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Unraveling the chromosome 17 patterns of FISH in interphase nuclei: An in-depth analysis of the HER2 amplicon and chromosome 17 centromere by karyotyping, FISH and M-FISH in breast cancer cells

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dc.creatorRondón-Lagos, Milenaspa
dc.creatorVerdun Di Cantogno, Ludovicaspa
dc.creatorRangel, Nelsonspa
dc.creatorMele, Teresaspa
dc.creatorRamírez Clavijo, Sandra Rocíospa
dc.creatorScagliotti, Giorgiospa
dc.creatorMarchiò, Caterinaspa
dc.creatorSapino, Annaspa
dc.date.accessioned2020-05-26T00:03:05Z
dc.date.available2020-05-26T00:03:05Z
dc.date.created2014spa
dc.description.abstractBackground: In diagnostic pathology, HER2 status is determined in interphase nuclei by fluorescence in situ hybridization (FISH) with probes for the HER2 gene and for the chromosome 17 centromere (CEP17). The latter probe is used as a surrogate for chromosome 17 copies, however chromosome 17 (Chr17) is frequently rearranged. The frequency and type of specific structural Chr17 alterations in breast cancer have been studied by using comparative genomic hybridization and spectral karyotyping, but not fully detailed. Actually, balanced chromosome rearrangements (e.g. translocations or inversions) and low frequency mosaicisms are assessable on metaphases using G-banding karyotype and multicolor FISH (M-FISH) only. Methods: We sought to elucidate the CEP17 and HER2 FISH patterns of interphase nuclei by evaluating Chr17 rearrangements in metaphases of 9 breast cancer cell lines and a primary culture from a triple negative breast carcinoma by using G-banding, FISH and M-FISH. Results: Thirty-nine rearranged chromosomes containing a portion of Chr17 were observed. Chromosomes 8 and 11 were the most frequent partners of Chr17 translocations. The lowest frequency of Chr17 abnormalities was observed in the HER2-negative cell lines, while the highest was observed in the HER2-positive SKBR3 cells. The MDA-MB231 triple negative cell line was the sole to show only non-altered copies of Chr17, while the SKBR3, MDA-MB361 and JIMT-1 HER2-positive cells carried no normal Chr17 copies. True polysomy was observed in MDA-MB231 as the only Chr17 alteration. In BT474 cells polysomy was associated to Chr17 structural alterations. By comparing M-FISH and FISH data, in 8 out of 39 rearranged chromosomes only CEP17 signals were detectable, whereas in 14 rearranged chromosomes HER2 and STARD3 genes were present without CEP17 signals. HER2 and STARD3 always co-localized on the same chromosomes and were always co-amplified, whereas TOP2A also mapped to different derivatives and was co-amplified with HER2 and STARD3 on SKBR3 cells only. Conclusion: The high frequency of complex Chr17 abnormalities suggests that the interpretation of FISH results on interphase nuclei using a dual probe assay to assess gene amplification should be performed 'with caution', given that CEP17 signals are not always indicative of normal unaltered or rearranged copies of Chr17. © 2014 Rondón-Lagos et al.eng
dc.format.mimetypeapplication/pdf
dc.identifier.doihttps://doi.org/10.1186/1471-2407-14-922
dc.identifier.issn14712407
dc.identifier.urihttps://repository.urosario.edu.co/handle/10336/23559
dc.language.isoengspa
dc.publisherBioMed Central Ltd.spa
dc.relation.citationIssueNo. 1
dc.relation.citationTitleBMC Cancer
dc.relation.citationVolumeVol. 14
dc.relation.ispartofBMC Cancer, ISSN:14712407, Vol.14, No.1 (2014)spa
dc.relation.urihttps://www.scopus.com/inward/record.uri?eid=2-s2.0-84924406034&doi=10.1186%2f1471-2407-14-922&partnerID=40&md5=15a4b472ef70231b4612d202839a542espa
dc.rights.accesRightsinfo:eu-repo/semantics/openAccess
dc.rights.accesoAbierto (Texto Completo)spa
dc.source.instnameinstname:Universidad del Rosariospa
