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Article: Expression of c-myc, c-fos, and c-jun in hepatocellular carcinoma

TitleExpression of c-myc, c-fos, and c-jun in hepatocellular carcinoma
Authors
KeywordsCell cycle
Hepatocarcinogenesis
Immunohistochemistry
Proliferation
Issue Date2001
PublisherJohn Wiley & Sons, Inc. The Journal's web site is located at http://www3.interscience.wiley.com/cgi-bin/jhome/28741
Citation
Cancer, 2001, v. 91 n. 1, p. 106-112 How to Cite?
AbstractBACKGROUND. Increased expression of the proto-oncogene c-myc is a common phenomenon in hepatocellular carcinoma (HCC). The proto-oncogenes c-fos and c-jun are involved in cell cycle progression and cellular proliferation. METHODS. The objective of this study was to elucidate the mechanism of hepatocarcinogenesis with regard to the expressions of c-myc, c-fos, and c-jun. One hundred fifty biopsied HCC specimens were stained immunohistochemically for the above phenotypic markers both in tumor tissue and in adjacent nontumor tissue. RESULTS. Although the expression of c-myc was high (74%) in tumor tissue, it was significantly less compared with the expression in nontumor tissue (100%; P = 0.0002). The expression of c-myc was inversely proportional to the grade of differentiation in tumor tissue (P = 0.0108; correlation coefficient [r] = -0.244); that is, tissue with poorer histologic differentiation had a lower level of c-myc expression. There were inverse associations between the expression of c-myc and the expression of mutated p53 (P = 0.0017; r = -0.285) as well as the expression of Ki67 (P = 0.057; r = -0.147). There was significantly high expression of c-fos in tumor tissue compared with the expression in nontumor tissue (91% vs. 0%; P < 0.0001). Both the tumor tissue and the nontumor tissue had high levels of expression of c-jun (96.53% and 100%, respectively). There was a trend toward a positive association between the expression of c-fos and the expression of c-jun in tumor tissue (P = 0.07; r = 0.162). CONCLUSIONS. Because c-myc is a known inducer of wild type p53, decreased c-myc expression may lead to uncontrolled cell growth because of the lack of p53 expression that normally induces apoptosis. The coordinated expression of c-fos and c-jun in HCC may reflect the coordinated tumor cell cycle of progression and proliferation; however, future studies are required to elucidate this possibility. © 2001 American Cancer Society.
Persistent Identifierhttp://hdl.handle.net/10722/77346
ISSN
2021 Impact Factor: 6.921
2020 SCImago Journal Rankings: 3.052
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorYuen, MFen_HK
dc.contributor.authorWu, PCen_HK
dc.contributor.authorLai, VCHen_HK
dc.contributor.authorLau, JYNen_HK
dc.contributor.authorLai, CLen_HK
dc.date.accessioned2010-09-06T07:30:55Z-
dc.date.available2010-09-06T07:30:55Z-
dc.date.issued2001en_HK
dc.identifier.citationCancer, 2001, v. 91 n. 1, p. 106-112en_HK
dc.identifier.issn0008-543Xen_HK
dc.identifier.urihttp://hdl.handle.net/10722/77346-
dc.description.abstractBACKGROUND. Increased expression of the proto-oncogene c-myc is a common phenomenon in hepatocellular carcinoma (HCC). The proto-oncogenes c-fos and c-jun are involved in cell cycle progression and cellular proliferation. METHODS. The objective of this study was to elucidate the mechanism of hepatocarcinogenesis with regard to the expressions of c-myc, c-fos, and c-jun. One hundred fifty biopsied HCC specimens were stained immunohistochemically for the above phenotypic markers both in tumor tissue and in adjacent nontumor tissue. RESULTS. Although the expression of c-myc was high (74%) in tumor tissue, it was significantly less compared with the