ArticlePathology oncology research : POR2007
HER-2, TOP2A and chromosome 17 alterations in breast cancer.
Article in Pathology oncology research : POR, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 35 citations in OpenAlex.
- Review
- Current State of Breast Cancer Diagnosis, Treatment, and Theranostics.Pharmaceutics · 2021Review
- The Research Progress of Trastuzumab-Induced Cardiotoxicity in HER-2-Positive Breast Cancer Treatment.Frontiers in cardiovascular medicine · 2021Review
- Monosomy of chromosome 17 in breast cancer during interpretation of HER2 gene amplification.American journal of cancer research · 2015Article
- Article
- Prognostic value of TOP2A gene amplification and chromosome 17 polysomy in early breast cancer.Pathology oncology research : POR · 2012Article
- Lack of independent prognostic and predictive value of centromere 17 copy number changes in breast cancer patients with known HER2 and TOP2A status.Molecular oncology · 2012Article
- The nucleosome remodeling factor.FEBS letters · 2011Review
- Topoisomerase IIalpha maintains genomic stability through decatenation G(2) checkpoint signaling.Oncogene · 2010Article
- A novel translocation breakpoint within the BPTF gene is associated with a pre-malignant phenotype.PloS one · 2010Article
- Breast cancer and aneusomy 17: implications for carcinogenesis and therapeutic response.The Lancet. Oncology · 2009Review
- Targeted therapeutic options and future perspectives for HER2-positive breast cancer.Signal transduction and targeted therapyReview
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
HER-2 amplification is a biomarker for identifying patients who respond to trastuzumab and has been evaluated as a factor predicting the response to anthracyclines. The relationship between HER-2 and response to anthracycline therapy may also be the result of the close localization of TOP2A on 17q. It has been a matter of debate whether these two genes, HER-2 and TOP2A, behave separately on different amplicons or act together thus making it possible to predict the TOP2A status from the HER-2 status. In this study TOP2A, HER-2 and chromosome 17 aneusomy were investigated by fluorescent in situ hybridization (FISH) in 50 consecutive breast cancer patients. HER-2 amplification was detected in 11 patients (22%) and TOP2A changes were seen in 6 patients (12%); two amplifications and two deletions were observed in HER-2-amplified cases and two deletions in HER-2-nonamplified cases. Three of the TOP2A-deleted cases had polysomy 17. HER-2 copy number was higher than the TOP2A copy number in one patient with co-amplification. Polysomy was observed in 9 cases (18%) and monosomy in 6 cases (12%). Aneusomy was the sole anomaly in 11 patients (22%). We conclude that the TOP2A status cannot be predicted from the HER-2 status and evaluation of the TOP2A status only in patients with HER-2 overexpression may lead to missing cases with TOP2A deletion with possible resistance to therapy. Other factors modulating topo II activity may also affect the response to therapy. Studies evaluating different parameters that can modulate topo II activity and the response to the drugs targeting the enzyme are necessary.
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