File Download

There are no files associated with this item.

  Links for fulltext
     (May Require Subscription)
Supplementary

Article: Functional evidence of decreased tumorigenicity associated with monochromosome transfer of chromosome 14 in esophageal cancer and the mapping of tumor-suppressive regions to 14q32

TitleFunctional evidence of decreased tumorigenicity associated with monochromosome transfer of chromosome 14 in esophageal cancer and the mapping of tumor-suppressive regions to 14q32
Authors
Issue Date2005
PublisherJohn Wiley & Sons, Inc. The Journal's web site is located at http://www3.interscience.wiley.com/cgi-bin/jhome/38250
Citation
Genes Chromosomes And Cancer, 2005, v. 43 n. 3, p. 284-293 How to Cite?
AbstractDespite the abundant evidence of high allelic loss of chromosome arm 14q in human cancers, tumor-suppressor genes mapped to this chromosome have yet to be identified. To narrow the search for candidate genes, we performed monochromosome transfer of chromosome 14 into an esophageal carcinoma cell line, SLMT-I SI. Statistically significant suppression of the tumorigenic potential of microcell hybrids containing the transferred chromosome 14 provided functional evidence that tumor-suppressive regions of chromosome 14 are essential for esophageal cancer. Tumor segregants emerging in nude mice during the tumorigenicity assay were analyzed by detailed PCR-microsatellite typing to identify critical nonrandomly eliminated regions (CRs). A 680-kb CR mapped to 14q32.13 and an ∼2.2-Mb CR mapped to 14q32.33 were delineated. Dual-color BAC FISH analysis of microcell hybrids and tumor segregants verified the selective loss of the 14q32.13 region. In contrast, similar transfers of an intact chromosome 11 into SLMT-I SI did not significantly suppress tumor formation. These functional complementation studies showing the correlation of tumorigenic potential with critical regions of chromosome 14 validated the importance of the 14q32 region in tumor suppression in esophageal cancer. The present study also paved the path for further identification of novel tumor-suppressor genes that are relevant to the molecular pathogenesis of esophageal cancer. © 2005 Wiley-Liss, Inc.
Persistent Identifierhttp://hdl.handle.net/10722/88664
ISSN
2015 Impact Factor: 3.96
2015 SCImago Journal Rankings: 2.210
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorKo, JMYen_HK
dc.contributor.authorYau, WLen_HK
dc.contributor.authorChan, PLen_HK
dc.contributor.authorLung, HLen_HK
dc.contributor.authorYang, Len_HK
dc.contributor.authorLo, PHYen_HK
dc.contributor.authorTang, JCOen_HK
dc.contributor.authorSrivastava, Gen_HK
dc.contributor.authorStanbridge, EJen_HK
dc.contributor.authorLung, MLen_HK
dc.date.accessioned2010-09-06T09:46:20Z-
dc.date.available2010-09-06T09:46:20Z-
dc.date.issued2005en_HK
dc.identifier.citationGenes Chromosomes And Cancer, 2005, v. 43 n. 3, p. 284-293en_HK
dc.identifier.issn1045-2257en_HK
dc.identifier.urihttp://hdl.handle.net/10722/88664-
dc.description.abstractDespite the abundant evidence of high allelic loss of chromosome arm 14q in human cancers, tumor-suppressor genes mapped to this chromosome have yet to be identified. To narrow the search for candidate genes, we performed monochromosome transfer of chromosome 14 into an esophageal carcinoma cell line, SLMT-I SI. Statistically significant suppression of the tumorigenic potential of microcell hybrids containing the transferred chromosome 14 provided functional evidence that tumor-suppressive regions of chromosome 14 are essential for esophageal cancer. Tumor segregants emerging in nude mice during the tumorigenicity assay were analyzed by detailed PCR-microsatellite typing to identify critical nonrandomly eliminated regions (CRs). A 680-kb CR mapped to 14q32.13 and an ∼2.2-Mb CR mapped to 14q32.33 were delineated. Dual-color BAC FISH analysis of microcell hybrids and tumor segregants verified the selective loss of the 14q32.13 region. In contrast, similar transfers of an intact chromosome 11 into SLMT-I SI did not significantly suppress tumor formation. These functional complementation studies showing the correlation of tumorigenic potential with critical regions of chromosome 14 validated the importance of the 14q32 region in tumor suppression in esophageal cancer. The present study also paved the path for further identification of novel tumor-suppressor genes that are relevant to the molecular pathogenesis of esophageal cancer. © 2005 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/cgi-bin/jhome/38250en_HK
dc.relation.ispartofGenes Chromosomes and Canceren_HK
dc.rightsGenes, Chromosomes & Cancer. Copyright © John Wiley & Sons, Inc.en_HK
dc.subject.meshAnimalsen_HK
dc.subject.meshCarcinoma, Squamous Cell - geneticsen_HK
dc.subject.meshCell Line, Tumoren_HK
dc.subject.meshChromosome Mappingen_HK
dc.subject.meshChromosomes, Human, Pair 14en_HK
dc.subject.meshEsophageal Neoplasms - geneticsen_HK
dc.subject.meshGenes, Tumor Suppressoren_HK
dc.subject.meshHumansen_HK
dc.subject.meshIn Situ Hybridization, Fluorescenceen_HK
dc.subject.meshLoss of Heterozygosityen_HK
dc.subject.meshMiceen_HK
dc.subject.meshMicrosatellite Repeats - geneticsen_HK
dc.subject.meshNucleic Acid Hybridizationen_HK
dc.subject.meshTransplantation, Heterologousen_HK
dc.titleFunctional evidence of decreased tumorigenicity associated with monochromosome transfer of chromosome 14 in esophageal cancer and the mapping of tumor-suppressive regions to 14q32en_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=1045-2257&volume=43&issue=3&spage=284&epage=293&date=2005&atitle=Functional+evidence+of+decreased+tumorigenicity+associated+with+monochromosome+transfer+of+chromosome+14+in+esophageal+cancer+and+the+mapping+of+tumor-suppressive+regions+to+14q32en_HK
dc.identifier.emailLung, HL:hllung2@hku.hken_HK
dc.identifier.emailSrivastava, G:gopesh@pathology.hku.hken_HK
dc.identifier.emailLung, ML:mlilung@hku.hken_HK
dc.identifier.authorityLung, HL=rp00299en_HK
dc.identifier.authoritySrivastava, G=rp00365en_HK
dc.identifier.authorityLung, ML=rp00300en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1002/gcc.20190en_HK
dc.identifier.pmid15834943en_HK
dc.identifier.scopuseid_2-s2.0-21144456793en_HK
dc.identifier.hkuros105071en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-21144456793&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume43en_HK
dc.identifier.issue3en_HK
dc.identifier.spage284en_HK
dc.identifier.epage293en_HK
dc.identifier.isiWOS:000229262800006-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridKo, JMY=35725559400en_HK
dc.identifier.scopusauthoridYau, WL=36914040600en_HK
dc.identifier.scopusauthoridChan, PL=8603309800en_HK
dc.identifier.scopusauthoridLung, HL=6603819904en_HK
dc.identifier.scopusauthoridYang, L=14827615000en_HK
dc.identifier.scopusauthoridLo, PHY=36762664000en_HK
dc.identifier.scopusauthoridTang, JCO=14056850300en_HK
dc.identifier.scopusauthoridSrivastava, G=7202242238en_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