Risk factors of invasive cervical cancer in Morocco.

It is now well established that infection with oncogenic human papillomavirus (HPV) types is the necessary cause of cervical cancer (CC) and its immediate precursor cervical intraepithelial neoplasia 3. However, HPV infection alone may not be sufficient to cause CC, and other exogenous and endogenous factors may exist that, in conjunction with HPV, influence the risk of progression from cervical HPV infection to CC. In this chapter, we review the evidence for the role of parity, oral contraceptive (OC) use, and tobacco smoking in CC. In this study, molecular detection of HPV by PCR using consensus primers MY09/MY11 able to amplify the L1 gene present in all types of HPV from fresh frozen biopsies showed that the virus is present in 88% (99/113) of cases. The viral typing, carried out on HPV positive cases through hybridization using specifics probes MY14, WD74, WD126, MY16, MY70 and MY115 which correspond respectively to HPV 16, 18, 31, 33, 45 and 59 has revealed the prevalence of HPV 16 and 18 respectively with 65% (64/99) and 44.4% (44/99). Several combinations of double and multiple infections were also observed. Another part of this work has been devoted to the study of risk factors associated with the development of cancerous cervical lesions. The study is based on a questionnaire during the sampling and also on data collected from clinical records and records of hospital patients.

Molecular detection and genotyping of human papillomavirus in cervical carcinoma biopsies in an area of high incidence of cancer from Moroccan women.

Cervical cancer is a leading cause of cancer-related deaths in developing countries, and the human papillomavirus (HPV) is linked etiologically to cervical cancer. Eighty nine cervical carcinoma biopsies collected from women visiting the Oncologic Center in Casablanca (Centre Hospitalier Universitaire Ibn Rochd, Morocco) for cervical cancer symptoms, were screened for HPV DNA by polymerase chain reaction amplification with subsequent typing by hybridization with specific oligonucleotides for HPV types 16, 18, 31, 33, 45, and 59. Using very high stringency hybridization the HPV types could be easily distinguished. After preliminary clinical sorting, 92% (82/89) of the samples were found to be HPV-positive. Among the samples infected by a single HPV, type 16 was the most frequent 36.6% (30/82) of the positive samples, followed by HPV 18; 19.5% (16/82). Double or even multiple infections by the different HPV types were also detected (35.5% of the positive samples); dual infections were the more frequent, with the following combinations of HPVs: HPV16/HPV18 (21% of the positives samples) and HPV16/HPV45 (8.5%).