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Article: High-throughput tissue microarray analysis of c-myc activation in chronic liver diseases and hepatocellular carcinoma

TitleHigh-throughput tissue microarray analysis of c-myc activation in chronic liver diseases and hepatocellular carcinoma
Authors
Keywordsc-myc amplification
FISH
fluorescence in situ hybridization
HbsAG
HCC
hepatitis B surface antigen
hepatocellular carcinoma
immunohistochemistry
Issue Date2004
PublisherWB Saunders Co. The Journal's web site is located at http://www.elsevier.com/locate/humpath
Citation
Human Pathology, 2004, v. 35 n. 11, p. 1324-1331 How to Cite?
AbstractAmplification of 8q23-qter is common in human hepatocellular carcinoma (HCC). c-myc, an oncogene located on 8q24, may be important in hepatocarcinogenesis. The present study aimed to evaluate c-myc activation in hepatocarcinogenesis and its clinicopathological significance. High-throughput analysis of c-myc gene amplification and expression using dual-color fluorescence in situ hybridization and immunohistochemistry was performed on tissue microarrays consisting of 458 liver samples comprising HCCs, nontumorous livers and normal livers. HCCs demonstrated frequent c-myc amplification (30% when corrected for chromosome 8 aneusomy). In contrast, the noncancerous livers, which were mostly chronic hepatitis and cirrhosis, exhibited no c-myc amplification. Despite c-myc amplification, the HCCs exhibited less nuclear c-myc expression than the livers with chronic liver diseases and normal livers (P <0.001 and 0.004, respectively). The HCCs also had less cytoplasmic c-myc staining than the livers with chronic liver diseases (P = 0.002). Despite their absence of c-myc amplification, however, the livers with chronic disease had significantly increased expression of both nuclear and cytoplasmic c-myc protein compared with normal livers (P = 0.015 and 0.009, respectively). Clinicopathologically, the reduction in nuclear c-myc was more marked in HCCs with venous permeation and absence of tumor encapsulation (P = 0.013 and 0.021, respectively), whereas HCCs with cytoplasmic c-myc were positively associated with larger tumor size (P = 0.027). There was no significant association between c-myc amplification and protein expression levels in HCC. Our results suggest that overexpression of c-myc in chronic liver diseases may play an important role in the predisposition to hepatocarcinogenesis. Although c-myc was amplified in HCC, there appears to be a tight regulation by independent pathways of c-myc activation in hepatocarcinogenesis. © 2004 Elsevier Inc. All rights reserved.
Persistent Identifierhttp://hdl.handle.net/10722/71958
ISSN
2015 Impact Factor: 2.791
2015 SCImago Journal Rankings: 1.363
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorChan, KLen_HK
dc.contributor.authorGuan, XYen_HK
dc.contributor.authorNg, IOLen_HK
dc.date.accessioned2010-09-06T06:36:54Z-
dc.date.available2010-09-06T06:36:54Z-
dc.date.issued2004en_HK
dc.identifier.citationHuman Pathology, 2004, v. 35 n. 11, p. 1324-1331en_HK
dc.identifier.issn0046-8177en_HK
dc.identifier.urihttp://hdl.handle.net/10722/71958-
dc.description.abstractAmplification of 8q23-qter is common in human hepatocellular carcinoma (HCC). c-myc, an oncogene located on 8q24, may be important in hepatocarcinogenesis. The present study aimed to evaluate c-myc activation in hepatocarcinogenesis and its clinicopathological significance. High-throughput analysis of c-myc gene amplification and expression using dual-color fluorescence in situ hybridization and immunohistochemistry was performed on tissue microarrays consisting of 458 liver samples comprising HCCs, nontumorous livers and normal livers. HCCs demonstrated frequent c-myc amplification (30% when corrected for chromosome 