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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...
Autores principales: | , |
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Formato: | Texto |
Lenguaje: | English |
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Yonsei University College of Medicine
2005
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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. |
format | Text |
id | pubmed-2810564 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2005 |
publisher | Yonsei University College of Medicine |
record_format | MEDLINE/PubMed |
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 |
work_keys_str_mv | AT kimyoungtae aberrantcellcycleregulationincervicalcarcinoma AT zhaomin aberrantcellcycleregulationincervicalcarcinoma |