File Download
  Links for fulltext
     (May Require Subscription)
Supplementary

Article: Mandatory chromosomal segment balance in aneuploid tumor cells

TitleMandatory chromosomal segment balance in aneuploid tumor cells
Authors
KeywordsAneuploidy
Animal Cell
Animal Experiment
Animal Model
Article
Cancer Cell Culture
Cancer Inhibition
Chromosome 3P
Chromosome 3Q
Chromosome Analysis
Chromosome Inactivation
Chromosome Loss
Chromosome Structure
Controlled Study
Fluorescence In Situ Hybridization
Gene Deletion
Gene Sequence
Genetic Polymorphism
In Vitro Study
In Vivo Study
Microsatellite Marker
Mouse
Nonhuman
Qualitative Research
Quantitative Study
Scid Mouse
Supernumerary Chromosome
Tumor Suppressor Gene
Issue Date2007
PublisherBioMed Central Ltd. The Journal's web site is located at http://www.biomedcentral.com/bmccancer/
Citation
Bmc Cancer, 2007, v. 7 How to Cite?
AbstractBackground: Euploid chromosome balance is vitally important for normal development, but is profoundly changed in many tumors. Is each tumor dependent on its own structurally and numerically changed chromosome complement that has evolved during its development and progression? We have previously shown that normal chromosome 3 transfer into the KH39 renal cell carcinoma line and into the Hone1 nasopharyngeal carcinoma line inhibited their tumorigenicity. The aim of the present study was to distinguish between a qualitative and a quantitative model of this suppression. According to the former, a damaged or deleted tumor suppressor gene would be restored by the transfer of a normal chromosome. If so, suppression would be released only when the corresponding sequences of the exogenous normal chromosome are lost or inactivated. According to the alternative quantitative model, the tumor cell would not tolerate an increased dosage of the relevant gene or segment. If so, either a normal cell derived, or, a tumor derived endogenous segment could be lost. Methods: Fluorescence in Situ Hybridization based methods, as well as analysis of polymorphic microsatellite markers were used to follow chromosome 3 constitution changes in monochromosomal hybrids. Results: In both tumor lines with introduced supernumerary chromosomes 3, the copy number of 3p21 or the entire 3p tended to fall back to the original level during both in vitro and in vivo growth. An exogenous, normal cell derived, or an endogenous, tumor derived, chromosome segment was lost with similar probability. Identification of the lost versus retained segments showed that the intolerance for increased copy number was particularly strong for 3p14-p21, and weaker for other 3p regions. Gains in copy number were, on the other hand, well tolerated in the long arm and particularly the 3q26-q27 region. Conclusion: The inability of the cell to tolerate an experimentally imposed gain in 3p14-p21 in contrast to the well tolerated gain in 3q26-q27 is consistent with the fact that the former is often deleted in human tumors, whereas the latter is frequently amplified. The findings emphasize the importance of even minor changes in copy number in seemingly unbalanced aneuploid tumors. © 2007 Kost-Alimova et al; licensee BioMed Central Ltd.
Persistent Identifierhttp://hdl.handle.net/10722/91292
ISSN
2015 Impact Factor: 3.265
2015 SCImago Journal Rankings: 1.627
PubMed Central ID
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorKostAlimova, Men_HK
dc.contributor.authorDaraiRamqvist, Een_HK
dc.contributor.authorYau, WLen_HK
dc.contributor.authorSandlund, Aen_HK
dc.contributor.authorFedorova, Len_HK
dc.contributor.authorYang, Yen_HK
dc.contributor.authorKholodnyuk, Ien_HK
dc.contributor.authorCheng, Yen_HK
dc.contributor.authorLung, MLen_HK
dc.contributor.authorStanbridge, Een_HK
dc.contributor.authorKlein, Gen_HK
dc.contributor.authorImreh, Sen_HK
dc.date.accessioned2010-09-17T10:16:20Z-
dc.date.available2010-09-17T10:16:20Z-
dc.date.issued2007en_HK
dc.identifier.citationBmc Cancer, 2007, v. 7en_HK
dc.identifier.issn1471-2407en_HK
dc.identifier.urihttp://hdl.handle.net/10722/91292-