8 aneusomy). In contrast, the noncancerous livers, which were mostly chronic hepatitis and cirrhosis, exhibited no c-myc amplification. Despite c-myc amplification, the HCCs exhibited less nuclear c-myc expression than the livers with chronic liver diseases and normal livers (P <0.001 and 0.004, respectively). The HCCs also had less cytoplasmic c-myc staining than the livers with chronic liver diseases (P = 0.002). Despite their absence of c-myc amplification, however, the livers with chronic disease had significantly increased expression of both nuclear and cytoplasmic c-myc protein compared with normal livers (P = 0.015 and 0.009, respectively). Clinicopathologically, the reduction in nuclear c-myc was more marked in HCCs with venous permeation and absence of tumor encapsulation (P = 0.013 and 0.021, respectively), whereas HCCs with cytoplasmic c-myc were positively associated with larger tumor size (P = 0.027). There was no significant association between c-myc amplification and protein expression levels in HCC. Our results suggest that overexpression of c-myc in chronic liver diseases may play an important role in the predisposition to hepatocarcinogenesis. Although c-myc was amplified in HCC, there appears to be a tight regulation by independent pathways of c-myc activation in hepatocarcinogenesis. © 2004 Elsevier Inc. All rights reserved.en_HK
dc.languageengen_HK
dc.publisherWB Saunders Co. The Journal's web site is located at http://www.elsevier.com/locate/humpathen_HK
dc.relation.ispartofHuman Pathologyen_HK
dc.subjectc-myc amplificationen_HK
dc.subjectFISHen_HK
dc.subjectfluorescence in situ hybridizationen_HK
dc.subjectHbsAGen_HK
dc.subjectHCCen_HK
dc.subjecthepatitis B surface antigenen_HK
dc.subjecthepatocellular carcinomaen_HK
dc.subjectimmunohistochemistryen_HK
dc.subject.meshAdolescenten_HK
dc.subject.meshAdulten_HK
dc.subject.meshAgeden_HK
dc.subject.meshAged, 80 and overen_HK
dc.subject.meshCarcinoma, Hepatocellular - genetics - metabolism - pathologyen_HK
dc.subject.meshChilden_HK
dc.subject.meshChild, Preschoolen_HK
dc.subject.meshChronic Diseaseen_HK
dc.subject.meshFemaleen_HK
dc.subject.meshHumansen_HK
dc.subject.meshImmunohistochemistryen_HK
dc.subject.meshIn Situ Hybridization, Fluorescenceen_HK
dc.subject.meshLiver Neoplasms - genetics - metabolism - pathologyen_HK
dc.subject.meshMaleen_HK
dc.subject.meshMiddle Ageden_HK
dc.subject.meshOligonucleotide Array Sequence Analysisen_HK
dc.subject.meshProto-Oncogene Proteins c-myc - biosynthesis - geneticsen_HK
dc.subject.meshTumor Markers, Biological - metabolismen_HK
dc.titleHigh-throughput tissue microarray analysis of c-myc activation in chronic liver diseases and hepatocellular carcinomaen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0046-8177&volume=35&issue=11&spage=1324&epage=1331&date=2004&atitle=High-throughput+tissue+microarray+analysis+of+c-myc+activation+in+chronic+liver+diseases+and+hepatocellular+carcinomaen_HK
dc.identifier.emailGuan, XY:xyguan@hkucc.hku.hken_HK
dc.identifier.emailNg, IOL:iolng@hkucc.hku.hken_HK
dc.identifier.authorityGuan, XY=rp00454en_HK
dc.identifier.authorityNg, IOL=rp00335en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1016/j.humpath.2004.06.012en_HK
dc.identifier.pmid15668888-
dc.identifier.scopuseid_2-s2.0-10044285749en_HK
dc.identifier.hkuros100399en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-10044285749&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume35en_HK
dc.identifier.issue11en_HK
dc.identifier.spage1324en_HK
dc.identifier.epage1331en_HK
dc.identifier.isiWOS:000225940800004-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridChan, KL=8277448400en_HK
dc.identifier.scopusauthoridGuan, XY=7201463221en_HK
dc.identifier.scopusauthoridNg, IOL=7102753722en_HK

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