G2 checkpoint in uterine cervical cancer with HPV 16 E6 according to p53 polymorphism and its screening value☆

Cho, Nam Hoon; Lim, Shin Young; Kim, Young Tae; Kim, Dongki; Kim, Young Sun; Kim, Jae Wook

doi:10.1016/s0090-8258(03)00198-7

Cited by 11 publications

(7 citation statements)

References 29 publications

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“…According to the inclusion criteria, 28 studies (Minaguchi et al, 1998;Ngan et al, 1999;Baek et al, 2000;Kim et al, 2000;Kim et al, 2001;Yang et al, 2001;Bhattacharya et al, 2002;Kawamata et al, 2002;Nagpal et al, 2002;Saranath et al, 2002;Xi et al, 2002;Cho et al, 2003;Katiyar et al, 2003;Cho et al, 2004;Lee et al, 2004;Li et al, 2004;Wang et al, 2004;Wu et al, 2004;Yoshimitsu et al, 2004;Masatsugu et al, 2005;Mitra et Yao et al, 2008;Zheng et al, 2008;Zhou et al, 2009) were included and 103 were excluded in this meta-analysis. The flow chart of study selection is shown in Figure 1.…”

Section: Studies Included In the Meta-analysismentioning

confidence: 99%

Association Between p53 codon 72 Polymorphism and Cervical Cancer Risk Among Asians: a Huge Review and Meta-analysis

Zhou¹,

Gu²,

Zhang³

2012

Asian Pacific Journal of Cancer Prevention

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Section: Studies Included In the Meta-analysismentioning

confidence: 99%

Association Between p53 codon 72 Polymorphism and Cervical Cancer Risk Among Asians: a Huge Review and Meta-analysis

Zhou¹,

Gu²,

Zhang³

2012

Asian Pacific Journal of Cancer Prevention

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“…The arginine variant was found to interfere with one of the p53 polyproline regions that play a role in the induction of apoptosis (Mantovani and Banks, 1999). HPV 16 E6 alters the G2 checkpoint, and this shows a relation to the disruption of p53-regulated G2/M checkpoint (Cho et al, 2003). It has been reported that individuals who possess the Arg allele at codon 72 of p53 are susceptible to the development of HPV-associated cervical cancer, when compared to those who have the Pro allele.…”

Section: P53 Tumour Suppressormentioning

confidence: 99%

Molecular genetics of human cervical cancer: role of papillomavirus and the apoptotic cascade

Ledwaba

Dlamini

Naicker

et al. 2004

Biological Chemistry

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Cervical cancer is rated the second most common malignant tumour globally, and is aetiologically linked to human papillomavirus (HPV) infection. Here the cellular pathology under consideration of stem/progenitor cell carcinogenesis is reviewed. Of the three causative molecular mechanisms of cervical cancer, two are associated with HPV: firstly, the effect of the viral oncogenes, E6 and E7; and secondly, integration of the viral DNA into chromosomal regions of tumour phenotype. The third process involved is the repetitive loss of heterozygosity in some chromosomal regions. HPV can be classified into high- and low-risk types; the high-risk types encode two oncoproteins, E6 and E7, which interact with tumour suppressor proteins. The association results in the inactivation of tumour suppressor proteins and the abrogation of apoptosis. Apoptosis is referred to as programmed cell death, whereby a cell deliberately commits suicide, and thus regulates cell numbers during development and maintenance of cellular homeostasis. This review attempts to elucidate the role of apoptotic genes, and considers external factors that interact with HPV in the development and progression of cervical cancer. Therefore, an in-depth understanding of the apoptotic genes that control molecular mechanisms in cervical cancer are of critical importance. Useful targets for therapeutic strategies would be those that alter apoptotic pathways in a manner where the escape of HPV from surveillance by the host immune system is prevented. Such an approach directed at the apoptotic genes maybe useful in the treatment of cervical cancer.

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“…The oncogenic potential of HPV appears to be mediated by the E6 and E7 proteins, which are known to bind and inactivate the p53 and pRb proteins, respectively. Furthermore, the HPV E7 oncoprotein has been shown to abrogate p21 and p27 function 103,106,107. In addition to inactivation of the p53 and pRb proteins, other cell cycle regulatory proteins may be involved in the carcinogenesis of cervical cancer.…”

Section: Introductionmentioning

confidence: 99%

“…Cho et al found that cyclin B/p34cdc2 is significantly increased in HPV-16 or -18 positive cervical lesions, including CIN and SCC, in comparison with HPV-16 or -18 negative lesions 107. Southern et al demonstrated that expression of the cyclin B protein was up-regulated and persisted into the upper epithelial layers, in parallel with cyclin A expression, in HSIL infected with human papillomaviruses 16, 31, 33, 51, 58, 66, and 67 77.…”

Section: Introductionmentioning

confidence: 99%

Aberrant Cell Cycle Regulation in Cervical Carcinoma

Kim

Zhao

2005

Yonsei Med J

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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 p16INK4A-cyclin D1-CDK4/6-pRb-E2F, p21WAF1-p27KIP1-cyclinE-CDK2, and p14ARF-MDM2-p53 pathways. The results from several studies showed aberrant regulation of several cell cycle proteins, such as cyclin D, cyclin E, p16INK4A, p21WAF1, and p27KIP1, 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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G2 checkpoint in uterine cervical cancer with HPV 16 E6 according to p53 polymorphism and its screening value☆

Cited by 11 publications

References 29 publications

Association Between p53 codon 72 Polymorphism and Cervical Cancer Risk Among Asians: a Huge Review and Meta-analysis

Association Between p53 codon 72 Polymorphism and Cervical Cancer Risk Among Asians: a Huge Review and Meta-analysis

Molecular genetics of human cervical cancer: role of papillomavirus and the apoptotic cascade

Aberrant Cell Cycle Regulation in Cervical Carcinoma

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