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Expression levels of HMGA2 in adipocytic tumors correlate with morphologic and cytogenetic subgroups

Bartuma, H; Panagopoulos, I; Collin, A; Trombetta, D; Domanski, HA; Mandahl, N; Mertens, F; (2009) Expression levels of HMGA2 in adipocytic tumors correlate with morphologic and cytogenetic subgroups. Molecular Cancer , 8 , Article 36. 10.1186/1476-4598-8-36. Green open access

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Abstract

Background: The HMGA2 gene encodes a protein that alters chromatin structure. Deregulation, typically through chromosomal rearrangements, of HMGA2 has an important role in the development of several mesenchymal neoplasms. These rearrangements result in the expression of a truncated protein lacking the acidic C-terminus, a fusion protein consisting of the AT-hook domains encoded by exons 1-3 and parts from another gene, or a full-length protein; loss of binding sites for regulatory microRNA molecules from the 3' untranslated region (UTR) of HMGA2 has been suggested to be a common denominator.Methods: Seventy adipocytic tumors, representing different morphologic and cytogenetic subgroups, were analyzed by qRT-PCR to study the expression status of HMGA2; 18 of these tumors were further examined by PCR to search for mutations or deletions in the 3'UTR.Results: Type (full-length or truncated) and level of expression varied with morphology and karyotype, with the highest levels in atypical lipomatous tumors and lipomas with rearrangements of 12q13-15 and the lowest in lipomas with 6p- or 13q-rearrangements, hibernomas, spindle cell lipomas and myxoid liposarcomas. All 18 examined tumors showed reduced or absent expression of the entire, or parts of, the 3'UTR, which was not due to mutations at the DNA level.Conclusion: In adipocytic tumors with deregulated HMGA2 expression, the 3'UTR is consistently lost, either due to physical disruption of HMGA2 or a shift to production of shorter 3'UTR.

Type: Article
Title: Expression levels of HMGA2 in adipocytic tumors correlate with morphologic and cytogenetic subgroups
Open access status: An open access version is available from UCL Discovery
DOI: 10.1186/1476-4598-8-36
Publisher version: http://dx.doi.org/10.1186/1476-4598-8-36
Language: English
Additional information: © 2009 Bartuma et al; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
Keywords: BENIGN MESENCHYMAL TUMORS, ADIPOSE-TISSUE TUMORS, PULMONARY CHONDROID HAMARTOMAS, IN-SITU HYBRIDIZATION, LIPOMATOUS TUMORS, ARCHITECTURAL FACTOR, UTERINE LEIOMYOMAS, SUPERNUMERARY RING, PROTEIN GENE, WILD-TYPE
UCL classification: UCL
UCL > Provost and Vice Provost Offices
UCL > Provost and Vice Provost Offices > School of Life and Medical Sciences
UCL > Provost and Vice Provost Offices > School of Life and Medical Sciences > Faculty of Medical Sciences
URI: https://discovery.ucl.ac.uk/id/eprint/1312900
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