{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,17]],"date-time":"2026-08-17T23:59:25Z","timestamp":1787011165691,"version":"build-2736575974"},"reference-count":44,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[2002,11,19]],"date-time":"2002-11-19T00:00:00Z","timestamp":1037664000000},"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":[[2003,1]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>The cribriform\u2010morular variant (C\u2010MV), an unusual and peculiar subtype of papillary thyroid carcinoma (PTC), has been observed frequently in familial adenomatous polyposis (FAP)\u2010associated thyroid carcinoma and also in sporadic thyroid carcinoma. In this paper, five young women with the C\u2010MV of PTC, aged 22\u201334 years at cancer diagnosis, are reported; two of them had attenuated FAP. Grossly, one FAP\u2010associated tumour and one sporadic tumour were multicentric and the others were solitary. Histologically, the tumours were encapsulated and exhibited a combination of cribriform, follicular, trabecular, solid, and papillary patterns of growth, with morular areas. Immunohistochemically, the tumour cells showed cytoplasmic expression of thyroglobulin, neuron\u2010specific enolase, epithelial membrane antigen, high\u2010 and low\u2010molecular\u2010weight cytokeratins, vimentin, and bcl\u20102 protein; nuclear expression of oestrogen and progesterone receptors, and retinoblastoma protein; and cytoplasmic and nuclear accumulation of \u03b2\u2010catenin. Germline mutations of the adenomatous polyposis coli (APC) gene were investigated using the protein truncation test in four subjects, including two FAP individuals. Germline APC mutation was identified in only one FAP patient with the multicentric C\u2010MV of PTC, who had a thymidine deletion at codon 512, resulting in a frameshift leading to a premature stop codon. No loss of heterozygosity of loci close to the APC gene was detected in tumour tissues from these four patients. Somatic mutation analysis of exon 3 of the \u03b2\u2010catenin gene (CTNNB1) revealed alterations in seven tumours from all five individuals: one at a serine residue (codon 29), three at amino acids adjacent to serine or threonine residues (codons 22, 39, and 44), and three at other amino acids (codons 49, 54, and 56). Moreover, each of two different tumours examined from two patients with the multicentric C\u2010MV of PTC, had different somatic mutations of the CTNNB1 gene. Taken together, these data suggest that accumulation of mutant \u03b2\u2010catenin contributes to the development of the C\u2010MV of PTC. Copyright \u00a9 2002 John Wiley &amp; Sons, Ltd.<\/jats:p>","DOI":"10.1002\/path.1225","type":"journal-article","created":{"date-parts":[[2002,12,10]],"date-time":"2002-12-10T08:43:28Z","timestamp":1039509808000},"page":"58-67","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":117,"title":["Cribriform\u2010morular variant of papillary thyroid carcinoma: a pathological and molecular genetic study with evidence of frequent somatic mutations in exon 3 of the \u03b2\u2010catenin 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