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- Publisher Website: 10.1016/j.humpath.2004.06.012
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- PMID: 15668888
- WOS: WOS:000225940800004
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Article: High-throughput tissue microarray analysis of c-myc activation in chronic liver diseases and hepatocellular carcinoma
Title | High-throughput tissue microarray analysis of c-myc activation in chronic liver diseases and hepatocellular carcinoma |
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Authors | |
Keywords | c-myc amplification FISH fluorescence in situ hybridization HbsAG HCC hepatitis B surface antigen hepatocellular carcinoma immunohistochemistry |
Issue Date | 2004 |
Publisher | WB 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? |
Abstract | Amplification 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 Identifier | http://hdl.handle.net/10722/71958 |
ISSN | 2023 Impact Factor: 2.7 2023 SCImago Journal Rankings: 0.936 |
ISI Accession Number ID | |
References |
DC Field | Value | Language |
---|---|---|
dc.contributor.author | Chan, KL | en_HK |
dc.contributor.author | Guan, XY | en_HK |
dc.contributor.author | Ng, IOL | en_HK |
dc.date.accessioned | 2010-09-06T06:36:54Z | - |
dc.date.available | 2010-09-06T06:36:54Z | - |
dc.date.issued | 2004 | en_HK |
dc.identifier.citation | Human Pathology, 2004, v. 35 n. 11, p. 1324-1331 | en_HK |
dc.identifier.issn | 0046-8177 | en_HK |
dc.identifier.uri | http://hdl.handle.net/10722/71958 | - |
dc.description.abstract | Amplification 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.language | eng | en_HK |
dc.publisher | WB Saunders Co. The Journal's web site is located at http://www.elsevier.com/locate/humpath | en_HK |
dc.relation.ispartof | Human Pathology | en_HK |
dc.subject | c-myc amplification | en_HK |
dc.subject | FISH | en_HK |
dc.subject | fluorescence in situ hybridization | en_HK |
dc.subject | HbsAG | en_HK |
dc.subject | HCC | en_HK |
dc.subject | hepatitis B surface antigen | en_HK |
dc.subject | hepatocellular carcinoma | en_HK |
dc.subject | immunohistochemistry | en_HK |
dc.subject.mesh | Adolescent | en_HK |
dc.subject.mesh | Adult | en_HK |
dc.subject.mesh | Aged | en_HK |
dc.subject.mesh | Aged, 80 and over | en_HK |
dc.subject.mesh | Carcinoma, Hepatocellular - genetics - metabolism - pathology | en_HK |
dc.subject.mesh | Child | en_HK |
dc.subject.mesh | Child, Preschool | en_HK |
dc.subject.mesh | Chronic Disease | en_HK |
dc.subject.mesh | Female | en_HK |
dc.subject.mesh | Humans | en_HK |
dc.subject.mesh | Immunohistochemistry | en_HK |
dc.subject.mesh | In Situ Hybridization, Fluorescence | en_HK |
dc.subject.mesh | Liver Neoplasms - genetics - metabolism - pathology | en_HK |
dc.subject.mesh | Male | en_HK |
dc.subject.mesh | Middle Aged | en_HK |
dc.subject.mesh | Oligonucleotide Array Sequence Analysis | en_HK |
dc.subject.mesh | Proto-Oncogene Proteins c-myc - biosynthesis - genetics | en_HK |
dc.subject.mesh | Tumor Markers, Biological - metabolism | en_HK |
dc.title | High-throughput tissue microarray analysis of c-myc activation in chronic liver diseases and hepatocellular carcinoma | en_HK |
dc.type | Article | en_HK |
dc.identifier.openurl | http://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+carcinoma | en_HK |
dc.identifier.email | Guan, XY:xyguan@hkucc.hku.hk | en_HK |
dc.identifier.email | Ng, IOL:iolng@hkucc.hku.hk | en_HK |
dc.identifier.authority | Guan, XY=rp00454 | en_HK |
dc.identifier.authority | Ng, IOL=rp00335 | en_HK |
dc.description.nature | link_to_subscribed_fulltext | - |
dc.identifier.doi | 10.1016/j.humpath.2004.06.012 | en_HK |
dc.identifier.pmid | 15668888 | - |
dc.identifier.scopus | eid_2-s2.0-10044285749 | en_HK |
dc.identifier.hkuros | 100399 | en_HK |
dc.relation.references | http://www.scopus.com/mlt/select.url?eid=2-s2.0-10044285749&selection=ref&src=s&origin=recordpage | en_HK |
dc.identifier.volume | 35 | en_HK |
dc.identifier.issue | 11 | en_HK |
dc.identifier.spage | 1324 | en_HK |
dc.identifier.epage | 1331 | en_HK |
dc.identifier.isi | WOS:000225940800004 | - |
dc.publisher.place | United States | en_HK |
dc.identifier.scopusauthorid | Chan, KL=8277448400 | en_HK |
dc.identifier.scopusauthorid | Guan, XY=7201463221 | en_HK |
dc.identifier.scopusauthorid | Ng, IOL=7102753722 | en_HK |
dc.identifier.issnl | 0046-8177 | - |