High resolution SNP array genomic profiling of peripheral T cell lymphomas,not otherwise specified,identifies a subgroup with chromosomal aberrations affecting the REL locus |
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| Authors: | Sylvia Hartmann Stefan Gesk René Scholtysik Markus Kreuz Stefanie Bug Inga Vater Claudia Döring Sergio Cogliatti Marie Parrens Jean‐Philippe Merlio Anna Kwiecinska Anna Porwit Pier Paolo Piccaluga Stefano Pileri Gerald Hoefler Ralf Küppers Reiner Siebert Martin‐Leo Hansmann |
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| Institution: | 1. Senckenberg Institute of Pathology, University of Frankfurt, Frankfurt;2. Institute of Human Genetics, Christian‐Albrechts‐University Kiel, University Hospital Schleswig‐Holstein, Campus Kiel;3. Institute of Cell Biology, University of Duisburg‐Essen, Medical School Essen, Essen;4. Institute of Medical Informatics, Statistics and Epidemiology, University of Leipzig, Leipzig;5. Institute for Informatics, University of Frankfurt, Frankfurt, Germany;6. Institute of Pathology, Kantonsspital St.Gallen, St.Gallen, Switzerland;7. Department of Pathology and Tumour Genetics, CHU Bordeaux and EA2406, Bordeaux, France;8. Department of Pathology, Karolinska Institutet and Karolinska University Hospital Solna, Stockholm, Sweden;9. Institute of Haematology and Medical Oncology “L. and A. Seràgnoli,”, Sant’Orsola‐Malpighi Hospital, University of Bologna, Bologna, Italy;10. Institute of Pathology, Medical School University of Graz, Graz, Austria |
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| Abstract: | Little is known about genomic aberrations in peripheral T cell lymphoma, not otherwise specified (PTCL NOS). We studied 47 PTCL NOS by 250k GeneChip single nucleotide polymorphism arrays and detected genomic imbalances in 22 of the cases. Recurrent gains and losses were identified, including gains of chromosome regions 1q32–43, 2p15–16, 7, 8q24, 11q14–25, 17q11–21 and 21q11–21 (≥5 cases each) as well as losses of chromosome regions 1p35–36, 5q33, 6p22, 6q16, 6q21–22, 8p21–23, 9p21, 10p11–12, 10q11–22, 10q25–26, 13q14, 15q24, 16q22, 16q24, 17p11, 17p13 and Xp22 (≥4 cases each). Genomic imbalances affected several regions containing members of nuclear factor‐kappaB signalling and genes involved in cell cycle control. Gains of 2p15–16 were confirmed in each of three cases analysed by fluorescence in situ hybridization (FISH) and were associated with breakpoints at the REL locus in two of these cases. Three additional cases with gains of the REL locus were detected by FISH among 18 further PTCL NOS. Five of 27 PTCL NOS investigated showed nuclear expression of the REL protein by immunohistochemistry, partly associated with genomic gains of the REL locus. Therefore, in a subgroup of PTCL NOS gains/rearrangements of REL and expression of REL protein may be of pathogenetic relevance. |
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| Keywords: | non‐Hodgkin‐lymphoma peripheral T cell lymphoma NOS SNP array genomic profiling REL |
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