D-68135 Mannheim [K. G.]; General Hospital, D-36043 Fulda [U. B.]; and Institute of Pathology, Charité, Humboldt University, D-10098 Berlin [I. P.], Germany

Mutations and interaction with high-risk human papillomavirus (HPV) E6 oncoprotein are well-established mechanisms of p53 inactivation. In a series of 123 unselected squamous cell carcinomas of the head and neck (SCCHN), we performed sequence analysis of the entire coding region of p53 transcript and determined the presence of the E6 transcripts of HPV 16 and 18. Aberrant p53 transcripts were identified in 97 (79%) SCCHN. HPV 16 and/or 18 E6 transcripts were detected in 37 (30%) tumor specimens, including 20 (77%) of the 26 p53 wild-type tumors. The likely inactivation of p53 in 117 (95%) of the 123 SCCHN suggests that this event could be obligatory in the multistep process of carcinogenesis.




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