The human papillomavirus E6 protein and its contribution to malignant progression.
Fiamma Mantovani,Lawrence Banks +1 more
TLDR
This review discusses the interactions of the cellular proteins with which E6 interacts in the light of their respective contributions to the malignant progression of HPV transformed cells.Abstract:
The Human Papillomavirus (HPV) E6 protein is one of three oncoproteins encoded by the virus. It has long been recognized as a potent oncogene and is intimately associated with the events that result in the malignant conversion of virally infected cells. In order to understand the mechanisms by which E6 contributes to the development of human malignancy many laboratories have focused their attention on identifying the cellular proteins with which E6 interacts. In this review we discuss these interactions in the light of their respective contributions to the malignant progression of HPV transformed cells.read more
Citations
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Human papillomavirus and cervical cancer
TL;DR: The new HPV-oriented model of cervical carcinogenesis should gradually replace older morphological models based only on cytology and histology, and can minimise the incidence of cervical cancer, and the morbidity and mortality it causes, even in low-resource settings.
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Epithelial polarity and proliferation control: links from the Drosophila neoplastic tumor suppressors
TL;DR: In this article, the role of the fly nTSGs in controlling cell polarity and cell proliferation was reviewed. But whether the loss of polarity loss might causally contribute to cancer has remained unclear.
Journal ArticleDOI
Targeting proteins for destruction by the ubiquitin system: implications for human pathobiology.
TL;DR: This review focuses on the response to hypoxia, inflammatory diseases, neurodegenerative diseases, and muscle-wasting disorders, as well as human papillomaviruses, cervical cancer and other malignancies.
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Systematic Review of Genomic Integration Sites of Human Papillomavirus Genomes in Epithelial Dysplasia and Invasive Cancer of the Female Lower Genital Tract
TL;DR: It is confirmed that HPV integration sites are randomly distributed over the whole genome with a clear predilection for genomic fragile sites, and no evidence for targeted disruption or functional alteration of critical cellular genes by the integrated viral sequences could be found.
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The Epidemiology and Risk Factors of Head and Neck Cancer: a Focus on Human Papillomavirus
TL;DR: Not all HPV-positive HNSCC express the viral oncogenes (E6 and E7), which suggests that HPV may function as a carcinogen in a smaller proportion of H NSCC.
References
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WAF1, a potential mediator of p53 tumor suppression
Wafik S. El-Deiry,Takashi Tokino,Victor E. Velculescu,Daniel B. Levy,Ramon Parsons,Jeffrey M. Trent,D Lin,W. Edward Mercer,Kenneth W. Kinzler,Bert Vogelstein +9 more
TL;DR: A gene is identified, named WAF1, whose induction was associated with wild-type but not mutant p53 gene expression in a human brain tumor cell line and that could be an important mediator of p53-dependent tumor growth suppression.
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THE NF-κB AND IκB PROTEINS: New Discoveries and Insights
TL;DR: The transcription factor NF-κB has attracted widespread attention among researchers in many fields based on its unusual and rapid regulation, the wide range of genes that it controls, its central role in immunological processes, the complexity of its subunits, and its apparent involvement in several diseases.
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The p21 Cdk-interacting protein Cip1 is a potent inhibitor of G1 cyclin-dependent kinases
TL;DR: In this article, an improved two-hybrid system was employed to isolate human genes encoding Cdk-interacting proteins (Cips) and found that CIP1 is a potent, tight-binding inhibitor of Cdks and can inhibit the phosphorylation of Rb by cyclin A-Cdk2.
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Lessons from Hereditary Colorectal Cancer
TL;DR: The authors are grateful to the members of their laboratories for their contributions to the reviewed studies and to F. Giardiello and S. Hamilton for photographs of colorectal lesions.
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Mice deficient for p53 are developmentally normal but susceptible to spontaneous tumours
Lawrence A. Donehower,Michele Harvey,Betty L. Slagle,Mark J. McArthur,Charles A. Montgomery,Janet S. Butel,Allan Bradley +6 more
TL;DR: Observations indicate that a normal p53 gene is dispensable for embryonic development, that its absence predisposes the animal to neoplastic disease, and that an oncogenic mutant form of p53 is not obligatory for the genesis of many types of tumours.