Molecular events in uterine cervical cancer.
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.


METHODS
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.
Southern
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SA
Department of Pathology, University of Liverpool, Royal Liverpool University Hospital.
Herrington
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CS
D002453:Cell Cycle; D004198:Disease Susceptibility / Q000276:immunology; D005260:Female; D006801:Humans; D019656:Loss of Heterozygosity; D027383:Papillomaviridae; D012307:Risk Factors; D014412:Tumor Virus Infections / Q000150:complications* / Q000235:genetics; D002583:Uterine Cervical Neoplasms / Q000235:genetics / Q000473:pathology / Q000821:virology*