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Article: Identification of tumor suppressive activity by irradiation microcell-mediated chromosome transfer and involvement of alpha B-crystallin in nasopharyngeal carcinoma

TitleIdentification of tumor suppressive activity by irradiation microcell-mediated chromosome transfer and involvement of alpha B-crystallin in nasopharyngeal carcinoma
Authors
KeywordsAlpha B-crystallin (CRYAB)
Chromosome 11q
Irradiation microcell-mediated chromosome transfer
Microcell hybrid
Nasopharyngeal carcinoma
Issue Date2008
PublisherJohn Wiley & Sons, Inc.. The Journal's web site is located at http://www3.interscience.wiley.com/journal/29331/home
Citation
International Journal Of Cancer, 2008, v. 122 n. 6, p. 1288-1296 How to Cite?
AbstractIn previous studies, we successfully refined nasopharyngeal carcinoma (NPC) critical regions (CRs) mapping to chromosome 11q13 and 11q22-23. The chromosome 11 fragment containing the 1.8 Mb NPC CR at 11q13 (CR1), the CR at 11q22.3 mapped near D11S2000 (CR2), part of the CR at 11q23.1-11q23.2 overlapping with D11S1300 and D11S1391 (CR3), and the CR at cell adhesion molecule 1 (CADM1) locus (CR4), was chosen as the chromosome 11 donor cell line for the present study. Gamma irradiation was applied to cleave this truncated chromosome into smaller fragments and a new panel of donor cells containing further deleted fragments was produced. Subclones XMCH3.2 and XMCH3.4 were chosen for subsequent transfer to HONE1 cells; each contains a single copy of deleted chromosome 11 fragment with or without CR2 and the THY1 locus, previously shown to be involved in NPC. Both resultant chromosome 11 fragments in XMCH3.2 and XMCH3.4 caused tumor suppression. The association of alpha B-crystallin (CRYAB), a gene identified as being differentially expressed by gene profiling of NPC and an immortalized nasopharyngeal epithelial cell line, and which is located near CR3, was found to be associated with tumor suppression in all the tumor-suppressive hybrids. In addition, the expression level of this gene was down-regulated in the 7 NPC cell lines and in 5 out of 14 normal/tumor tissue pairs in the present study. Both promoter hypermethylation and allelic loss may be involved in the inactivation of this gene, suggesting its possible role in NPC development. © 2007 Wiley-Liss, Inc.
Persistent Identifierhttp://hdl.handle.net/10722/58245
ISSN
2015 Impact Factor: 5.531
2015 SCImago Journal Rankings: 2.657
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorHong, LLen_HK
dc.contributor.authorLo, CCen_HK
dc.contributor.authorWong, CCLen_HK
dc.contributor.authorCheung, AKLen_HK
dc.contributor.authorKa, FCen_HK
dc.contributor.authorWong, Nen_HK
dc.contributor.authorFung, MKen_HK
dc.contributor.authorKing, CCen_HK
dc.contributor.authorLaw, EWLen_HK
dc.contributor.authorSai, WTen_HK
dc.contributor.authorChua, Den_HK
dc.contributor.authorSham, JSen_HK
dc.contributor.authorCheng, Yen_HK
dc.contributor.authorStanbridge, EJen_HK
dc.contributor.authorRobertson, GPen_HK
dc.contributor.authorLung, MLen_HK
dc.date.accessioned2010-05-31T03:26:32Z-
dc.date.available2010-05-31T03:26:32Z-
dc.date.issued2008en_HK
dc.identifier.citationInternational Journal Of Cancer, 2008, v. 122 n. 6, p. 1288-1296en_HK
dc.identifier.issn0020-7136en_HK
dc.identifier.urihttp://hdl.handle.net/10722/58245-
dc.description.abstractIn previous studies, we successfully refined nasopharyngeal carcinoma (NPC) critical regions (CRs) mapping to chromosome 11q13 and 11q22-23. The chromosome 11 fragment containing the 1.8 Mb NPC CR at 11q13 (CR1), the CR at 11q22.3 mapped near D11S2000 (CR2), part of the CR at 11q23.1-11q23.2 overlapping with D11S1300 and D11S1391 (CR3), and the CR at cell adhesion molecule 1 (CADM1) locus (CR4), was chosen as the chromosome 11 donor cell line for the present study. Gamma irradiation was applied to cleave this truncated chromosome into smaller fragments and a new panel of donor cells containing further deleted fragments was produced. Subclones XMCH3.2 and XMCH3.4 were chosen for subsequent transfer to HONE1 