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Blood, 1 September 2006, Vol. 108, No. 5, pp. 1733-1743. Prepublished online as a Blood First Edition Paper on May 16, 2006; DOI 10.1182/blood-2006-02-005496. This Article Full Text (PDF) Supplemental Tables All Versions of this Article: blood-2006-02-005496v1 108/5/1733    most recent Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Walker, B. A Articles by Morgan, G. J Search for Related Content PubMed PubMed Citation Articles by Walker, B. A Articles by Morgan, G. J Social Bookmarking                   What's this?  Previous Article  |  Next Article  Submitted February 27, 2006 Accepted April 26, 2006 Integration of global SNP-based mapping and expression arrays reveals key regions, mechanisms and genes important in the pathogenesis of multiple myeloma Brian A Walker, Paola E Leone, Matthew W Jenner, Cheng Li, David Gonzalez, David C Johnson, Fiona M Ross, Faith E Davies, and Gareth J Morgan* Section of Haemato-Oncology, Institute of Cancer Research, Surrey, UK Harvard School of Public Health, Boston, MA, USA Wessex Regional Cytogenetic Laboratory, Salisbury, UK * Corresponding author; email: gareth.morgan{at}icr.ac.uk. Multiple myeloma is characterized by genomic alterations frequently involving gains and losses of chromosomes. SNP-based mapping arrays allow the identification of copy number changes at the sub-megabase level and the identification of loss of heterozygosity (LOH) due to monosomy and uniparental disomy (UPD). We have found that SNP-based mapping array data and FISH copy number data correlated well, making the technique robust as a tool to investigate myeloma genomics. The most frequently identified alterations are located at 1p, 1q, 6q, 8p, 13, and 16q. LOH is found in these large regions and also in smaller regions throughout the genome with a median size of 1 Mb. We have identified that UPD is prevalent in myeloma and occurs through a number of mechanisms including mitotic nondisjunction and mitotic recombination. For the first time in myeloma, integration of mapping and expression data has allowed us to reduce the complexity of standard gene expression data and identify candidate genes important in both the transition from normal to MGUS to myeloma and in different subgroups within myeloma. We have documented these genes providing a focus for further studies to identify and characterize those that are key in the pathogenesis of myeloma. 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