{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,23]],"date-time":"2026-07-23T16:31:01Z","timestamp":1784824261251,"version":"3.55.0"},"reference-count":24,"publisher":"Wiley","issue":"3","license":[{"start":{"date-parts":[[2012,12,13]],"date-time":"2012-12-13T00:00:00Z","timestamp":1355356800000},"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":[[2013,2]]},"abstract":"Aims<\/jats:title>Several cases of focal nodular hyperplasia (FNH<\/jats:styled-content>) or similar hyperplastic lesions have been reported adjacent to hepatic neoplasms, including hepatocellular carcinoma, epithelioid haemangioendothelioma and hepatoblastoma. We refer to this hyperplastic response as peritumoral hyperplasia (PTH<\/jats:styled-content>). Here, we report eight cases of PTH<\/jats:styled-content> adjacent to primary hepatocellular carcinomas (two) and metastatic neuroendocrine tumours (three), gastrointestinal stromal tumour (one) and colon carcinomas (two).<\/jats:p><\/jats:sec>Methods and results<\/jats:title>Sections were stained with H&E<\/jats:styled-content> and trichrome, and for glutamine synthetase, CD<\/jats:styled-content>34 and cytokeratin 7. PTH<\/jats:styled-content> was composed of a peritumoral rim of hyperplastic hepatocytes up to 7.0\u00a0mm wide, delimited by adjacent hepatocellular atrophy. PTH<\/jats:styled-content> had altered plate architecture, strong glutamine synthetase expression and variable sinusoidal endothelial cell CD<\/jats:styled-content>34 expression. The central tumour deposit typically invaded portal veins and was markedly hypervascular with CD<\/jats:styled-content>34\u2010positive capillaries.<\/jats:p><\/jats:sec>Conclusions<\/jats:title>We suggest that PTH<\/jats:styled-content> is a hyperplastic response to increased blood flow in the peritumoral parenchyma. The increased flow occurs when portal vein invasion by a hypervascular tumour causes arterio\u2010portal shunting. While PTH<\/jats:styled-content> shares some morphological features with FNH<\/jats:styled-content>, it lacks the defining nodular architecture, central scar and bile ductules. PTH<\/jats:styled-content> may be related pathophysiologically to FNH<\/jats:styled-content>, but should be classified as a separate entity because of its distinct morphology and peritumoral location.<\/jats:p><\/jats:sec>","DOI":"10.1111\/his.12032","type":"journal-article","created":{"date-parts":[[2012,9,18]],"date-time":"2012-09-18T02:27:07Z","timestamp":1347935227000},"page":"458-464","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":36,"title":["Peritumoral hyperplasia of the liver: a response to portal vein invasion by hypervascular neoplasms"],"prefix":"10.1111","volume":"62","author":[{"given":"Thomas","family":"Arnason","sequence":"first","affiliation":[{"name":"Division of Anatomical Pathology Queen Elizabeth II Health Sciences Centre and Dalhousie University Halifax NS Canada"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kirsten E","family":"Fleming","sequence":"additional","affiliation":[{"name":"Division of Anatomical Pathology Queen Elizabeth II Health Sciences Centre and Dalhousie University Halifax NS Canada"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ian R","family":"Wanless","sequence":"additional","affiliation":[{"name":"Division of Anatomical Pathology Queen Elizabeth II Health Sciences Centre and Dalhousie University Halifax NS Canada"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2012,12,13]]},"reference":[{"key":"e_1_2_5_2_1","doi-asserted-by":"publisher","DOI":"10.1111\/j.1365-2559.1994.tb01328.x"},{"key":"e_1_2_5_3_1","first-page":"1105","article-title":"Focal nodular hyperplasia of the liver: comments on the pathogenesis","volume":"124","author":"Wanless IR","year":"2000","journal-title":"Arch. 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