{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,4]],"date-time":"2026-10-04T18:59:39Z","timestamp":1791140379691,"version":"4.1.0"},"reference-count":43,"publisher":"BMJ","issue":"9","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["J Clin Pathol"],"published-print":{"date-parts":[[2003,9]]},"abstract":"<jats:p>\n                    <jats:bold>Background:<\/jats:bold>\n                    Premalignant Barrett\u2019s oesophagus (BO) and gastric intestinal metaplasia (IM) show phenotypic variability. Incompletely differentiated sulfomucin rich gastric IM (type III) may have increased malignant potential. The types of sulfated oligosaccharide structures present in IM, BO, and colon have not been fully characterised.\n                  <\/jats:p>\n                  <jats:p>\n                    <jats:bold>Aims:<\/jats:bold>\n                    To compare sulfo-Lewis\n                    <jats:sup>a<\/jats:sup>\n                    epitope tissue distribution with high iron diamine (HID) positive sulfomucin in metaplastic, dysplastic, and neoplastic tissues from oesophagus and stomach.\n                  <\/jats:p>\n                  <jats:p>\n                    <jats:bold>Methods:<\/jats:bold>\n                    Sections containing gastric IM or BO (some associated with dysplasia or adenocarcinoma) were stained by the HID\/alcian blue (AB) method and immunohistochemically (antibody 91.9H) to detect sulfo-Lewis\n                    <jats:sup>a<\/jats:sup>\n                    . Based on HID\/AB staining, IM was subtyped into type I (complete) or types II and III (incomplete).\n                  <\/jats:p>\n                  <jats:p>\n                    <jats:bold>Results:<\/jats:bold>\n                    In total, 125 sections from 38 subjects were studied. Normal squamous oesophagus, normal gastric epithelium, and type I IM were negative for sulfomucin and sulfo-Lewis\n                    <jats:sup>a<\/jats:sup>\n                    . In type II IM, occasional goblet cells were HID and sulfo-Lewis\n                    <jats:sup>a<\/jats:sup>\n                    positive, but sialomucin secreting (AB positive) columnar cells were sulfo-Lewis\n                    <jats:sup>a<\/jats:sup>\n                    negative. Type III IM was always sulfo-Lewis\n                    <jats:sup>a<\/jats:sup>\n                    positive. Sulfomucin staining in dysplasia and cancer was variable, but HID positive areas were always sulfo-Lewis\n                    <jats:sup>a<\/jats:sup>\n                    positive.\n                  <\/jats:p>\n                  <jats:p>\n                    <jats:bold>Conclusions:<\/jats:bold>\n                    Sulfo-Le\n                    <jats:sup>a<\/jats:sup>\n                    , which is expressed on colonic mucin, is invariably present on sulfomucins in gastric IM and BO. Its presence in incomplete variants of IM and its absence from type I IM emphasises the phenotypic differences between complete and incomplete forms of metaplasia. 91.9H immunostaining is useful in IM subtyping. Characterising the molecular basis of sulfo-Lewis\n                    <jats:sup>a<\/jats:sup>\n                    expression may help understand the process of aberrant differentiation.\n                  <\/jats:p>","DOI":"10.1136\/jcp.56.9.703","type":"journal-article","created":{"date-parts":[[2003,8,27]],"date-time":"2003-08-27T18:39:43Z","timestamp":1062009583000},"page":"703-708","source":"Crossref","is-referenced-by-count":24,"title":["Detection of sulfated glycoproteins in intestinal metaplasia: a comparison of traditional mucin staining with immunohistochemistry for the sulfo-Lewis\n                    <sup>a<\/sup>\n                    carbohydrate epitope"],"prefix":"10.1136","volume":"56","author":[{"given":"K","family":"Bodger","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"F","family":"Campbell","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"J M","family":"Rhodes","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"239","published-online":{"date-parts":[[2003,8,27]]},"reference":[{"key":"2025121403533517000_56.9.703.1","doi-asserted-by":"publisher","DOI":"10.1136\/jcp.33.8.711"},{"key":"2025121403533517000_56.9.703.2","first-page":"3554","volume":"48","year":"1988","journal-title":"Cancer Res"},{"key":"2025121403533517000_56.9.703.3","doi-asserted-by":"crossref","first-page":"5","DOI":"10.1093\/ajcp\/98.1.5","volume":"98","year":"1992","journal-title":"Am J Clin Pathol"},{"key":"2025121403533517000_56.9.703.4","unstructured":"Nevalainen TJ. 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