dc.description.abstractBackground: Euploid chromosome balance is vitally important for normal development, but is profoundly changed in many tumors. Is each tumor dependent on its own structurally and numerically changed chromosome complement that has evolved during its development and progression? We have previously shown that normal chromosome 3 transfer into the KH39 renal cell carcinoma line and into the Hone1 nasopharyngeal carcinoma line inhibited their tumorigenicity. The aim of the present study was to distinguish between a qualitative and a quantitative model of this suppression. According to the former, a damaged or deleted tumor suppressor gene would be restored by the transfer of a normal chromosome. If so, suppression would be released only when the corresponding sequences of the exogenous normal chromosome are lost or inactivated. According to the alternative quantitative model, the tumor cell would not tolerate an increased dosage of the relevant gene or segment. If so, either a normal cell derived, or, a tumor derived endogenous segment could be lost. Methods: Fluorescence in Situ Hybridization based methods, as well as analysis of polymorphic microsatellite markers were used to follow chromosome 3 constitution changes in monochromosomal hybrids. Results: In both tumor lines with introduced supernumerary chromosomes 3, the copy number of 3p21 or the entire 3p tended to fall back to the original level during both in vitro and in vivo growth. An exogenous, normal cell derived, or an endogenous, tumor derived, chromosome segment was lost with similar probability. Identification of the lost versus retained segments showed that the intolerance for increased copy number was particularly strong for 3p14-p21, and weaker for other 3p regions. Gains in copy number were, on the other hand, well tolerated in the long arm and particularly the 3q26-q27 region. Conclusion: The inability of the cell to tolerate an experimentally imposed gain in 3p14-p21 in contrast to the well tolerated gain in 3q26-q27 is consistent with the fact that the former is often deleted in human tumors, whereas the latter is frequently amplified. The findings emphasize the importance of even minor changes in copy number in seemingly unbalanced aneuploid tumors. © 2007 Kost-Alimova et al; licensee BioMed Central Ltd.en_HK
dc.languageengen_HK
dc.publisherBioMed Central Ltd. The Journal's web site is located at http://www.biomedcentral.com/bmccancer/en_HK
dc.relation.ispartofBMC Canceren_HK
dc.subjectAneuploidyen_HK
dc.subjectAnimal Cellen_HK
dc.subjectAnimal Experimenten_HK
dc.subjectAnimal Modelen_HK
dc.subjectArticleen_HK
dc.subjectCancer Cell Cultureen_HK
dc.subjectCancer Inhibitionen_HK
dc.subjectChromosome 3Pen_HK
dc.subjectChromosome 3Qen_HK
dc.subjectChromosome Analysisen_HK
dc.subjectChromosome Inactivationen_HK
dc.subjectChromosome Lossen_HK
dc.subjectChromosome Structureen_HK
dc.subjectControlled Studyen_HK
dc.subjectFluorescence In Situ Hybridizationen_HK
dc.subjectGene Deletionen_HK
dc.subjectGene Sequenceen_HK
dc.subjectGenetic Polymorphismen_HK
dc.subjectIn Vitro Studyen_HK
dc.subjectIn Vivo Studyen_HK
dc.subjectMicrosatellite Markeren_HK
dc.subjectMouseen_HK
dc.subjectNonhumanen_HK
dc.subjectQualitative Researchen_HK
dc.subjectQuantitative Studyen_HK
dc.subjectScid Mouseen_HK
dc.subjectSupernumerary Chromosomeen_HK
dc.subjectTumor Suppressor Geneen_HK
dc.titleMandatory chromosomal segment balance in aneuploid tumor cellsen_HK
dc.typeArticleen_HK
dc.identifier.emailCheng, Y:yuecheng@hku.hken_HK
dc.identifier.emailLung, ML:mlilung@hku.hken_HK
dc.identifier.authorityCheng, Y=rp01320en_HK
dc.identifier.authorityLung, ML=rp00300en_HK
dc.description.naturepublished_or_final_version-
dc.identifier.doi10.1186/1471-2407-7-21en_HK
dc.identifier.pmid17257397-
dc.identifier.pmcidPMC1794251-
dc.identifier.scopuseid_2-s2.0-33846934262en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-33846934262&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume7en_HK
dc.identifier.isiWOS:000244016500001-
dc.publisher.placeUnited Kingdomen_HK
dc.identifier.scopusauthoridKostAlimova, M=6603933704en_HK
dc.identifier.scopusauthoridDaraiRamqvist, E=15831044400en_HK
dc.identifier.scopusauthoridYau, WL=36914040600en_HK
dc.identifier.scopusauthoridSandlund, A=6508273434en_HK
dc.identifier.scopusauthoridFedorova, L=18339040100en_HK
dc.identifier.scopusauthoridYang, Y=7409381085en_HK
dc.identifier.scopusauthoridKholodnyuk, I=6602995307en_HK
dc.identifier.scopusauthoridCheng, Y=36131038300en_HK
dc.identifier.scopusauthoridLung, ML=7006411788en_HK
dc.identifier.scopusauthoridStanbridge, E=7103249410en_HK
dc.identifier.scopusauthoridKlein, G=7403533715en_HK
dc.identifier.scopusauthoridImreh, S=7003485208en_HK
dc.identifier.citeulike1069590-

Export via OAI-PMH Interface in XML Formats


OR


Export to Other Non-XML Formats