This Article Order Full text via Infotrieve Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Kessis, T. D. Articles by Cho, K. R. Search for Related Content PubMed PubMed Citation Articles by Kessis, T. D. Articles by Cho, K. R.

American Journal of Pathology, Vol 143, 1398-1405, Copyright © 1993 by American Society for Investigative Pathology

REGULAR ARTICLES

p53 gene mutations and MDM2 amplification are uncommon in primary carcinomas of the uterine cervix

TD Kessis, RJ Slebos, SM Han, K Shah, XF Bosch, N Munoz, L Hedrick and KR Cho
School of Hygiene and Public Health, Johns Hopkins University, Baltimore, Maryland.

The p53 gene is the most frequently altered gene known thus far in a wide variety of human cancers. Inactivation of p53, either through mutation or through interaction with the human papillomavirus (HPV) E6 oncoprotein, is a characteristic feature of all cervical carcinoma cell lines that have been studied. These findings suggest that p53 inactivation is required for cervical carcinoma development and that HPV infection and p53 mutation may be mutually exclusive. We have studied the p53 gene in 35 primary cervical carcinomas. DNA sequence and single strand conformational polymorphism analyses were used to evaluate p53 in 27 squamous carcinomas (25 HPV-positive) and eight adenocarcinomas (four HPV-positive). A missense mutation of p53 was observed in one HPV 16-positive squamous carcinoma, demonstrating that p53 mutations can occur in combination with HPV infection. The HPV- negative tumors all lacked p53 gene mutations. The absence of p53 mutations in HPV-negative cases prompted an assessment of tumors for MDM2 gene amplification. The MDM2 gene encodes a p53 binding protein and has been found to be amplified in some human tumors lacking p53 mutations. MDM2 amplification was not identified in any of the tumors we examined, including four HPV-negative cases. Our findings show that HPV infection and p53 gene mutation are not mutually exclusive and suggest that many HPV-negative carcinomas may arise via a pathway independent of p53 inactivation.

This article has been cited by other articles:

				P. K. Ha and J. A. Califano THE ROLE OF HUMAN PAPILLOMAVIRUS IN ORAL CARCINOGENESIS Crit. Rev. Oral. Biol. Med., July 1, 2004; 15(4): 188 - 196. [Abstract] [Full Text] [PDF]

				C. T. Miller, S. Aggarwal, T. K. Lin, S. L. Dagenais, J. I. Contreras, M. B. Orringer, T. W. Glover, D. G. Beer, and L. Lin Amplification and Overexpression of the Dual-Specificity Tyrosine-(Y)-Phosphorylation Regulated Kinase 2 (DYRK2) Gene in Esophageal and Lung Adenocarcinomas Cancer Res., July 15, 2003; 63(14): 4136 - 4143. [Abstract] [Full Text] [PDF]

				X. Lin, M. Tascilar, W.-H. Lee, W. J. Vles, B. H. Lee, R. Veeraswamy, K. Asgari, D. Freije, B. van Rees, W. R. Gage, et al. GSTP1 CpG Island Hypermethylation Is Responsible for the Absence of GSTP1 Expression in Human Prostate Cancer Cells Am. J. Pathol., November 1, 2001; 159(5): 1815 - 1826. [Abstract] [Full Text] [PDF]

				A.-M. F. Kersemaekers, G. J. Fleuren, G. G. Kenter, L. J. C. M. Van den Broek, S. M. Uljee, J. Hermans, and M. J. Van de Vijver Oncogene Alterations in Carcinomas of the Uterine Cervix: Overexpression of the Epidermal Growth Factor Receptor Is Associated with Poor Prognosis Clin. Cancer Res., March 1, 1999; 5(3): 577 - 586. [Abstract] [Full Text] [PDF]