Original Article

Modern Pathology (2005) 18, 638–644, advance online publication, 12 November 2004; doi:10.1038/modpathol.3800326

Gains of 13q are correlated with a poor prognosis in liposarcoma

Hannelore Schmidt1, Frank Bartel1, Matthias Kappler1, Peter Würl2, Heidemarie Lange1, Matthias Bache3, Hans-Jürgen Holzhausen1 and Helge Taubert1

  1. 1Institute of Pathology, Martin Luther University Halle-Wittenberg, Halle, Germany
  2. 2Surgical Clinic 1, University of Ulm, Ulm, Germany
  3. 3Department of Radiotherapy, Martin Luther University Halle-Wittenberg, Halle, Germany

Correspondence: Dr H Schmidt, PhD, Institute of Pathology, Faculty of Medicine, Martin Luther University Halle-Wittenberg, Magdeburger Strasse 14, D-06097 Halle, Germany. E-mail: hannelore.schmidt@medizin.uni-halle.de

Received 22 June 2004; Revised 21 September 2004; Accepted 21 September 2004; Published online 12 November 2004.

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Abstract

Liposarcomas are a phenotypical heterogenous group of tumors divided into four main subtypes: well-differentiated, dedifferentiated, myxoid/round cell, and pleomorphic. The aim of this study was to compare DNA sequence copy number changes of these subtypes as investigated by comparative genomic hybridization in 36 patients. Comparative genomic hybridization revealed genomic imbalances in tumors of 27 patients (mean 5.6 imbalances per tumor). The most frequent gains were within single regions of 1q, 12q, and 13q. We found a significant correlation of poor overall survival and gain of 13q21 (P=0.0221), 13q22 (P=0.0341), 13q31 (P=0.0410), and 13q32 (P=0.0074). The univariate Cox regression analysis revealed an increased risk of tumor-related death for patients whose liposarcomas possess with gains of 13q21 and 13q32 simultaneously (P=0.010; RR=7.1; 95% CI 1.6–31.7). Furthermore, 12 high-level amplifications were found in tumors of seven patients. In four cases 12q14–q15 and in two cases 13q32–q33 were amplified. We identified in different liposarcoma subtypes characteristic genomic changes: Gains and high-level amplifications of 12q occurred in all 11 investigated well-differentiated liposarcomas, and these changes were often present simultaneously with gains of 1q (mean 5.5 changes). In the two dedifferentiated liposarcomas, gains of 1q in both liposarcomas, and a high-level amplification of 13q were striking. Only eight of the 17 patients with myxoid/round cell liposarcomas showed changes in DNA copy number (mean 3.4 imbalances). In four of these eight cases gains of 13q occurred. The six pleomorphic liposarcomas possessed the most frequent genomic imbalances (mean number 16.3) of all liposarcoma subtypes investigated. These imbalances were in almost all chromosomal regions detected predominantly as over-representations of chromosomes 1, 5p, 13q, and 22q. Summarizing, all subtypes but well-differentiated liposarcomas showed gains of 13q, which were associated with a poor prognosis.

Keywords:

CGH, gain of 13q, liposarcoma subtypes, poor prognosis

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