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Article: Clinicopathological significance of loss of heterozygosity on chromosome 13q in hepatocellular carcinoma

TitleClinicopathological significance of loss of heterozygosity on chromosome 13q in hepatocellular carcinoma
Authors
Issue Date2002
PublisherAmerican Association for Cancer Research.
Citation
Clinical Cancer Research, 2002, v. 8 n. 7, p. 2266-2272 How to Cite?
AbstractPurpose: Allelic loss is the most frequently genetic alteration found in hepatocellular carcinoma (HCC). Previous genome-wide studies have indicated that chromosome 13q is one of the most frequently affected chromosomes. However, reports on detailed deletion mapping as well as detailed clinicopathological correlation are scanty. Experimental Design: We performed high-density allelotyping on chromosome 13q in HCC from 60 patients and investigated the correlation between allelic losses on chromosome 13q and the clinicopathological features. Results: Allelic loss at one or more of the 29 microsatellite markers was found in 28 (47%) of the 60 HCCs. Allelic losses were more frequently found in tumors with larger size or in tumors at more advanced tumor stages (P = 0.015 and 0.012, respectively). These two clinicopathological features were also significantly associated with the accumulation of allelic losses in terms of fractional allelic loss index (P = 0.028 and 0.018, respectively). In addition, subchromosomal regions located at 13q12.3-14.1 and 13q32 were found to be significantly associated with advanced tumor stages and larger tumor size, respectively (P = 0.008 and 0.007). Conclusions: The overall findings suggested that allelic losses on 13q might play an important role in contributing to a more aggressive tumor behavior. Putative tumor suppressor genes might be harbored at 13q12.3-14.1 and 13q32, and inactivation of these genes via allelic losses might enhance tumor progression in HCC.
Persistent Identifierhttp://hdl.handle.net/10722/88483
ISSN
2015 Impact Factor: 8.738
2015 SCImago Journal Rankings: 5.314
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorWong, CMen_HK
dc.contributor.authorLee, JMFen_HK
dc.contributor.authorLau, TCMen_HK
dc.contributor.authorFan, STen_HK
dc.contributor.authorNg, IOLen_HK
dc.date.accessioned2010-09-06T09:43:58Z-
dc.date.available2010-09-06T09:43:58Z-
dc.date.issued2002en_HK
dc.identifier.citationClinical Cancer Research, 2002, v. 8 n. 7, p. 2266-2272en_HK
dc.identifier.issn1078-0432en_HK
dc.identifier.urihttp://hdl.handle.net/10722/88483-
dc.description.abstractPurpose: Allelic loss is the most frequently genetic alteration found in hepatocellular carcinoma (HCC). Previous genome-wide studies have indicated that chromosome 13q is one of the most frequently affected chromosomes. However, reports on detailed deletion mapping as well as detailed clinicopathological correlation are scanty. Experimental Design: We performed high-density allelotyping on chromosome 13q in HCC from 60 patients and investigated the correlation between allelic losses on chromosome 13q and the clinicopathological features. Results: Allelic loss at one or more of the 29 microsatellite markers was found in 28 (47%) of the 60 HCCs. Allelic losses were more frequently found in tumors with larger size or in tumors at more advanced tumor stages (P = 0.015 and 0.012, respectively). These two clinicopathological features were also significantly associated with the accumulation of allelic losses in terms of fractional allelic loss index (P = 0.028 and 0.018, respectively). In addition, subchromosomal regions located at 13q12.3-14.1 and 13q32 were found to be significantly associated with advanced tumor stages and larger tumor size, respectively (P = 0.008 and 0.007). Conclusions: The overall findings suggested that allelic losses on 13q might play an important role in contributing to a more aggressive tumor behavior. Putative tumor suppressor genes might be harbored at 13q12.3-14.1 and 13q32, and inactivation of these genes via allelic losses might enhance tumor progression in HCC.en_HK
dc.languageengen_HK
dc.publisherAmerican Association for Cancer Research.en_HK
dc.relation.ispartofClinical Cancer Researchen_HK
dc.subject.meshAdulten_HK
dc.subject.meshAgeden_HK
dc.subject.meshAged, 80 and overen_HK
dc.subject.meshAllelesen_HK
dc.subject.meshCarcinoma, Hepatocellular - genetics - pathologyen_HK
dc.subject.meshCell Differentiationen_HK
dc.subject.meshChromosome Deletionen_HK
dc.subject.meshChromosomes, Human, Pair 13 - geneticsen_HK
dc.subject.meshDNA, Neoplasm - metabolismen_HK
dc.subject.meshFemaleen_HK
dc.subject.meshHepatitis B Antigens - metabolismen_HK
dc.subject.meshHumansen_HK
dc.subject.meshLiver Diseases - genetics - pathologyen_HK
dc.subject.meshLiver Neoplasms - genetics - pathologyen_HK
dc.subject.meshLoss of Heterozygosityen_HK
dc.subject.meshMaleen_HK
dc.subject.meshMicrosatellite Repeatsen_HK
dc.subject.meshMiddle Ageden_HK
dc.subject.meshNeoplasm Invasivenessen_HK
dc.titleClinicopathological significance of loss of heterozygosity on chromosome 13q in hepatocellular carcinomaen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=1078-0432&volume=8&spage=2266&epage=2272&date=2002&atitle=Clinicopathological+significance+of+loss+of+heterozygosity+on+chromosome+13q+in+hepatocellular+carcinomaen_HK
dc.identifier.emailWong, CM: jackwong@pathology.hku.hken_HK
dc.identifier.emailFan, ST: stfan@hku.hken_HK
dc.identifier.emailNg, IOL: iolng@hkucc.hku.hken_HK
dc.identifier.authorityWong, CM=rp00231en_HK
dc.identifier.authorityFan, ST=rp00355en_HK
dc.identifier.authorityNg, IOL=rp00335en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.pmid12114430-
dc.identifier.scopuseid_2-s2.0-0035992384en_HK
dc.identifier.hkuros76735en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0035992384&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume8en_HK
dc.identifier.issue7en_HK
dc.identifier.spage2266en_HK
dc.identifier.epage2272en_HK
dc.identifier.isiWOS:000176740300032-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridWong, CM=16314668400en_HK
dc.identifier.scopusauthoridLee, JMF=36065603500en_HK
dc.identifier.scopusauthoridLau, TCM=17341008600en_HK
dc.identifier.scopusauthoridFan, ST=7402678224en_HK
dc.identifier.scopusauthoridNg, IOL=7102753722en_HK

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