Association of FOSL1 copy number alteration and triple negative breast tumors

• Published in: Genetics and molecular biology Vol. 42; no. 1; pp. 26 - 31
• Main Authors: 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
• Format: Journal Article
• Language: English
• Published: Brazil Sociedade Brasileira de Genetica 01.01.2019; Sociedade Brasileira de Genética
• Subjects: BIOCHEMISTRY & MOLECULAR BIOLOGY; Breast cancer; Chromosome 11; CNA; Copy number; DNA copy number alterations; ErbB-2 protein; Genes; GENETICS & HEREDITY; Genomic instability; Glutathione transferase; Health risk assessment; Human and Medical Genetics; Invasiveness; Phenotypes; Stability; Statistical analysis; TNBC; Triple negative breast cancer; Tumors; DNA copy number alterations; TNBC; Triple negative breast cancer; CNA
• ISSN: 1415-4757; 1678-4685; 1678-4685
• DOI: 10.1590/1678-4685-GMB-2017-0267

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.