Array comparative genomic hybridization analysis reveals a limited number of genomic alterations in familial adenomatous polyposis-associated and sporadic desmoid tumors

ABSTRACT: Desmoid tumors (also called deep or aggressive fibromatoses) are potentially life-threatening fibromatous lesions. Hereditary desmoid tumors arise in individuals affected by either familial adenomatous polyposis (FAP) or hereditary desmoid disease (HDD) carrying germline mutations in APC. Most non-FAP (sporadic) desmoids carry somatic mutations in the beta-catenin gene. Previous studies identified losses on 5q and 6q, and gains on 8q and 20q as recurrent genetic changes in desmoids. However, virtually all genetic changes were derived from sporadic tumors. To investigate the somatic alterations in FAP-associated desmoids and to compare them with changes occurring in sporadic tumors, we analyzed 17 FAP-associated and 38 sporadic desmoids for copy number abnormalities (CNAs) by means of array

ORGANISM(S): Homo sapiens

SUBMITTER: Els Robanus-Maandag 

PROVIDER: E-GEOD-28458 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress