{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,12,13]],"date-time":"2025-12-13T05:02:23Z","timestamp":1765602143573,"version":"3.48.0"},"reference-count":37,"publisher":"BMJ","issue":"12","content-domain":{"domain":["bmj.com"],"crossmark-restriction":true},"short-container-title":["J Clin Pathol"],"accepted":{"date-parts":[[2013,7,4]]},"published-print":{"date-parts":[[2013,12]]},"abstract":"<jats:sec>\n                    <jats:title>Aims<\/jats:title>\n                    <jats:p>\n                      <jats:italic>HER2NEU<\/jats:italic>\n                      gene amplification is present in the majority of invasive breast carcinomas that have HER2 protein overexpression. A subset of breast cancers harbour an increased chromosome 17 (CEP17) copy number (polysomy 17). We investigated the clinicopathologic significance of polysomy 17 in correlation with various histological parameters and\n                      <jats:italic>HER2NEU<\/jats:italic>\n                      gene amplification.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>\n                      We collected the surgical specimens of 266 consecutive cases of primary invasive breast carcinomas.\n                      <jats:italic>HER2NEU<\/jats:italic>\n                      gene status and CEP17 copy numbers were assessed by fluorescent in situ hybridisation (FISH). Chromosome 17 polysomy was determined by the presence of \u22653 average CEP17 signals per nucleus.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      63 tumours (23.7%) harboured polysomy 17. Carcinomas with polysomy 17 were associated with adverse histological indicators including high histological grade, high nuclear grade, poor Nottingham Prognostic Index, advanced local tumour extent and progesterone receptor negativity. Polysomy 17 was common to\n                      <jats:italic>HER2NEU<\/jats:italic>\n                      amplified and unamplified tumours, and more frequently observed in\n                      <jats:italic>HER2NEU<\/jats:italic>\n                      unamplified (71.4%) cases.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>In the absence of the gene amplification, HER2 protein overexpression may be explained by other mechanisms including polysomy 17.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1136\/jclinpath-2013-201506","type":"journal-article","created":{"date-parts":[[2013,8,2]],"date-time":"2013-08-02T01:06:24Z","timestamp":1375405584000},"page":"1070-1075","update-policy":"https:\/\/doi.org\/10.1136\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":10,"title":["Chromosome 17 polysomy: correlation with histological parameters and\n                    <i>HER2NEU<\/i>\n                    gene amplification"],"prefix":"10.1136","volume":"66","author":[{"given":"Maria","family":"Orsaria","sequence":"first","affiliation":[{"name":"Department of Pathology, Azienda Ospedaliero-Universitaria S. 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