dc.source.reponamereponame:Repositorio Institucional EdocURspa
dc.subject.keywordEpidermal growth factor receptor 2spa
dc.subject.keywordhumaneng
dc.subject.keywordtype iieng
dc.subject.keywordtumoreng
dc.subject.keywordneoplasmeng
dc.subject.keywordgeneticeng
dc.subject.keywordfluorescenceeng
dc.subject.keyworderbb-2eng
dc.subject.keywordhumaneng
dc.subject.keywordCarrier proteinspa
dc.subject.keywordpair 17eng
dc.subject.keywordDna binding proteinspa
dc.subject.keywordDna topoisomerase (atp hydrolysing)spa
dc.subject.keywordDna topoisomerase ii alphaspa
dc.subject.keywordMembrane proteinspa
dc.subject.keywordStard3 proteineng
dc.subject.keywordTumor antigenspa
dc.subject.keywordAmpliconspa
dc.subject.keywordArticlespa
dc.subject.keywordBreast cancer cell linespa
dc.subject.keywordBt474 cell linespa
dc.subject.keywordCentromerespa
dc.subject.keywordChromosome 11spa
dc.subject.keywordChromosome 17spa
dc.subject.keywordChromosome 8spa
dc.subject.keywordChromosome g bandspa
dc.subject.keywordChromosome rearrangementspa
dc.subject.keywordChromosome translocationspa
dc.subject.keywordFluorescence in situ hybridizationspa
dc.subject.keywordGene locationspa
dc.subject.keywordGene mappingspa
dc.subject.keywordHumanspa
dc.subject.keywordHuman tissuespa
dc.subject.keywordInterphasespa
dc.subject.keywordInvestigative proceduresspa
dc.subject.keywordJimt 1 cell linespa
dc.subject.keywordKaryotypingspa
dc.subject.keywordKpl4 cell linespa
dc.subject.keywordMcf 7 cell linespa
dc.subject.keywordMda mb231 cell linespa
dc.subject.keywordMda mb361 cell linespa
dc.subject.keywordMulticolor fluorescence in situ hybridizationspa
dc.subject.keywordOncogenespa
dc.subject.keywordOncogene neuspa
dc.subject.keywordPolysomespa
dc.subject.keywordSignal transductionspa
dc.subject.keywordSkbr3 cell linespa
dc.subject.keywordStard3 genespa
dc.subject.keywordT47d cell linespa
dc.subject.keywordTnbc case cell linespa
dc.subject.keywordTop2a genespa
dc.subject.keywordTriple negative breast cancerspa
dc.subject.keywordZr 75 1 cell linespa
dc.subject.keywordCarcinomaspa
dc.subject.keywordCell nucleusspa
dc.subject.keywordCentromerespa
dc.subject.keywordCytologyspa
dc.subject.keywordFluorescence in situ hybridizationspa
dc.subject.keywordGene translocationspa
dc.subject.keywordGeneticsspa
dc.subject.keywordInterphasespa
dc.subject.keywordKaryotypingspa
dc.subject.keywordMetaphasespa
dc.subject.keywordProceduresspa
dc.subject.keywordProto oncogenespa
dc.subject.keywordTumor cell linespa
dc.subject.keywordAntigenseng
dc.subject.keywordCarcinomaspa
dc.subject.keywordCarrier proteinsspa
dc.subject.keywordCell lineeng
dc.subject.keywordCell nucleusspa
dc.subject.keywordCentromerespa
dc.subject.keywordChromosomeseng
dc.subject.keywordDna topoisomeraseseng
dc.subject.keywordDna-binding proteinsspa
dc.subject.keywordGeneseng
dc.subject.keywordHumansspa
dc.subject.keywordIn situ hybridizationeng
dc.subject.keywordInterphasespa
dc.subject.keywordKaryotypingspa
dc.subject.keywordMembrane proteinsspa
dc.subject.keywordMetaphasespa
dc.subject.keywordTranslocationeng
dc.subject.keywordTriple negative breast neoplasmsspa
dc.subject.keywordBreast cancerspa
dc.subject.keywordCep17spa
dc.subject.keywordChromosomal rearrangementsspa
dc.subject.keywordChromosome 17spa
dc.subject.keywordHer2spa
dc.subject.keywordM-fishspa
dc.subject.keywordPolysomyspa
dc.subject.keywordStard3spa
dc.subject.keywordTop2aspa
dc.titleUnraveling the chromosome 17 patterns of FISH in interphase nuclei: An in-depth analysis of the HER2 amplicon and chromosome 17 centromere by karyotyping, FISH and M-FISH in breast cancer cellsspa
dc.typearticleeng
dc.type.hasVersioninfo:eu-repo/semantics/publishedVersion
dc.type.spaArtículospa
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