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Article: Disruption of p53-p21/WAF1 cell cycle pathway contributes to progression and worse clinical outcome of hepatocellular carcinoma.

TitleDisruption of p53-p21/WAF1 cell cycle pathway contributes to progression and worse clinical outcome of hepatocellular carcinoma.
Authors
Issue Date2004
PublisherDemetrios A Spandidos Ed & Pub. The Journal's web site is located at http://147.52.72.117/OR/or.htm
Citation
Oncology Reports, 2004, v. 12 n. 1, p. 25-31 How to Cite?
Abstractp53-p21/WAF1 cell cycle pathway plays an important role in growth control, and the inappropriate deregulation of this pathway has been implicated in carcinogenesis. Although the role of p53 in hepatocellular carcinoma (HCC) has been suggested, its exact molecular mechanism in relation to its down-stream gene p21/WAF1 remains unclear. To investigate the relationship between the expression of p53 and p21/WAF1 and the possible roles of the 2 proteins in HCC, we examined the intracellular expression of p53, p21/WAF1 and PCNA immunohistochemically, together with apoptosis by terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick-end labeling assay in 35 clinical tissue specimens. The correlation between the clinicopathologic parameters and the intracellular gene expression were analyzed. The results showed that p53 over-expression is a reliable marker for mutational modulation of p53 function. p53 was negatively correlated with p21/WAF1 in hepatitis B virus-related HCC (p=0.024, r=-0.432). Patients with a high p53 expression had a significantly higher Edmondson grading (12/21 vs 13/14, p=0.024) and larger tumor size (10 vs 6 cm, p=0.029). Patients with higher p53 expression had shorter disease-free survival (4 vs 19 months, p=0.0131) and overall survival (11 vs 42 months, p=0.0031). Intracellular expression of p21/WAF1 was positively correlated to proliferating cell nuclear antigen (p=0.001, r=0.776) and apoptosis (p=0.003, r=0.639). Our findings suggest that disruption of p53-p21/WAF1 cell cycle pathways contributes to tumor progression and worse clinical outcome of HCC.
Persistent Identifierhttp://hdl.handle.net/10722/148417
ISSN
2015 Impact Factor: 2.486
2015 SCImago Journal Rankings: 0.968
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorLee, TKen_US
dc.contributor.authorMan, Ken_US
dc.contributor.authorPoon, RTen_US
dc.contributor.authorLo, CMen_US
dc.contributor.authorNg, IOen_US
dc.contributor.authorFan, STen_US
dc.date.accessioned2012-05-29T06:12:51Z-
dc.date.available2012-05-29T06:12:51Z-
dc.date.issued2004en_US
dc.identifier.citationOncology Reports, 2004, v. 12 n. 1, p. 25-31en_US
dc.identifier.issn1021-335Xen_US
dc.identifier.urihttp://hdl.handle.net/10722/148417-
dc.description.abstractp53-p21/WAF1 cell cycle pathway plays an important role in growth control, and the inappropriate deregulation of this pathway has been implicated in carcinogenesis. Although the role of p53 in hepatocellular carcinoma (HCC) has been suggested, its exact molecular mechanism in relation to its down-stream gene p21/WAF1 remains unclear. To investigate the relationship between the expression of p53 and p21/WAF1 and the possible roles of the 2 proteins in HCC, we examined the intracellular expression of p53, p21/WAF1 and PCNA immunohistochemically, together with apoptosis by terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick-end labeling assay in 35 clinical tissue specimens. The correlation between the clinicopathologic parameters and the intracellular gene expression were analyzed. The results showed that p53 over-expression is a reliable marker for mutational modulation of p53 function. p53 was negatively correlated with p21/WAF1 in hepatitis B virus-related HCC (p=0.024, r=-0.432). Patients with a high p53 expression had a significantly higher Edmondson grading (12/21 vs 13/14, p=0.024) and larger tumor size (10 vs 6 cm, p=0.029). Patients with higher p53 expression had shorter disease-free survival (4 vs 19 months, p=0.0131) and overall survival (11 vs 42 months, p=0.0031). Intracellular expression of p21/WAF1 was positively correlated to proliferating cell nuclear antigen (p=0.001, r=0.776) and apoptosis (p=0.003, r=0.639). Our findings suggest that disruption of p53-p21/WAF1 cell cycle pathways contributes to tumor progression and worse clinical outcome of HCC.en_US
dc.languageengen_US
dc.publisherDemetrios A Spandidos Ed & Pub. The Journal's web site is located at http://147.52.72.117/OR/or.htmen_US
dc.relation.ispartofOncology reportsen_US
dc.subject.meshCarcinoma, Hepatocellular - Genetics - Mortality - Pathology - Surgery - Therapyen_US
dc.subject.meshCell Cycle - Geneticsen_US
dc.subject.meshCell Cycle Proteins - Geneticsen_US
dc.subject.meshCyclin-Dependent Kinase Inhibitor P21en_US
dc.subject.meshDisease Progressionen_US
dc.subject.meshGenes, P53 - Geneticsen_US
dc.subject.meshHepatectomyen_US
dc.subject.meshHumansen_US
dc.subject.meshImmunohistochemistryen_US
dc.subject.meshLiver Neoplasms - Genetics - Mortality - Pathology - Surgery - Therapyen_US
dc.subject.meshProliferating Cell Nuclear Antigen - Analysisen_US
dc.subject.meshSurvival Analysisen_US
dc.subject.meshTreatment Outcomeen_US
dc.titleDisruption of p53-p21/WAF1 cell cycle pathway contributes to progression and worse clinical outcome of hepatocellular carcinoma.en_US
dc.typeArticleen_US
dc.identifier.emailLee, TK:tkwlee@hkucc.hku.hken_US
dc.identifier.emailMan, K:kwanman@hkucc.hku.hken_US
dc.identifier.emailPoon, RT:poontp@hkucc.hku.hken_US
dc.identifier.emailLo, CM:chungmlo@hkucc.hku.hken_US
dc.identifier.emailNg, IO:iolng@hkucc.hku.hken_US
dc.identifier.emailFan, ST:stfan@hku.hken_US
dc.identifier.authorityLee, TK=rp00447en_US
dc.identifier.authorityMan, K=rp00417en_US
dc.identifier.authorityPoon, RT=rp00446en_US
dc.identifier.authorityLo, CM=rp00412en_US
dc.identifier.authorityNg, IO=rp00335en_US
dc.identifier.authorityFan, ST=rp00355en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.pmid15201954-
dc.identifier.scopuseid_2-s2.0-21644447666en_US
dc.identifier.hkuros90452-
dc.identifier.volume12en_US
dc.identifier.issue1en_US
dc.identifier.spage25en_US
dc.identifier.epage31en_US
dc.identifier.isiWOS:000222169100004-
dc.publisher.placeGreeceen_US
dc.identifier.scopusauthoridLee, TK=7501439435-
dc.identifier.scopusauthoridMan, K=7101754072-
dc.identifier.scopusauthoridPoon, RT=7103097223-
dc.identifier.scopusauthoridLo, CM=7401771672-
dc.identifier.scopusauthoridNg, IO=7102753722-
dc.identifier.scopusauthoridFan, ST=7402678224-

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