{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,1]],"date-time":"2026-10-01T05:57:58Z","timestamp":1790834278939,"version":"4.1.0"},"reference-count":59,"publisher":"Wiley","issue":"7","license":[{"start":{"date-parts":[[2018,2,13]],"date-time":"2018-02-13T00:00:00Z","timestamp":1518480000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Histopathology"],"published-print":{"date-parts":[[2018,6]]},"abstract":"<jats:p>Despite the significant biological, behavioural and management differences between ductal carcinoma <jats:italic>in situ<\/jats:italic> (<jats:styled-content style=\"fixed-case\">DCIS<\/jats:styled-content>) and invasive carcinoma of the breast, they share many morphological and molecular similarities. Differentiation of these two different lesions in breast pathological diagnosis is based typically on the presence of an intact barrier between the malignant epithelial cells and stroma; namely, the myoepithelial cell (<jats:styled-content style=\"fixed-case\">MEC<\/jats:styled-content>) layer and surrounding basement membrane (<jats:styled-content style=\"fixed-case\">BM<\/jats:styled-content>). Despite being robust diagnostic criteria, the identification of <jats:styled-content style=\"fixed-case\">MEC<\/jats:styled-content>s and <jats:styled-content style=\"fixed-case\">BM<\/jats:styled-content> to differentiate <jats:italic>in\u2010situ<\/jats:italic> from invasive carcinoma is not always straightforward. The <jats:styled-content style=\"fixed-case\">MEC<\/jats:styled-content> layer around <jats:styled-content style=\"fixed-case\">DCIS<\/jats:styled-content> may be interrupted and\/or show an altered immunoprofile. <jats:styled-content style=\"fixed-case\">MEC<\/jats:styled-content>s may be absent in some benign locally infiltrative lesions such as microglandular adenosis and infiltrating epitheliosis, and occasionally in non\u2010infiltrative conditions such as apocrine lesions, and in these contexts this does not denote malignancy or invasive disease with metastatic potential. <jats:styled-content style=\"fixed-case\">MEC<\/jats:styled-content>s may also be absent around some malignant lesions such as some forms of papillary carcinoma, yet these behave in an indolent fashion akin to some <jats:styled-content style=\"fixed-case\">DCIS<\/jats:styled-content>. In Paget's disease, malignant mammary epithelial cells extend anteriorly from the ducts to infiltrate the epidermis of the nipple but do not typically infiltrate through the <jats:styled-content style=\"fixed-case\">BM<\/jats:styled-content> into the dermis. Conversely, <jats:styled-content style=\"fixed-case\">BM<\/jats:styled-content>\u2010like material can be seen around invasive carcinoma cells and around metastatic tumour cell deposits. Here, we review the role of <jats:styled-content style=\"fixed-case\">MEC<\/jats:styled-content>s and <jats:styled-content style=\"fixed-case\">BM<\/jats:styled-content> in breast pathology and highlight potential clinical implications. We advise caution in interpretation of <jats:styled-content style=\"fixed-case\">MEC<\/jats:styled-content> features in breast pathology and mindfulness of the substantive evidence base in the literature associated with behaviour and clinical outcome of lesions classified as benign on conventional morphological examination before changing classification to an invasive lesion on the sole basis of <jats:styled-content style=\"fixed-case\">MEC<\/jats:styled-content> characteristics.<\/jats:p>","DOI":"10.1111\/his.13446","type":"journal-article","created":{"date-parts":[[2017,12,2]],"date-time":"2017-12-02T07:32:35Z","timestamp":1512199955000},"page":"1075-1083","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":40,"title":["Invasion in breast lesions: the role of the epithelial\u2013stroma barrier"],"prefix":"10.1111","volume":"72","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-5009-5525","authenticated-orcid":false,"given":"Emad A","family":"Rakha","sequence":"first","affiliation":[{"name":"Department of Histopathology Nottingham City Hospital NHS Trust Nottingham University Nottingham UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Islam M","family":"Miligy","sequence":"additional","affiliation":[{"name":"Department of Histopathology Nottingham City Hospital NHS Trust Nottingham University Nottingham UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kylie L","family":"Gorringe","sequence":"additional","affiliation":[{"name":"Cancer Genomics Program Peter MacCallum Cancer Centre Melbourne Vic. 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