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Nucleoli are inconspicuous, and atypia and nuclear hyperchromasia are not seen. The overall cellularity and mitotic activity is variable, but mitoses are generally sparse and do not appear to be predictive of outcome. Cellularity can range from very sparse and fibrotic (perhaps best exemplified by Gardner-type fibromas, but also seen in sporadic cases) to relatively cellular, appearing almost storiform in areas. Generally, though, the overall pattern is mostly enlongated fascicles. Ultrastructural studies indicate that the spindle cells have features of both fibroblasts and myofibroblasts, but this is not useful in making diagnostic distinctions.

Adv Anat Pathol 12(6):350–356 21. Montgomery E, Torbenson MS et al (2002) Beta-catenin immunohistochemistry separates mesenteric fibromatosis from gastrointestinal stromal tumor and sclerosing mesenteritis. Am J Surg Pathol 26(10):1296–1301 22. Ng TL, Gown AM et al (2005) Nuclear beta-catenin in mesenchymal tumors. Mod Pathol 18(1):68–74 23. Pignatti G, Barbanti-Brodano G et al (2000) Extraabdominal desmoid tumor. A study of 83 cases. Clin Orthop Relat Res 375:207–213 24. Rock MG, Pritchard DJ et al (1984) Extra-abdominal desmoid tumors.

1 CTNNB1 mutation prevalence documented in various neoplasms C. Colombo and D. sanger. uk/perl/genetics/CGP/cosmic), was utilized to acquire the frequency of APC and β-catenin somatic mutation in a variety of tumor types gene led to the search for other possible Wnt pathway deregulations [61]. These investigations highlighted the propensity of direct CTNBB1 (the gene coding for β-catenin) mutations in sporadic DTs. CTNBB1 and APC mutations are mutually exclusive [62]. 1) [3, 61, 63–66]. CTNBB1 mutations almost exclusively occur in exon 3 of gene in the region encoding the phosphorylation domain of β-catenin.

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