p53 and p21 Expression in Precancerous Lesions and Carcinomas of the Uterine Cervix: Overexpression of p53 Predicts Poor Disease Outcome

Huang, Lee-Wen; Chou, Yuh-Yu; Chao, Shiouh-Lirng; Chen, Tong‐Jong; Lee, Tigris T.Y.

doi:10.1006/gyno.2001.6397

Cited by 40 publications

(25 citation statements)

References 22 publications

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“…Thus, HPV E6 is incompletely inactivating p53 at all evaluated tissue sites. The analysis of human cervical cancers has led to the same conclusion in that some human cervical cancers still express detectable p53 protein, indicative of E6 not completely degrading it (41,42). Thus, our mouse model for cervical cancer recapitulates a feature of human cervical cancer in that p53 is not completely inactivated by E6.…”

Section: Discussionsupporting

confidence: 57%

p53 Loss Synergizes with Estrogen and Papillomaviral Oncogenes to Induce Cervical and Breast Cancers

2008

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Section: Discussionsupporting

confidence: 57%

p53 Loss Synergizes with Estrogen and Papillomaviral Oncogenes to Induce Cervical and Breast Cancers

2008

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“…However, Nadal et al reported that high p21 expression was noted in squamous cell differentiation of laryngeal carcinomas, whereas poorly differentiated carcinomas had low p21 protein expression [32]. In our previous study, p21 was abundantly expressed in precancerous lesions but was down regulated in the microinvasive carcinoma and further down regulated in the invasive carcinoma [19]. This paradoxical increase in p21 expression might be related to the role of p21 in cell differentiation.…”

Section: Discussionmentioning

confidence: 78%

“…In addition, we found that there was significantly increased expression of p53 in advanced-stage cervical carcinomas, which implies that inactivation of p53 is associated with tumor progression [19]. In vitro, high-risk HPV E6 protein can bind to p53, which results in the rapid ubiquitin-dependent degradation of p53 [20].…”

Section: Introductionmentioning

confidence: 97%

Decreased p21 Expression in HPV-18 Positive Cervical Carcinomas

Huang

Seow

Lee

et al. 2009

Pathol. Oncol. Res.

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The aim of this study was to investigate the relationship between different human papillomavirus (HPV) genotypes and the expression of p53, p21 and p27 in cervical carcinomas. A total of 103 cases of cervical carcinomas were assayed for expression of p53, p21 and p27 by immunohistochemistry. HPV typing was carried out by two polymerase chain reaction-based methods. Overall, HPV prevalence was 97.1% among the cervical carcinomas in this study. HPV-16 was detected in 66% of the tumors, HPV-18 in 7.8%, HPV-16/18 in 7.8% and other HPV types in 15.5%. The expression of p53 and p27 was not related to HPV genotype. However, in the HPV-18 positive cervical carcinomas, expression of p21 was significantly decreased or completely absent (P = 0.019). Our results indicated that down-regulation of p21 was strongly associated with HPV-18 positive cervical carcinomas. The significantly lower expression of p21 protein in HPV-18 positive samples compared to HPV-18 negative cervical carcinomas supports the hypothesis that inactivation and degradation of p21 proteins by HPV-18 E7 may play an important role in the carcinogenesis of HPV-18 positive cervical neoplasia.

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“…The major consequence of inhibiting p53 function is to inhibit a key inducer of apoptosis in transformed cells. Paradoxically, many cervical tumors often reveal detectable levels of p53 (22,14), possibly reflecting incomplete degradation by E6. Alternative possibilities to explain the detection of the p53 protein include the presence of variants of E6 incapable of degrading p53 (16) and the presence of feedback loops that lead to high p53 levels consequent to E6 expression.…”

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confidence: 99%

Activated Notch1 Inhibits p53-Induced Apoptosis and Sustains Transformation by Human Papillomavirus Type 16 E6 and E7 Oncogenes through a PI3K-PKB/Akt-Dependent Pathway

Nair

Somasundaram

Krishna

2003

J Virol

150

123

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Activated Notch1 (AcN1) alleles cooperate with oncogenes from DNA tumor viruses in transformation of epithelial cells. AcN1 signaling has pleiotropic effects, and suggested oncogenic roles include driving proliferation through cyclin D1 or the generation of resistance to apoptosis on matrix withdrawal through a phosphatidylinositol 3-kinase (PI3K)-PKB/Akt-dependent pathway. Here, we extend the antiapoptotic role for AcN1 by showing inhibition of p53-induced apoptosis and transactivation. Chemical inhibitors of the PI3K pathway block AcN1-induced inhibition of p53-dependent apoptosis and nuclear localization of Hdm2. We show that expression of wild-type p53 does not inhibit synergistic transformation by AcN1 and human papillomavirus E6 and E7 oncogenes. We suggest that activation of Notch signaling may serve as an additional mechanism to inhibit wild-type p53 function in papillomavirus-associated neoplasia.

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p53 and p21 Expression in Precancerous Lesions and Carcinomas of the Uterine Cervix: Overexpression of p53 Predicts Poor Disease Outcome

Cited by 40 publications

References 22 publications

p53 Loss Synergizes with Estrogen and Papillomaviral Oncogenes to Induce Cervical and Breast Cancers

p53 Loss Synergizes with Estrogen and Papillomaviral Oncogenes to Induce Cervical and Breast Cancers

Decreased p21 Expression in HPV-18 Positive Cervical Carcinomas

Activated Notch1 Inhibits p53-Induced Apoptosis and Sustains Transformation by Human Papillomavirus Type 16 E6 and E7 Oncogenes through a PI3K-PKB/Akt-Dependent Pathway

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