Anthracycline-‐based treatment for HER2-‐positive breast cancer is associated with serious side effects. The topoisomerase II alpha protein is the mechanical target of anthracyclines, but its role as a biomarker has yet to be established. Amplification of TOP2A is reported in 24-‐54% of HER2 positive tumours. Co-‐amplification has been proposed as one explanation due to the close proximity of the two genes, but it is also possible that the TOP2A DNA probes are too large, giving false positives. Chromosome 17 anomalies have also been suggested. In this study, we use new, smaller DNA probes for in situ hybridization in 153 HER2-‐positive tumours. 33% were TOP2A-‐amplified, and we found only three cases of CEP17 anomaly (deletions). A smaller DNA probe is less likely to overlap with adjacent regions, and as such is more specific. The incidence of TOP2A amplification in our material was consistent with current research, indicating that DNA probe overlap cannot explain the amplification of TOP2A seen in HER2-‐ positive tumours.