Human papillomavirus oncoproteins: pathways to transformation.
An association between human papillomavirus (HPV) infection and the development of cervical cancer was initially reported over 30 years ago, and today there is overwhelming evidence that certain subtypes of HPV are the causative agents of these malignancies. The p53 and retinoblastoma proteins are well-characterized targets of the HPV E6 and E7 oncoproteins, but recent studies have shown that the alteration of additional pathways are equally important for transformation. These additional factors are crucial regulators of cell cycle progression, telomere maintenance, apoptosis and chromosomal stability. Understanding how HPV oncoproteins modify these activities provides novel insights into the basic mechanisms of oncogenesis.
Moody
Cary A
CA
Department of MicrobiologyImmunology, Feinberg School of Medicine, Northwestern University, Chicago, Illinois 60611, USA.
Laimins
Laimonis A
LA
D017209:Apoptosis; D002471:Cell Transformation, Neoplastic; D018385:Centrosome; D051357:Cyclin-Dependent Kinase 2 / Q000378:metabolism; D004249:DNA Damage; D050684:E2F Transcription Factors / Q000502:physiology; D005260:Female; D042822:Genomic Instability; D006801:Humans; D009856:Oncogene Proteins, Viral / Q000502:physiology*; D027383:Papillomaviridae / Q000502:physiology; D030361:Papillomavirus Infections / Q000150:complications*; D011401:Promoter Regions, Genetic; D016160:Retinoblastoma Protein / Q000378:metabolism; D016159:Tumor Suppressor Protein p53 / Q000378:metabolism; D002583:Uterine Cervical Neoplasms / Q000209:etiology* / Q000821:virology
D050684:E2F Transcription Factors; D009856:Oncogene Proteins, Viral; D016160:Retinoblastoma Protein; D016159:Tumor Suppressor Protein p53; D051357:Cyclin-Dependent Kinase 2