Gene copy numbers of HER family in breast cancer

Aim The aim of the study was to analyze the occurrence of abnormal gene copy numbers of all HER oncogenes and to correlate these alterations to other clinicopathological variables in a consecutive series of 225 breast cancer patients. Methods Gene copy number of HER oncogenes was analyzed with double differential polymerase chain reaction (ddPCR). Statistical analysis was performed with a set of nonparametric tests. Results Sixty-five percent of the tumors contained abnormal gene copy number of at least one HER oncogene. Alterations of at least two oncogenes were found in 31% of cases. The correlations between average gene copy numbers (AGCNs) of particular HER oncogenes were much stronger in node positive compared to node-negative tumors. Deletions of EGFR were associated with the lack of steroid hormone receptors. The HER3 and HER4 amplifications were more common in well differentiated tumors. Conclusions Our results indicate a key role of HER heterodimers in tumor progression and confirm earlier data that HER2 is the preferred partner for other HER oncogenes in this process. Deletions of EGFR were associated with unfavorable characteristics, whereas HER3 and HER4 amplifications may be linked with less aggressive phenotypes.