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Human Molecular Genetics Advance Access published online on June 30, 2004
Human Molecular Genetics, doi:10.1093/hmg/ddh195
© 2004 by Oxford University Press
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Comprehensive whole genome array CGH profiling of mantle cell lymphoma model genomes

Ronald J. deLeeuw 1*, Jonathan J. Davies 2, Andreas Rosenwald 3, Gwyn Bebb 2, Randy D. Gascoyne 2, Martin J.S. Dyer 4, Louis M. Staudt 5, Jose A. Martinez-Climent 6, Wan L. Lam 2

1 Departments of Cancer Genetics, Medical Oncology, and Pathology, British Columbia Research Centre Agency, 601 W. 10th Ave., Vancouver, British Columbia V5Z 1L3, Canada
2 Departments of Cancer Genetics, Medical Oncology, and Pathology, British Columbia Cancer Agency, Vancouver, British Columbia, Canada
3 Institute of Pathology, University of Wuerzburg, Germany; Center for Cancer Research, National Cancer Institute, Bethesda, Maryland, USA
4 MRC Toxicology Unit, University of Leicester, United Kingdom
5 Center for Cancer Research, National Cancer Institute, Bethesda, Maryland, USA
6 Department of Hematology and Medical Oncology, Hospital Clinico, University of Valencia, Spain

* To whom correspondence should be addressed. E-mail: rdeleeuw{at}bccrc.ca.


  Abstract

Mantle cell lymphoma is an aggressive non-Hodgkin's lymphoma with median patient survival times of approximately 3 years. Although the characteristic t(11;14)(q13;q32) is found in virtually all cases, experimental evidence suggests that this event alone is insufficient to result in lymphoma and secondary genomic alterations are required. Using a newly developed DNA microarray of 32,433 overlapping genomic segments spanning the entire human genome, we can for the first time, move beyond marker based analysis and comprehensively search for secondary genomic alterations concomitant with the t(11;14) in eight commonly used cell models of MCL (Granta-519, HBL-2, NCEB-1, Rec-1, SP49, UPN-1, Z138C, and JVM-2). Examining these genomes at tiling resolution identified an unexpected average of 35 genetic alterations per cell line, with equal numbers of amplifications and deletions. Recurrent high level amplifications were identified at 18q21 containing BCL2, and 13q31 containing GPC5. In addition, a recurrent homozygous deletion was identified at 9p21 containing p15 and p16 Alignment of these profiles revealed 14 recurrent losses and 21 recurrent gains as small as 130 Kb. Remarkably, even the intra immunoglobulin gene deletions at 2p11 and 22q11 were detected, demonstrating the power of combining the detection sensitivity of array CGH with the resolution of an overlapping whole genome tiling-set. These alterations not only coincided with previously described aberrations in MCL, but also defined 13 novel regions. Further characterization of such minimally altered genomic regions identified using whole genome array CGH will define novel dominant oncogenes and tumor suppressor genes that play important roles in the pathogenesis of MCL.


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