Registro completo |
Provedor de dados: |
Genet. Mol. Biol.
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País: |
Brazil
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Título: |
Association of FOSL1 copy number alteration and triple negative breast tumors
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Autores: |
Serino,Leandro Tamião Rodrigues
Jucoski,Tayana Schultz
Morais,Stephanie Bath de
Fernandes,Cíntia Callegari Coêlho
Lima,Rubens Silveira de
Urban,Cícero Andrade
Cavalli,Luciane Regina
Cavalli,Iglenir João
Ribeiro,Enilze Maria de Souza Fonseca
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Data: |
2019-03-01
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Ano: |
2019
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Palavras-chave: |
Triple negative breast cancer
TNBC
DNA copy number alterations
CNA
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Resumo: |
Abstract Copy number alterations (CNAs) are a frequent feature in human breast cancer, and one of the hallmarks of genomic instability. The FOSL1, GSTP1 and CCND1 genes are located at 11q13, a cytoband commonly affected by CNA in breast cancer, with relevant function in progression and invasion. Our main goal was to analyze CNAs of these genes and determine their association with breast cancer subtypes. Seventy-three cases of invasive breast tumors [52 Luminal, 7 HER2+ and 14 triple negative (TNBC) subtypes] were analyzed by TaqMan assays. CNAs were observed for all genes, with gains more frequently observed. Gains of the FOSL1 gene were observed in 71% of the cases. This gene was the only one with a statistically significant difference (p<0.001) among tumor subtypes, with increased copy number in TNBC compared to luminal and HER2+. No significant association of CNA and clinical and histopathological parameters from the patients was observed. Additional studies in larger breast cancer patient cohorts based on more refined molecular subtypes are necessary to confirm the observed association of FOSL1 gain with aggressive breast tumors phenotypes.
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Tipo: |
Info:eu-repo/semantics/article
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Idioma: |
Inglês
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Identificador: |
http://www.scielo.br/scielo.php?script=sci_arttext&pid=S1415-47572019000100026
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Editor: |
Sociedade Brasileira de Genética
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Relação: |
10.1590/1678-4685-gmb-2017-0267
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Formato: |
text/html
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Fonte: |
Genetics and Molecular Biology v.42 n.1 2019
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Direitos: |
info:eu-repo/semantics/openAccess
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