ORIGINAL PAPER p53 codon 72 polymorphism and risk of cervical carcinoma in Moroccan women M. Meftah El khair M. M. Ennaji R. El kebbaj R. Ait Mhand M. Attaleb M. El Mzibri Received: 12 June 2009 / Accepted: 18 August 2009 / Published online: 23 September 2009 Ó Humana Press Inc. 2009 Abstract Human papillomavirus (HPV) has been impli- cated in cervical carcinoma and the p53 gene is polymor- phic at amino acid 72 of the protein that it encodes. The association between p53 polymorphisms and risk for HPV- associated cervical cancer has been examined, but the results have been conflicting. It has been reported that patients with the arginine form have a higher risk of developing cervical cancer than those with the proline form. The purpose of this study was to examine whether p53 Arg at the polymorphic position 72 could represents a risk factor for women with high-risk HPV-associated malignant cervical lesions. In this study, the polymorphism was examined by both allele-specific PCR and RFLP analysis in 113 patients with cervical cancer and in 100 healthy controls. There was no statistical difference in the subtype distribution between the cervix cancer and the control groups. There was no significant association between genotype distribution of the p53 codon 72 poly- morphism and HPV infection. Thus, polymorphism of the p53 itself as well as in combination with HPV infection may not be a genetic risk for cervical cancer and therefore much attention should be paid to other risk factors such as sexual behavior and smoking. Keywords Cervical cancer  HPV  p53 codon 72 polymorphism Introduction Cervical carcinoma in women is the second most common type of cancer worldwide. The incidence is greater in developing countries where this disease is one of the major causes of death from cancer in women, with an overall survival rate of 40% [1]. Human papillomavirus (HPV) is considered as a necessary cause of most cervical cancers; HPV positivity in cervical cancer is estimated to be between 90 and 95% [2, 3]. Up to now, more than 200 HPV genotypes were recensed, but the interest is focused only on 30 types that are closely associated to cervical lesions. Among them, 15 HPV types have been classified as high- risk types (16, 18, 31, 33, 35, 39, 45, 51, 52, 56, 58, 59, 68, 73 and 82); 3 have been classified as probable high-risk types (26, 53 and 66); and 12 have been classified as low risk types (6, 11, 40, 42, 43, 44, 54, 61, 70, 72, 81 and CP6108) [3]. Among the high-risk HPV genotypes, HPV 16 is the most common in squamous cell carcinoma of the cervix (50–60%), followed by HPV 18, which is present in about 11–15% of cervical cancer cases [3, 4]. Oncogenicity of HPVs is due to the activity of two oncoproteins E6 and E7 [5]. E7 protein can bind to and render inactive the retinoblastoma cellular tumor suppressor protein pRB [6]. E6 protein interacts with protein p53 and inhibits its activity, followed by proteolytic degradation through the ubiquitin pathway [7, 8]. In addition to inducing the rapid degradation of p53, E6 also binds to and degrades FADD, preventing the trans- mission of apoptotic signals via the Fas pathway [5]. Recently, it was shown that sustained inactivation of the M. M. El khair  M. M. Ennaji (&)  R. El kebbaj  R. A. Mhand Laboratory of Virology and Hygiene & Microbiology, Department of Biology, Faculty of Science and Technology, University Hassan II-Mohammedia, 20650 Mohammedia, Morocco e-mail: m.ennaji@univh2m.ac.ma; m.ennaji@yahoo.fr M. M. El khair  R. El kebbaj  M. Attaleb  M. El Mzibri Molecular Biology Laboratory, National Center for Energy, Nuclear Science and Technology (CNESTEN), Rabat, Morocco e-mail: mzibri@yahoo.com Med Oncol (2010) 27:861–866 DOI 10.1007/s12032-009-9297-6