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Query: UNIPROT:P04637 (p53)
 77,613 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Human papillomavirus (HPV) infection has been recognized as the major cause of cervical cancer. This article summarizes the functions of HPV gene products that cause abnormal cell growth--E6 and E7--and reviews how cellular and viral factors influence their synthesis. E6 and E7 inactivate two cellular tumor-suppressor gene products, p53 and RB. In cervical cancer, E6-E7 gene control is deranged by mutations in viral control sequences and in integrated HPV fragments by the disruption of the viral repressor E2. Elimination of this sequence makes E6-E7 mRNAs unstable, and deranges cellular regulation at the integration site. It is apparent that an intricate interplay of cellular and viral factors determines whether the outcome is active papillomavirus infection, viral latency, or ultimately, genital cancer.
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PMID:The genetic program of genital human papillomaviruses in infection and cancer. 898 74

Human papillomaviruses (HPVs) are a group of host-specific DNA viruses, with a remarkable epithelial cell specificity: they have been reported principally in the ano-genital tract, urethra, skin, larynx, tracheo-bronchial and oral mucosa. More than 100 different HPV types have been identified and classified as high (e.g. 16, 18, 31) or low (e.g. 11, 42, 36) -risk (HR and LR), based on their association with cervical carcinoma. The carcinogenic role of HR-HPV revolves mainly around two of its oncoproteins: HPV-E6 which promotes degradation of the p53 tumour suppressor gene product and HPV-E7 which modifies the pRb tumour suppressor gene product, inhibiting the activity of TGF-beta2. Since these viral oncoproteins are capable of transforming primary human keratinocytes from either genital or upper respiratory tract epithelia, they have been considered to play a role in disrupting cell-cycle regulatory pathways leading to a genetic progression to ano-genital cancer and, possibly, also to oral squamous cell carcinoma (OSCC). Recently, the oncogene HPV-E5 has also been found to transform cells by modulating growth factor receptors. On the basis of the high, although very variable, frequency of HR-HPV in OSCC, an oral malignant potential of HPV infection has been hypothesised but not definitively confirmed. Major aims of this review are to update the understanding of HPV activities with respect to oral oncology and to comment on the HPV DNA reported frequencies in OSCC and potentially malignant oral lesions. A computer database search was performed, through the use of MEDLINE (PubMED) and Cochrane Library, for the last three decades. Search key words used were: human papillomavirus, HPV and cancer, HPV and oral lesions, HPV and oral premalignant lesions, HPV and oral cancer, HPV and HNSCC, HPV and oral mucosa. The search was of all fields, all languages and all dates available.
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PMID:Human papillomavirus: its identity and controversial role in oral oncogenesis, premalignant and malignant lesions (review). 1733 19

The association between human papillomaviruses (HPV) and oral cancer was initially suggested nearly 30 years ago by us. Today, the research interest of head and neck squamous cell carcinoma (HNSCC) has substantially increased. HPV-associated HNSCC is considered a distinct clinical entity with better prognosis than the classical tobacco and alcohol associated cancers. HPV 16 seems to be the main genotype present in HNSCC and it most probably utilizes the same pathways in epithelial cell transformation as established for genital cancer. High-risk HPV E6 and E7 target the well characterized cellular proteins p53 and Rb, respectively. In addition, several other cellular targets of E6 and E7 have been identified. This review gives an overview on the biology of HPV which aids in dissecting the role of HPV in head and neck carcinogenesis. It also summarizes the possible pathways involved in creating new tools for diagnosis and therapy of HPV-associated HNSCC.
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PMID:Biology of human papillomavirus infections in head and neck carcinogenesis. 2278 19