File Download

There are no files associated with this item.

  Links for fulltext
     (May Require Subscription)
Supplementary

Article: Fine mapping of the 11q22-23 tumor suppressive region and involvement of TSLC1 in nasopharyngeal carcinoma

TitleFine mapping of the 11q22-23 tumor suppressive region and involvement of TSLC1 in nasopharyngeal carcinoma
Authors
KeywordsChemicals And Cas Registry Numbers
Issue Date2004
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, 2004, v. 112 n. 4, p. 628-635 How to Cite?
AbstractPrevious studies transferring an intact chromosome 11 into HONE1 cells demonstrated the functional significance of chromosome regions, 11q13 and 11q22-23, in nasopharyngeal carcinoma (NPC) development. In our study the 11q22-23 region was comprehensively re-investigated by detailed microsatellite and single nucleotide polymorphism genotyping and by fluorescence in situ hybridization to map precisely the regions containing tumor suppressive activity. We observed 3 chromosomal intervals within 11q22-23 that were commonly lost in the tumor segregants derived from HONE1/chromosome 11 hybrids. One critical region of 0.36 Mb was mapped near the marker D11S2000 and a second 0.44 Mb region was located around the markers D11S1300 and D11S1391. In a third region high allelic loss was also observed at marker D11S4484, where a newly cloned tumor suppressor gene, TSLC1 (tumor suppressor in lung cancer I), is located. The gene expression analysis showed absence or low expression levels of TSLC1 mRNA in 4 highly tumorigenic NPC cell lines. In addition, the methylation study results show that the TSLC1 promoter region was hypermethylated in all 4 NPC cell lines and re-expression of the gene occurs in HONE1 cells after 5-aza-2′-deoxycytidine treatment. Hence, the mode of silencing of this candidate TSG in NPC may be attributed to promoter hypermethylation. We have obtained functional evidence for multiple critical tumor suppressive regions in 11q22-23 by fine deletion mapping and for inactivation of TSLC1 being one of these candidate TSGs in NPC development. © 2004 Wiley-Liss, Inc.
Persistent Identifierhttp://hdl.handle.net/10722/91281
ISSN
2015 Impact Factor: 5.531
2015 SCImago Journal Rankings: 2.657
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorLung, HLen_HK
dc.contributor.authorCheng, Yen_HK
dc.contributor.authorKumaran, MKen_HK
dc.contributor.authorLiu, ETBen_HK
dc.contributor.authorMurakami, Yen_HK
dc.contributor.authorChan, CYen_HK
dc.contributor.authorYau, WLen_HK
dc.contributor.authorKo, JMYen_HK
dc.contributor.authorStanbridge, EJen_HK
dc.contributor.authorLung, MLen_HK
dc.date.accessioned2010-09-17T10:16:09Z-
dc.date.available2010-09-17T10:16:09Z-
dc.date.issued2004en_HK
dc.identifier.citationInternational Journal Of Cancer, 2004, v. 112 n. 4, p. 628-635en_HK
dc.identifier.issn0020-7136en_HK
dc.identifier.urihttp://hdl.handle.net/10722/91281-
dc.description.abstractPrevious studies transferring an intact chromosome 11 into HONE1 cells demonstrated the functional significance of chromosome regions, 11q13 and 11q22-23, in nasopharyngeal carcinoma (NPC) development. In our study the 11q22-23 region was comprehensively re-investigated by detailed microsatellite and single nucleotide polymorphism genotyping and by fluorescence in situ hybridization to map precisely the regions containing tumor suppressive activity. We observed 3 chromosomal intervals within 11q22-23 that were commonly lost in the tumor segregants derived from HONE1/chromosome 11 hybrids. One critical region of 0.36 Mb was mapped near the marker D11S2000 and a second 0.44 Mb region was located around the markers D11S1300 and D11S1391. In a third region high allelic loss was also observed at marker D11S4484, where a newly cloned tumor suppressor gene, TSLC1 (tumor suppressor in lung cancer I), is located. The gene expression analysis showed absence or low expression levels of TSLC1 mRNA in 4 highly tumorigenic NPC cell lines. In addition, the methylation study results show that the TSLC1 promoter region was hypermethylated in all 4 NPC cell lines and re-expression of the gene occurs in HONE1 cells after 5-aza-2′-deoxycytidine treatment. Hence, the mode of silencing of this candidate TSG in NPC may be attributed to promoter hypermethylation. We have obtained functional evidence for multiple critical tumor suppressive regions in 11q22-23 by fine deletion mapping and for inactivation of TSLC1 being one of these candidate TSGs in NPC development. © 2004 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.subjectChemicals And Cas Registry Numbersen_HK
dc.subject.meshCarcinoma - genetics - pathologyen_HK
dc.subject.meshCell Adhesion Moleculesen_HK
dc.subject.meshChromosome Mappingen_HK
dc.subject.meshChromosomes, Human, Pair 11 - geneticsen_HK
dc.subject.meshDNA Methylationen_HK
dc.subject.meshDNA Primersen_HK
dc.subject.meshGenes, Tumor Suppressoren_HK
dc.subject.meshGenetic Markersen_HK
dc.subject.meshHumansen_HK
dc.subject.meshImmunoglobulins - geneticsen_HK
dc.subject.meshIn Situ Hybridization, Fluorescenceen_HK
dc.subject.meshLoss of Heterozygosityen_HK
dc.subject.meshMembrane Proteins - geneticsen_HK
dc.subject.meshNasopharyngeal Neoplasms - genetics - pathologyen_HK
dc.subject.meshPolymorphism, Single Nucleotideen_HK
dc.subject.meshPromoter Regions, Genetic - geneticsen_HK
dc.subject.meshReverse Transcriptase Polymerase Chain Reactionen_HK
dc.subject.meshTumor Suppressor Proteinsen_HK
dc.titleFine mapping of the 11q22-23 tumor suppressive region and involvement of TSLC1 in nasopharyngeal carcinomaen_HK
dc.typeArticleen_HK
dc.identifier.emailLung, HL:hllung2@hku.hken_HK
dc.identifier.emailCheng, Y:yuecheng@hku.hken_HK
dc.identifier.emailLung, ML:mlilung@hku.hken_HK
dc.identifier.authorityLung, HL=rp00299en_HK
dc.identifier.authorityCheng, Y=rp01320en_HK
dc.identifier.authorityLung, ML=rp00300en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1002/ijc.20454en_HK
dc.identifier.pmid15382043-
dc.identifier.scopuseid_2-s2.0-7044249519en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-7044249519&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume112en_HK
dc.identifier.issue4en_HK
dc.identifier.spage628en_HK
dc.identifier.epage635en_HK
dc.identifier.isiWOS:000224717000010-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridLung, HL=6603819904en_HK
dc.identifier.scopusauthoridCheng, Y=36131038300en_HK
dc.identifier.scopusauthoridKumaran, MK=8056747700en_HK
dc.identifier.scopusauthoridLiu, ETB=7202240109en_HK
dc.identifier.scopusauthoridMurakami, Y=7404145481en_HK
dc.identifier.scopusauthoridChan, CY=8056747300en_HK
dc.identifier.scopusauthoridYau, WL=36914040600en_HK
dc.identifier.scopusauthoridKo, JMY=35725559400en_HK
dc.identifier.scopusauthoridStanbridge, EJ=7103249410en_HK
dc.identifier.scopusauthoridLung, ML=7006411788en_HK

Export via OAI-PMH Interface in XML Formats


OR


Export to Other Non-XML Formats