cells; each contains a single copy of deleted chromosome 11 fragment with or without CR2 and the THY1 locus, previously shown to be involved in NPC. Both resultant chromosome 11 fragments in XMCH3.2 and XMCH3.4 caused tumor suppression. The association of alpha B-crystallin (CRYAB), a gene identified as being differentially expressed by gene profiling of NPC and an immortalized nasopharyngeal epithelial cell line, and which is located near CR3, was found to be associated with tumor suppression in all the tumor-suppressive hybrids. In addition, the expression level of this gene was down-regulated in the 7 NPC cell lines and in 5 out of 14 normal/tumor tissue pairs in the present study. Both promoter hypermethylation and allelic loss may be involved in the inactivation of this gene, suggesting its possible role in NPC development. © 2007 Wiley-Liss, Inc.en_HK
dc.languageengen_HK
dc.publisherJohn Wiley & Sons, Inc.. The Journal's web site is located at http://www3.interscience.wiley.com/journal/29331/homeen_HK
dc.relation.ispartofInternational Journal of Canceren_HK
dc.rightsInternational Journal of Cancer. Copyright © John Wiley & Sons, Inc.en_HK
dc.subjectAlpha B-crystallin (CRYAB)en_HK
dc.subjectChromosome 11qen_HK
dc.subjectIrradiation microcell-mediated chromosome transferen_HK
dc.subjectMicrocell hybriden_HK
dc.subjectNasopharyngeal carcinomaen_HK
dc.subject.meshAnimals-
dc.subject.meshBase Sequence-
dc.subject.meshChromosomes, Human, Pair 11-
dc.subject.meshDNA Methylation-
dc.subject.meshalpha-Crystallin B Chain - physiology-
dc.titleIdentification of tumor suppressive activity by irradiation microcell-mediated chromosome transfer and involvement of alpha B-crystallin in nasopharyngeal carcinomaen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0020-7136&volume=122&issue=6&spage=1288&epage=1296&date=2008&atitle=Identification+of+tumor+suppressive+activity+by+irradiation+microcell-mediated+chromosome+transfer+and+involvement+of+alpha+B-crystallin+in+nasopharyngeal+carcinomaen_HK
dc.identifier.emailHong, LL: hllung2@hku.hken_HK
dc.identifier.emailWong, CCL: carmencl@pathology.hku.hken_HK
dc.identifier.emailCheung, AKL: arthurhk@hku.hken_HK
dc.identifier.emailSai, WT: gswtsao@hkucc.hku.hken_HK
dc.identifier.emailChua, D: dttchua@hkucc.hku.hken_HK
dc.identifier.emailCheng, Y: yuecheng@hku.hken_HK
dc.identifier.emailLung, ML: mlilung@hku.hken_HK
dc.identifier.authorityHong, LL=rp00299en_HK
dc.identifier.authorityWong, CCL=rp01602en_HK
dc.identifier.authorityCheung, AKL=rp01769en_HK
dc.identifier.authoritySai, WT=rp00399en_HK
dc.identifier.authorityChua, D=rp00415en_HK
dc.identifier.authorityCheng, Y=rp01320en_HK
dc.identifier.authorityLung, ML=rp00300en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1002/ijc.23259en_HK
dc.identifier.pmid18027848-
dc.identifier.scopuseid_2-s2.0-39649108844en_HK
dc.identifier.hkuros173232en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-39649108844&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume122en_HK
dc.identifier.issue6en_HK
dc.identifier.spage1288en_HK
dc.identifier.epage1296en_HK
dc.identifier.eissn1097-0215-
dc.identifier.isiWOS:000253302800012-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridHong, LL=6603819904en_HK
dc.identifier.scopusauthoridLo, CC=35083898100en_HK
dc.identifier.scopusauthoridWong, CCL=24823630000en_HK
dc.identifier.scopusauthoridCheung, AKL=8967932600en_HK
dc.identifier.scopusauthoridKa, FC=35083577600en_HK
dc.identifier.scopusauthoridWong, N=7202836653en_HK
dc.identifier.scopusauthoridFung, MK=23570461000en_HK
dc.identifier.scopusauthoridKing, CC=23570603000en_HK
dc.identifier.scopusauthoridLaw, EWL=36742183700en_HK
dc.identifier.scopusauthoridSai, WT=7102813116en_HK
dc.identifier.scopusauthoridChua, D=7006773480en_HK
dc.identifier.scopusauthoridSham, JS=7101655565en_HK
dc.identifier.scopusauthoridCheng, Y=36131038300en_HK
dc.identifier.scopusauthoridStanbridge, EJ=7103249410en_HK
dc.identifier.scopusauthoridRobertson, GP=7402368503en_HK
dc.identifier.scopusauthoridLung, ML=7006411788en_HK

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