{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,9]],"date-time":"2026-10-09T19:44:31Z","timestamp":1791575071623,"version":"4.3.4"},"reference-count":48,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[2026,3,29]],"date-time":"2026-03-29T00:00:00Z","timestamp":1774742400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"},{"start":{"date-parts":[[2026,3,29]],"date-time":"2026-03-29T00:00:00Z","timestamp":1774742400000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Histopathology"],"published-print":{"date-parts":[[2026,7]]},"abstract":"<jats:sec>\n                    <jats:title>Aims<\/jats:title>\n                    <jats:p>De\u2010escalated treatment for ductal carcinoma in situ (DCIS) aims to prevent overtreatment of patients. However, patients diagnosed preoperatively with pure DCIS via core needle biopsy (CNB) may be upgraded to invasive cancer upon excision. Therefore, it is essential to stratify patients at low risk for upgrade to invasive disease during the biopsy to inform management decisions.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods and results<\/jats:title>\n                    <jats:p>\n                      In this study, we reviewed a cohort of patients with pure DCIS diagnosed by CNB and their corresponding excision specimens to identify predictive features for upgrading to microinvasion or invasive breast cancer (IBC). Of the 228 CNB cases, 82 (36%) were upgraded at excision, with 26.8% classified as microinvasion and 73.2% as frank invasion. Significant tumour intrinsic features associated with DCIS upgrade included larger tumour size, palpable mass, high grade and presence of necrosis (\n                      <jats:italic>P<\/jats:italic>\n                      \u2009\u2264\u20090.026). Factors related to sampling adequacy, such as the number of cores, total core length and length of the longest core, were also predictive features (\n                      <jats:italic>P<\/jats:italic>\n                      \u2009\u2264\u20090.027). Additionally, tumour microenvironment (TME) characteristics, including calcification and stromal tumour\u2010infiltrating lymphocytes (sTIL), were linked to upgrades, particularly in the human epidermal growth factor 2 (HER2)\u2010negative subgroup (\n                      <jats:italic>P<\/jats:italic>\n                      \u2009\u2264\u20090.004). These features were independently associated with frank invasion in HER2\u2010negative cancers.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>Our results provide valuable insights into additional predictive features for DCIS upgrade. When combined with adequate sampling and intrinsic tumour characteristics, TME features\u2014namely tumour infiltrating lymphocytes (TILs) and calcification\u2014are useful in predicting DCIS upgrades, especially in HER2\u2010negative cases.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1111\/his.70143","type":"journal-article","created":{"date-parts":[[2026,3,29]],"date-time":"2026-03-29T23:29:34Z","timestamp":1774826974000},"page":"122-135","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":1,"title":["Calcification and tumour\u2010infiltrating lymphocytes predict upgrade of human epidermal growth factor 2 (\n                    <scp>HER2)<\/scp>\n                    \u2010negative ductal carcinoma in situ diagnosed on core needle\u00a0biopsy"],"prefix":"10.1111","volume":"89","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-8758-1984","authenticated-orcid":false,"given":"Monalyn","family":"Marabi","sequence":"first","affiliation":[{"name":"Department of Anatomical and Cellular Pathology and State Key Laboratory of Translational Oncology Prince of Wales Hospital, The Chinese University of Hong Kong  Hong Kong Hong Kong"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yuyang","family":"Li","sequence":"additional","affiliation":[{"name":"Department of Pathology The First Affiliated Hospital of Fujian Medical University  Fuzhou Fujian China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-9185-4121","authenticated-orcid":false,"given":"Chaiwat","family":"Aphivatanasiri","sequence":"additional","affiliation":[{"name":"Department of Anatomical and Cellular Pathology and State Key Laboratory of Translational Oncology Prince of Wales Hospital, The Chinese University of Hong Kong  Hong Kong Hong Kong"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-6612-9622","authenticated-orcid":false,"given":"Julia Y","family":"Tsang","sequence":"additional","affiliation":[{"name":"Department of Anatomical and Cellular Pathology and State Key Laboratory of Translational Oncology Prince of Wales Hospital, The Chinese University of Hong Kong  Hong Kong Hong Kong"},{"name":"Li Ka Shing Institute of Health Sciences The Chinese University of Hong Kong  Hong Kong Hong Kong"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-2425-0314","authenticated-orcid":false,"given":"Joshua JX","family":"Li","sequence":"additional","affiliation":[{"name":"Department of Anatomical and Cellular Pathology and State Key Laboratory of Translational Oncology Prince of Wales Hospital, The Chinese University of Hong Kong  Hong Kong Hong Kong"},{"name":"Department of Pathology 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