Molecular events in uterine cervical cancer

• Published in: Sexually transmitted infections Vol. 74; no. 2; pp. 101 - 109
• Main Authors: Southern, S A, Herrington, C S
• Format: Journal Article
• Language: English
• Published: London BMJ 01.04.1998; BMJ Publishing Group LTD; BMJ Group
• Subjects: AIDS/HIV; Biological and medical sciences; Cell Cycle; Cervical cancer; Disease Susceptibility - immunology; Female; Female genital diseases; Gynecology. Andrology. Obstetrics; Humans; Loss of Heterozygosity; Medical sciences; Original; Papillomaviridae; Risk Factors; Tumor Virus Infections - complications; Tumor Virus Infections - genetics; Tumors; Uterine Cervical Neoplasms - genetics; Uterine Cervical Neoplasms - pathology; Uterine Cervical Neoplasms - virology; Human; Carcinoma; Etiopathogenesis; Papovaviridae; Malignant tumor; Review; Uterine cervix; Cofactor; Female genital diseases; Virology; Infection; Papillomavirus; Virus; Human papillomavirus; Viral disease; Risk factor; Female; Uterine cervix diseases
• ISSN: 1368-4973; 1472-3263
• DOI: 10.1136/sti.74.2.101

OBJECTIVE: To review the literature regarding the molecular events which occur in the development of uterine cervical cancer, with particular reference to human papillomavirus (HPV) infection. METHODOLOGY: Bibliographic searches of Medline and the ISI citation databases using appropriate keywords, including the following: papillomavirus, cervix, pathology, cyclin, chromosome, heterozygosity, telomerase, smoking, hormones, HLA, immune response, HIV, HSV, EBV. CONCLUSIONS: It has become clear that most cervical neoplasia, whether intraepithelial or invasive, is attributable in part to HPV infection. However, HPV infection alone is not sufficient, and, in a small proportion of cases, may not be necessary for malignant transformation. There is increasing evidence that HPV gene products interfere with cell cycle control leading to secondary accumulation of small and large scale genetic abnormalities. This may explain the association of viral persistence with lesion progression but, in many patients, secondary factors, such as smoking and immune response, are clearly important. However, the mechanisms involved in the interaction between HPV and host factors are poorly understood.