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Aberrant Cell Cycle Regulation in Cervical Carcinoma

Carcinoma of the uterine cervix is one of the most common malignancies among women worldwide. Human papillomaviruses (HPV) have been identified as the major etiological factor in cervical carcinogenesis. However, the time lag between HPV infection and the diagnosis of cancer indicates that multiple...

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Autores principales: Kim, Young Tae, Zhao, Min
Formato: Texto
Lenguaje:English
Publicado: Yonsei University College of Medicine 2005
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2810564/
https://www.ncbi.nlm.nih.gov/pubmed/16259056
http://dx.doi.org/10.3349/ymj.2005.46.5.597
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author Kim, Young Tae
Zhao, Min
author_facet Kim, Young Tae
Zhao, Min
author_sort Kim, Young Tae
collection PubMed
description Carcinoma of the uterine cervix is one of the most common malignancies among women worldwide. Human papillomaviruses (HPV) have been identified as the major etiological factor in cervical carcinogenesis. However, the time lag between HPV infection and the diagnosis of cancer indicates that multiple steps, as well as multiple factors, may be necessary for the development of cervical cancer. The development and progression of cervical carcinoma have been shown to be dependent on various genetic and epigenetic events, especially alterations in the cell cycle checkpoint machinery. In mammalian cells, control of the cell cycle is regulated by the activity of cyclin-dependent kinases (CDKs) and their essential activating coenzymes, the cyclins. Generally, CDKs, cyclins, and CDK inhibitors function within several pathways, including the p16(INK4A)-cyclin D1-CDK4/6-pRb-E2F, p21(WAF1)-p27(KIP1)-cyclinE-CDK2, and p14(ARF)-MDM2-p53 pathways. The results from several studies showed aberrant regulation of several cell cycle proteins, such as cyclin D, cyclin E, p16(INK4A), p21(WAF1), and p27(KIP1), as characteristic features of HPV-infected and HPV E6/E7 oncogene-expressing cervical carcinomas and their precursors. These data suggested further that interactions of viral proteins with host cellular proteins, particularly cell cycle proteins, are involved in the activation or repression of cell cycle progression in cervical carcinogenesis.
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spelling pubmed-28105642010-01-26 Aberrant Cell Cycle Regulation in Cervical Carcinoma Kim, Young Tae Zhao, Min Yonsei Med J Review Article Carcinoma of the uterine cervix is one of the most common malignancies among women worldwide. Human papillomaviruses (HPV) have been identified as the major etiological factor in cervical carcinogenesis. However, the time lag between HPV infection and the diagnosis of cancer indicates that multiple steps, as well as multiple factors, may be necessary for the development of cervical cancer. The development and progression of cervical carcinoma have been shown to be dependent on various genetic and epigenetic events, especially alterations in the cell cycle checkpoint machinery. In mammalian cells, control of the cell cycle is regulated by the activity of cyclin-dependent kinases (CDKs) and their essential activating coenzymes, the cyclins. Generally, CDKs, cyclins, and CDK inhibitors function within several pathways, including the p16(INK4A)-cyclin D1-CDK4/6-pRb-E2F, p21(WAF1)-p27(KIP1)-cyclinE-CDK2, and p14(ARF)-MDM2-p53 pathways. The results from several studies showed aberrant regulation of several cell cycle proteins, such as cyclin D, cyclin E, p16(INK4A), p21(WAF1), and p27(KIP1), as characteristic features of HPV-infected and HPV E6/E7 oncogene-expressing cervical carcinomas and their precursors. These data suggested further that interactions of viral proteins with host cellular proteins, particularly cell cycle proteins, are involved in the activation or repression of cell cycle progression in cervical carcinogenesis. Yonsei University College of Medicine 2005-10-31 2005-10-31 /pmc/articles/PMC2810564/ /pubmed/16259056 http://dx.doi.org/10.3349/ymj.2005.46.5.597 Text en Copyright © 2005 The Yonsei University College of Medicine http://creativecommons.org/licenses/by-nc/3.0 This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/3.0) which permits unrestricted noncommercial use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Review Article
Kim, Young Tae
Zhao, Min
Aberrant Cell Cycle Regulation in Cervical Carcinoma
title Aberrant Cell Cycle Regulation in Cervical Carcinoma
title_full Aberrant Cell Cycle Regulation in Cervical Carcinoma
title_fullStr Aberrant Cell Cycle Regulation in Cervical Carcinoma
title_full_unstemmed Aberrant Cell Cycle Regulation in Cervical Carcinoma
title_short Aberrant Cell Cycle Regulation in Cervical Carcinoma
title_sort aberrant cell cycle regulation in cervical carcinoma
topic Review Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2810564/
https://www.ncbi.nlm.nih.gov/pubmed/16259056
http://dx.doi.org/10.3349/ymj.2005.46.5.597
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