{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,11,2]],"date-time":"2025-11-02T16:21:39Z","timestamp":1762100499797},"reference-count":33,"publisher":"Wiley","issue":"3","license":[{"start":{"date-parts":[[2006,5,18]],"date-time":"2006-05-18T00:00:00Z","timestamp":1147910400000},"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":["Int J Experimental Path"],"published-print":{"date-parts":[[2006,6]]},"abstract":"<jats:title>Summary<\/jats:title><jats:p>Germ\u2010line mutation of the <jats:italic>Apc<\/jats:italic> gene has been linked to familial adenomatous polyposis (FAP) that predisposes to colon cancer. <jats:italic>Apc<\/jats:italic><jats:sup><jats:italic>Min\/+<\/jats:italic><\/jats:sup> mice, heterozygous for the <jats:italic>Apc<\/jats:italic> gene mutation, progressively develop small intestinal tumours in a manner that is analogous to that observed in the colon of patients with FAP (<jats:ext-link xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" xlink:href=\"#b1\">Su <jats:italic>et al<\/jats:italic>. 1992; <\/jats:ext-link><jats:ext-link xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" xlink:href=\"#b2\">Fodde <jats:italic>et al<\/jats:italic>. 1994; <\/jats:ext-link><jats:ext-link xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" xlink:href=\"#b3\">Moser <jats:italic>et al<\/jats:italic>. 1995<\/jats:ext-link>). We have studied the effects of <jats:italic>Apc<\/jats:italic> gene mutation on murine intestinal and extra\u2010intestinal, proliferatively active tissues. We have contrasted the histology to that of the age\u2010 and sex\u2010matched wild\u2010type C57BL\/6 mice. Histological assessment of the normal appearing intestinal mucosa demonstrates minimal change in size of crypts. In contrast, villi are longer in the ileum of <jats:italic>Apc<\/jats:italic><jats:sup><jats:italic>Min\/+<\/jats:italic><\/jats:sup> mice relative to C57BL\/6 mice at 12 and 15 weeks of age. Vigorous splenic haematopoiesis in <jats:italic>Apc<\/jats:italic><jats:sup><jats:italic>Min\/+<\/jats:italic><\/jats:sup> mice was seen at 12 and 15 weeks of age, as reflected by marked splenomegaly, increased splenic haematopoietic cells and megakaryocytes. Peripheral blood counts, however, did not differ between C57BL\/6 and <jats:italic>Apc<\/jats:italic><jats:sup><jats:italic>Min\/+<\/jats:italic><\/jats:sup> mice at 15 weeks of age. Lymphoid depletion in <jats:italic>Apc<\/jats:italic><jats:sup><jats:italic>Min\/+<\/jats:italic><\/jats:sup> mice was characterized by diminished numbers of splenic lymphoid follicles and small intestinal Peyer's patches. The ovaries of 12\u2010 and 15\u2010week\u2010old <jats:italic>Apc<\/jats:italic><jats:sup><jats:italic>Min\/+<\/jats:italic><\/jats:sup> mice exhibited increased numbers of atretic follicles, and estrous cycling by serial vaginal smears showed tendency of elongation in the mutant mice during these age ranges. The testicles of 10\u2010week\u2010old <jats:italic>Apc<\/jats:italic><jats:sup><jats:italic>Min\/+<\/jats:italic><\/jats:sup> mice showed increased numbers of underdeveloped seminiferous tubules. Collectively, these data suggest that, in addition to its obvious effects upon intestinal adenoma formation, <jats:italic>Apc<\/jats:italic> gene mutation causes impairment of developmental and apparent differentiation blockade in proliferative tissues, including those of the haematopoietic system, lymphoid and reproductive tract.<\/jats:p>","DOI":"10.1111\/j.1365-2613.2006.00477.x","type":"journal-article","created":{"date-parts":[[2006,5,18]],"date-time":"2006-05-18T15:21:31Z","timestamp":1147965691000},"page":"227-236","update-policy":"http:\/\/dx.doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":44,"title":["Developmental abnormalities in multiple proliferative tissues of <i>Apc<\/i><sup><i>Min\/+<\/i><\/sup> mice"],"prefix":"10.1111","volume":"87","author":[{"given":"Shaojin","family":"You","sequence":"first","affiliation":[]},{"given":"Masami","family":"Ohmori","sequence":"additional","affiliation":[]},{"given":"Maria Marjorette O.","family":"Pe\u00f1a","sequence":"additional","affiliation":[]},{"given":"Basel","family":"Nassri","sequence":"additional","affiliation":[]},{"given":"Jovelyn","family":"Quiton","sequence":"additional","affiliation":[]},{"given":"Ziad A.","family":"Al\u2010Assad","sequence":"additional","affiliation":[]},{"given":"Lucy","family":"Liu","sequence":"additional","affiliation":[]},{"given":"Patricia A.","family":"Wood","sequence":"additional","affiliation":[]},{"given":"Sondra H.","family":"Berger","sequence":"additional","affiliation":[]},{"given":"ZhiJian","family":"Liu","sequence":"additional","affiliation":[]},{"given":"Michael D.","family":"Wyatt","sequence":"additional","affiliation":[]},{"given":"Robert L.","family":"Price","sequence":"additional","affiliation":[]},{"given":"Franklin G.","family":"Berger","sequence":"additional","affiliation":[]},{"given":"William J. 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