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Human epidermal growth factor receptor 2 (HER2)-amplified breast cancers represent a tumor subtype with chromosome 17q rearrangements that lead to frequent gene amplifications. The aim of this study was to quantify the amplification of genes located on chromosome 17q and to analyze the relations between the pattern of gene amplifications and the patients' characteristics and survival.    Methods  Patients with HER2-positive breast tumors (HER2 score of 3+ by immunohistochemistry or positive for  HER2  amplification by fluorescence  in situ  hybridization (FISH)) ( n  = 86) and with HER2-negative breast tumors ( n  = 40) (negative controls) were included in this study. Using a quantitative polymerase chain reaction method and DNA extracted from frozen tumor specimens, 11 genes ( MED1 ,  STARD3 ,  HER2 ,  GRB7, THRA, RARA ,  TOP2A ,  IGFBP4 ,  CCR7 ,  KRT20, KRT19  and  GAS ), which are localized within Chr17q12-q21 and have a putative role in breast cancer development, were quantified. Relapse-free and overall survival rates were estimated from the date of surgery to the date of the event of interest (recurrence or death) using the Kaplan-Meier method.    Results  Gene amplification was observed only in HER2-positive tumors, and the frequency of amplification decreased with the distance of the gene from  HER2 .  HER2  presented the highest level of amplification.  TOP2A  was not included in the smallest region of amplification involving  HER2 . Amplification of  RARA ,  KRT20  and  KRT19  was significantly associated with node-positive breast cancer ( P  = 0.030,  P  = 0.002 and  P  = 0.033, respectively). During a median follow-up period of 55 months (range, 6 to 81 months), the subgroup of patients with hormone receptor-negative cancer and without  TOP2A  amplification showed the worst survival (relapse-free survival: hazard ratio (HR) = 0.29, 95% confidence interval (95% CI), 0.13 to 0.65,  P  = 0.001; and overall survival: HR = 0.28, 95% CI, 0.10 to 0.76,  P  = 0.008).    Conclusions   HER2  amplification seems to drive genomic instability along chromosome 17q, leading to different patterns of gene amplification. This study confirms the clinical importance of identifying, among patients with HER2-positive breast tumors, the subgroup of patients with hormone receptor-negative and nonamplified  TOP2A  cancers as they have the worst prognosis.

breast cancer research

Quantification and clinical relevance of gene amplification at chromosome 17q12-q21 in human epidermal growth factor receptor 2-amplified breast cancers