Original Article

Gene copy number analysis in malignant pleural mesothelioma using oligonucleotide array CGH
P.M. Lindholm^a, K. Salmenkivi^a, H. Vauhkonen^a, A.G. Nicholson^b, S. Anttila^c, V.L. Kinnula^d, S. Knuutila<sup>a

a</sup>Department of Pathology, Haartman Institute and HUSLAB, University of Helsinki and Helsinki University Central Hospital, Helsinki (Finland);
^bDepartment of Histopathology, Royal Brompton Hospital, London (UK)
^cHealth and Work Ability, Biological Mechanisms and Prevention of Work-related Diseases, Finnish Institute of Occupational Health,
^dDepartment of Medicine, Pulmonary Division, University of Helsinki and Helsinki University Hospital, Helsinki (Finland)

Address of Corresponding Author

Cytogenet Genome Res 2007;119:46-52 (DOI: 10.1159/000109618)

  Abstract.

Conventional cytogenetic analyses and comparative genomic hybridization have revealed a complex and even chaotic nature of chromosomal aberrations in pleural malignant mesothelioma (MM). We set out to describe the complex gene copy number changes and screen for novel genetic aberrations using a high-density oligonucleotide microarray platform for comparative genomic hybridization (aCGH) of a series of 26 well-characterized MM tumor samples. The number of copy number changes varied from zero to 40 per sample. Gene copy number losses predominated over gains, and the most frequent region of loss was 9p21.3 (17/26 cases), the locus of CDKN2A and CDKN2B, both known to be commonly lost in MM. The most recurrent minimal regions of losses were 1p31.1 p13.2, 3p22.1p14.2, 6q22.1, 9p21.3, 13cenq14.12, 14q22.1qter, and 22qcenq12.3. Previously unreported gains included 9p13.3, 7p22.3p22.2, 12q13.3, and 17q21.32qter. The results suggest that gene copy number losses are a major mechanism of MM carcinogenesis and reveal a recurrent pattern of copy number changes in MM.

Copyright © 2007 S. Karger AG, Basel

  Author Contacts

Request reprints from Sakari Knuutila
Department of Pathology, Haartman Institute, PO Box 21
(Haartmaninkatu 3), FI-00014 University of Helsinki (Finland)
telephone: +358 9 191 26527; fax: +358 9 191 26788
e-mail: sakari.knuutila@helsinki.fi

  Article Information

This work was supported by the K. Albin Johansson foundation, Foundation of the Finnish Anti-Tuberculosis Association, Finnish Cancer Society, Medicinska Understödsföreningen Liv och Hälsa, and Finnish Funding Agency for Technology and Innovation (TEKES).

Manuscript received: 30 April 2007
Accepted in revised form for publication by A. Geurts van Kessel,: 6 June 2007.
Published online: December 14, 2007
Number of Print Pages : 7
Number of Figures : 2, Number of Tables : 3, Number of References : 42