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Article: Microsatellite instability, Epstein-Barr virus, mutation of type II transforming growth factor β receptor and BAX in gastric carcinomas in Hong Kong Chinese

TitleMicrosatellite instability, Epstein-Barr virus, mutation of type II transforming growth factor β receptor and BAX in gastric carcinomas in Hong Kong Chinese
Authors
KeywordsBAX
Epstein-Barr virus
Gastric carcinoma
Hong Kong Chinese
Microsatellite instability
TβRII
Issue Date1999
PublisherNature Publishing Group. The Journal's web site is located at http://www.nature.com/bjc
Citation
British Journal Of Cancer, 1999, v. 79 n. 3-4, p. 582-588 How to Cite?
AbstractMicrosatellite instability (MI), the phenotypic manifestation of mismatch repair failure, is found in a proportion of gastric carcinomas. Little is known of the links between MI and Epstein-Barr virus (EBV) status and clinicopathological elements. Examination of genes mutated through the MI mechanism could also be expected to reveal important information on the carcinogenic pathway. Seventy-nine gastric carcinomas (61 EBV negative, 18 EBV positive) from local Hong Kong Chinese population, an intermediate-incidence area, were examined. Eight microsatellite loci, inclusive of the A10 tract of type II transforming growth factor β receptor (TβR-II), were used to evaluate the MI status. MI in the BAX and insulin-like growth factor II receptor (IGF-IIR) genes were also examined. High-level MI (> 40% unstable loci) was detected in ten cases (12.7%) and low-level MI (1-40% unstable loci) in three (3.8%). High-level MI was detected in two EBV-associated cases (11%) and the incidence was similar for the EBV-negative cases (13%). The high-level MIs were significantly associated with intestinal-type tumours (P = 0.03) and a more prominent lymphoid infiltrate (P = 0.04). Similar associations were noted in the EBV-positive carcinomas. The high-level MIs were more commonly located in the antrum, whereas the EBV-associated carcinomas were mostly located in body. Thirteen cardia cases were negative for both high-level MI and EBV. All patients aged below 55 were MI negative (P = 0.049). Of the high-level MIs, 80% had mutation in TβR-II, 40% in BAX and 0% in IGF-IIR. Of low-level MIs, 33% also had TβR-II mutation. These mutations were absent in the MI-negative cases. Of three lymphoepithelioma-like carcinomas, two cases were EBV positive and MI negative, one case was EBV negative but with high-level MI. In conclusion, high-level MIs were present regardless of the EBV status, and were found in a particular clinicopathological subset of gastric carcinoma patient. Inactivation of important growth regulatory genes observed in these carcinomas confirms the importance of MI in carcinogenesis.
Persistent Identifierhttp://hdl.handle.net/10722/148158
ISSN
2015 Impact Factor: 5.569
2015 SCImago Journal Rankings: 2.939
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorLeung, SYen_HK
dc.contributor.authorYuen, STen_HK
dc.contributor.authorChung, LPen_HK
dc.contributor.authorChu, KMen_HK
dc.contributor.authorWong, MPen_HK
dc.contributor.authorBranicki, FJen_HK
dc.contributor.authorHo, JCIen_HK
dc.date.accessioned2012-05-29T06:11:10Z-
dc.date.available2012-05-29T06:11:10Z-
dc.date.issued1999en_HK
dc.identifier.citationBritish Journal Of Cancer, 1999, v. 79 n. 3-4, p. 582-588en_HK
dc.identifier.issn0007-0920en_HK
dc.identifier.urihttp://hdl.handle.net/10722/148158-
dc.description.abstractMicrosatellite instability (MI), the phenotypic manifestation of mismatch repair failure, is found in a proportion of gastric carcinomas. Little is known of the links between MI and Epstein-Barr virus (EBV) status and clinicopathological elements. Examination of genes mutated through the MI mechanism could also be expected to reveal important information on the carcinogenic pathway. Seventy-nine gastric carcinomas (61 EBV negative, 18 EBV positive) from local Hong Kong Chinese population, an intermediate-incidence area, were examined. Eight microsatellite loci, inclusive of the A10 tract of type II transforming growth factor β receptor (TβR-II), were used to evaluate the MI status. MI in the BAX and insulin-like