ArticleScientific reports2019
HER2, chromosome 17 polysomy and DNA ploidy status in breast cancer; a translational study.
Article in Scientific reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 17 citations in OpenAlex.
- HER2 amplification as a resistance mechanism to osimertinib and its successful treatment with trastuzumab deruxtecan: a case report.Frontiers in oncology · 2026Article
- HER2 Low Breast Cancer: A New Subtype or a Trojan for Cytotoxic Drug Delivery?International journal of molecular sciences · 2023Review
- Resistance to antibody-drug conjugates in breast cancer: mechanisms and solutions.Cancer communications (London, England) · 2023Review
- Chinese expert consensus on the diagnosis and treatment of HER2-altered non-small cell lung cancer.Thoracic cancer · 2023Article
- The frequency and clinical significance of centromere enumeration probe 17 alterations in human epidermal growth factor receptor 2 immunohistochemistry-equivocal invasive breast cancer.Histopathology · 2022Article
- Validation of HER2 Status in Whole Genome Sequencing Data of Breast Cancers with the Ploidy-Corrected Copy Number Approach.Molecular diagnosis & therapy · 2022Article
- Rapid HER2 cytologic fluorescence in situ hybridization for breast cancer using noncontact alternating current electric field mixing.Cancer medicine · 2021Article
- Towards personalized treatment for early stage HER2-positive breast cancer.Nature reviews. Clinical oncology · 2020Review
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Authors and funding
18 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Breast cancer treatment depends on human epidermal growth factor receptor-2 (HER2) status, which is often determined using dual probe fluorescence in situ hybridisation (FISH). Hereby, also loss and gain of the centromere of chromosome 17 (CEP17) can be observed (HER2 is located on chromosome 17). CEP17 gain can lead to difficulty in interpretation of HER2 status, since this might represent true polysomy. With this study we investigated whether isolated polysomy is present and how this effects HER2 status in six breast cancer cell lines and 97 breast cancer cases, using HER2 FISH and immunohistochemistry, DNA ploidy assessment and multiplex ligation dependent probe amplification. We observed no isolated polysomy of chromosome 17 in any cell line. However, FISH analysis did show CEP17 gain in five of six cell lines, which reflected gains of the whole chromosome in metaphase spreads and aneuploidy with gain of multiple chromosomes in all these cases. In patients' samples, gain of CEP17 indeed correlated with aneuploidy of the tumour (91.1%; p < 0.001). Our results indicate that CEP17 gain is not due to isolated polysomy, but rather due to widespread aneuploidy with gain of multiple chromosomes. As aneuploidy is associated with poor clinical outcome, irrespective of tumour grade, this could improve future therapeutic decision making.
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