{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,6]],"date-time":"2026-10-06T10:27:21Z","timestamp":1791282441276,"version":"4.1.0"},"reference-count":51,"publisher":"Wiley","issue":"4","license":[{"start":{"date-parts":[[2005,5,19]],"date-time":"2005-05-19T00:00:00Z","timestamp":1116460800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":["pathsocjournals.onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["The Journal of Pathology"],"published-print":{"date-parts":[[2005,8]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>\n                    Vimentin expression is a rather rare finding in invasive breast cancer, and is associated with high tumour invasiveness and chemoresistance. It is currently explained by two different biological theories: direct histogenetic derivation from myoepithelial cells, and epithelial\u2013mesenchymal transition (EMT) reflecting the end\u2010stage of breast cancer dedifferentiation. In this study we aimed to obtain further insights into the biological hallmarks of these vimentin\u2010expressing breast cancers. We applied immunohistochemistry for vimentin and 15 other differentiation markers to a series of 364 invasive breast cancer cases, using tissue microarray technology. 7.7% of all tumours expressed vimentin. Almost all of these cases (19\/21) were Grade 3 invasive ductal carcinomas, and the majority (13\/21) of these were associated with a ductal\n                    <jats:italic>in situ<\/jats:italic>\n                    component. Vimentin expression was also seen in the respective\n                    <jats:italic>in situ<\/jats:italic>\n                    components and correlated positively with the expression of SMA, CD10, CK 5, p53, Mib\u20101 and EGFR. A negative correlation was seen for the expression of CK 8\/18 and the oestrogen receptor. Vimentin\u2010expressing carcinomas revealed a significantly higher average absolute number of cytogenetic alterations per case, but a significantly lower frequency of chromosome 16q losses compared to vimentin\u2010negative cases. Our present results demonstrate that, despite analogies between vimentin\u2010positive breast cancers and myoepithelial cells in their expression of differentiation\u2010related proteins, neither myoepithelial histogenesis nor EMT can exclusively explain the biology of these distinct tumours. This is mainly supported by the significantly higher incidence of vimentin\u2010expressing breast cancers compared to any other myoepithelial breast tumours and the fact that vimentin is already observed in ductal\n                    <jats:italic>in situ<\/jats:italic>\n                    components. We therefore propose the alternative hypothesis that vimentin\u2010expressing breast carcinomas may derive from breast progenitor cells with bilinear (glandular and myoepithelial) differentiation potential. Copyright \u00a9 2005 Pathological Society of Great Britain and Ireland. Published by John Wiley &amp; Sons, Ltd.\n                  <\/jats:p>","DOI":"10.1002\/path.1797","type":"journal-article","created":{"date-parts":[[2005,5,19]],"date-time":"2005-05-19T07:18:49Z","timestamp":1116487129000},"page":"451-457","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":179,"title":["The origin of vimentin expression in invasive breast cancer: epithelial\u2013mesenchymal transition, myoepithelial histogenesis or histogenesis from progenitor cells with bilinear differentiation 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