growth factor II receptor (IGF-IIR) genes were also examined. High-level MI (> 40% unstable loci) was detected in ten cases (12.7%) and low-level MI (1-40% unstable loci) in three (3.8%). High-level MI was detected in two EBV-associated cases (11%) and the incidence was similar for the EBV-negative cases (13%). The high-level MIs were significantly associated with intestinal-type tumours (P = 0.03) and a more prominent lymphoid infiltrate (P = 0.04). Similar associations were noted in the EBV-positive carcinomas. The high-level MIs were more commonly located in the antrum, whereas the EBV-associated carcinomas were mostly located in body. Thirteen cardia cases were negative for both high-level MI and EBV. All patients aged below 55 were MI negative (P = 0.049). Of the high-level MIs, 80% had mutation in TβR-II, 40% in BAX and 0% in IGF-IIR. Of low-level MIs, 33% also had TβR-II mutation. These mutations were absent in the MI-negative cases. Of three lymphoepithelioma-like carcinomas, two cases were EBV positive and MI negative, one case was EBV negative but with high-level MI. In conclusion, high-level MIs were present regardless of the EBV status, and were found in a particular clinicopathological subset of gastric carcinoma patient. Inactivation of important growth regulatory genes observed in these carcinomas confirms the importance of MI in carcinogenesis.en_HK
dc.languageengen_US
dc.publisherNature Publishing Group. The Journal's web site is located at http://www.nature.com/bjcen_HK
dc.relation.ispartofBritish Journal of Canceren_HK
dc.subjectBAXen_HK
dc.subjectEpstein-Barr virusen_HK
dc.subjectGastric carcinomaen_HK
dc.subjectHong Kong Chineseen_HK
dc.subjectMicrosatellite instabilityen_HK
dc.subjectTβRIIen_HK
dc.subject.meshAdulten_US
dc.subject.meshAgeden_US
dc.subject.meshCarcinoma - Genetics - Pathology - Virologyen_US
dc.subject.meshCell Transformation, Neoplastic - Geneticsen_US
dc.subject.meshDna Mutational Analysisen_US
dc.subject.meshDna, Neoplasm - Geneticsen_US
dc.subject.meshFemaleen_US
dc.subject.meshGenes, Tumor Suppressor - Geneticsen_US
dc.subject.meshHerpesviridae Infections - Complicationsen_US
dc.subject.meshHerpesvirus 4, Human - Pathogenicityen_US
dc.subject.meshHong Kongen_US
dc.subject.meshHumansen_US
dc.subject.meshMaleen_US
dc.subject.meshMicrosatellite Repeats - Geneticsen_US
dc.subject.meshMiddle Ageden_US
dc.subject.meshProto-Oncogene Proteins - Geneticsen_US
dc.subject.meshProto-Oncogene Proteins C-Bcl-2en_US
dc.subject.meshReceptors, Transforming Growth Factor Beta - Geneticsen_US
dc.subject.meshStomach Neoplasms - Genetics - Pathology - Virologyen_US
dc.subject.meshTumor Virus Infections - Complicationsen_US
dc.subject.meshBcl-2-Associated X Proteinen_US
dc.titleMicrosatellite instability, Epstein-Barr virus, mutation of type II transforming growth factor β receptor and BAX in gastric carcinomas in Hong Kong Chineseen_HK
dc.typeArticleen_HK
dc.identifier.emailLeung, SY: suetyi@hku.hken_HK
dc.identifier.emailChung, LP: lpchung@hkucc.hku.hken_HK
dc.identifier.emailChu, KM: chukm@hkucc.hku.hken_HK
dc.identifier.emailWong, MP: mwpik@hkucc.hku.hken_HK
dc.identifier.authorityLeung, SY=rp00359en_HK
dc.identifier.authorityChung, LP=rp00249en_HK
dc.identifier.authorityChu, KM=rp00435en_HK
dc.identifier.authorityWong, MP=rp00348en_HK
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1038/sj.bjc.6690092en_HK
dc.identifier.pmid10027334-
dc.identifier.scopuseid_2-s2.0-0032938931en_HK
dc.identifier.hkuros39506en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0032938931&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume79en_HK
dc.identifier.issue3-4en_HK
dc.identifier.spage582en_HK
dc.identifier.epage588en_HK
dc.identifier.isiWOS:000078165200033-
dc.publisher.placeUnited Kingdomen_HK
dc.identifier.scopusauthoridLeung, SY=7202044886en_HK
dc.identifier.scopusauthoridYuen, ST=7103160927en_HK
dc.identifier.scopusauthoridChung, LP=24315879100en_HK
dc.identifier.scopusauthoridChu, KM=7402453538en_HK
dc.identifier.scopusauthoridWong, MP=7403907887en_HK
dc.identifier.scopusauthoridBranicki, FJ=7003617514en_HK
dc.identifier.scopusauthoridHo, JCI=15029093800en_HK

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