expression in nontumor tissue (100%; P = 0.0002). The expression of c-myc was inversely proportional to the grade of differentiation in tumor tissue (P = 0.0108; correlation coefficient [r] = -0.244); that is, tissue with poorer histologic differentiation had a lower level of c-myc expression. There were inverse associations between the expression of c-myc and the expression of mutated p53 (P = 0.0017; r = -0.285) as well as the expression of Ki67 (P = 0.057; r = -0.147). There was significantly high expression of c-fos in tumor tissue compared with the expression in nontumor tissue (91% vs. 0%; P < 0.0001). Both the tumor tissue and the nontumor tissue had high levels of expression of c-jun (96.53% and 100%, respectively). There was a trend toward a positive association between the expression of c-fos and the expression of c-jun in tumor tissue (P = 0.07; r = 0.162). CONCLUSIONS. Because c-myc is a known inducer of wild type p53, decreased c-myc expression may lead to uncontrolled cell growth because of the lack of p53 expression that normally induces apoptosis. The coordinated expression of c-fos and c-jun in HCC may reflect the coordinated tumor cell cycle of progression and proliferation; however, future studies are required to elucidate this possibility. © 2001 American Cancer Society.en_HK
dc.languageengen_HK
dc.publisherJohn Wiley & Sons, Inc. The Journal's web site is located at http://www3.interscience.wiley.com/cgi-bin/jhome/28741en_HK
dc.relation.ispartofCanceren_HK
dc.rightsCancer. Copyright © John Wiley & Sons, Inc.en_HK
dc.subjectCell cycle-
dc.subjectHepatocarcinogenesis-
dc.subjectImmunohistochemistry-
dc.subjectProliferation-
dc.subject.meshAdolescenten_HK
dc.subject.meshAdulten_HK
dc.subject.meshAgeden_HK
dc.subject.meshAged, 80 and overen_HK
dc.subject.meshApoptosisen_HK
dc.subject.meshBiopsyen_HK
dc.subject.meshCarcinoma, Hepatocellular - genetics - physiopathologyen_HK
dc.subject.meshCell Cycleen_HK
dc.subject.meshCell Transformation, Neoplasticen_HK
dc.subject.meshFemaleen_HK
dc.subject.meshGene Expression Regulation, Neoplasticen_HK
dc.subject.meshGenes, fos - geneticsen_HK
dc.subject.meshGenes, jun - geneticsen_HK
dc.subject.meshGenes, myc - geneticsen_HK
dc.subject.meshHumansen_HK
dc.subject.meshImmunohistochemistryen_HK
dc.subject.meshLiver Neoplasms - genetics - physiopathologyen_HK
dc.subject.meshMaleen_HK
dc.subject.meshMiddle Ageden_HK
dc.subject.meshPhenotypeen_HK
dc.titleExpression of c-myc, c-fos, and c-jun in hepatocellular carcinomaen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0008-543X&volume=91&issue=1&spage=106&epage=112&date=2001&atitle=Expression+of+c-Myc,+c-Fos,+and+c-Jun+in+hepatocellular+carcinomaen_HK
dc.identifier.emailYuen, MF:mfyuen@hkucc.hku.hken_HK
dc.identifier.emailLai, CL:hrmelcl@hku.hken_HK
dc.identifier.authorityYuen, MF=rp00479en_HK
dc.identifier.authorityLai, CL=rp00314en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1002/1097-0142(20010101)91:1<106::AID-CNCR14>3.0.CO;2-2en_HK
dc.identifier.pmid11148566-
dc.identifier.scopuseid_2-s2.0-0035173815en_HK
dc.identifier.hkuros59908en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0035173815&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume91en_HK
dc.identifier.issue1en_HK
dc.identifier.spage106en_HK
dc.identifier.epage112en_HK
dc.identifier.isiWOS:000168675200014-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridYuen, MF=7102031955en_HK
dc.identifier.scopusauthoridWu, PC=7403119323en_HK
dc.identifier.scopusauthoridLai, VCH=36757583700en_HK
dc.identifier.scopusauthoridLau, JYN=7402446047en_HK
dc.identifier.scopusauthoridLai, CL=7403086396en_HK
dc.identifier.issnl0008-543X-

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