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Human papillomavirus and cervical carcinogenesis
1Department of Pathology, Tennis Court Road, Cambridge, CB2 1QP, UK.
Best Practice & Research. Clinical Obstetrics & Gynaecology
|September 21, 2001
Summary
Genital human papillomavirus (HPV) infections are a major cause of cervical cancer. Oncogenic HPV E6 and E7 genes deregulate cell cycle controls, leading to cancer development through rare genetic events.
Area of Science:
- Oncology
- Virology
- Cell Biology
Background:
- Genital human papillomavirus (HPV) infection is a primary risk factor for cervical cancer.
- High-risk HPV types possess E6 and E7 oncogenes that disrupt cellular cycle regulation.
Purpose of the Study:
- To elucidate the mechanisms by which high-risk HPV oncogenes contribute to cervical cancer development.
- To understand the role of viral and cellular gene deregulation in HPV-driven oncogenesis.
Main Methods:
- Review of epidemiological and experimental studies on HPV infection and cervical cancer.
- Analysis of the function of HPV E6 and E7 oncogenes in cell cycle control.
- Investigation of factors influencing viral and cellular gene deregulation.
Main Results:
- High-level expression of HPV E6 and E7 genes is normally restricted to differentiated, non-dividing cells.
- HPV oncogenesis necessitates the deregulation of viral and cellular genes, allowing aberrant E6 and E7 expression.
- Viral persistence and sustained exposure to steroid hormones increase the likelihood of this critical deregulation.
Conclusions:
- Deregulation of viral and cellular genes is a key event in HPV-induced cervical carcinogenesis.
- Factors such as viral persistence and hormone exposure can promote the oncogenic transformation process initiated by HPV.