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The molecular biology of cervical cancer
Author(s) -
Münger Karl
Publication year - 1995
Publication title -
journal of cellular biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.028
H-Index - 165
eISSN - 1097-4644
pISSN - 0730-2312
DOI - 10.1002/jcb.240590908
Subject(s) - biology , cancer research , cervical cancer , retinoblastoma , cervix , genome instability , gene , suppressor , cancer , human papillomavirus , retinoblastoma protein , immunology , cell cycle , genetics , medicine , dna damage , dna
Infections with specific high‐risk types of human papillomavirus constitute a major risk factor in development of precancerous and cancerous lesions of the uterine cervix. Laboratory studies suggest that the human papillomavirus has a mechanistic role in development of these lesions. The two viral proteins consistently expressed in cervical carcinomas functionally abrogate critical cell cycle regulatory pathways, including those governed by the p53 tumor suppressor protein and the product of the retinoblastoma susceptibility gene, pRB. Subversion of these pathways by viral proteins causes genomic instability, resulting in the accumulation of chromosomal abnormalities followed by clonal expansion of malignant cells. Since continued expression of the papillomavirus proteins is critical for maintenance of the transformed state, they are attractive targets for prevention and therapy of precursor as well as cancerous lesions of the cervix.