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Int J Hematol. 2013 Mar;97(3):313-23. doi: 10.1007/s12185-013-1291-2. Epub 2013 Feb 28.

Molecular pathogenesis of multiple myeloma: basic and clinical updates.

Author information

1
Mayo Clinic Arizona, 13400 E Shea Blvd, Scottsdale, AZ 85259, USA.

Abstract

Multiple myeloma is divided into two distinct genetic subtypes based on chromosome content. Hyperdiploid myeloma is characterized by multiple trisomies of chromosomes 3, 5, 7, 9 11, 15, 19 and 21, and lacks recurrent immunoglobulin gene translocations. Non-hyperdiploid myeloma in contrast is characterized by chromosome translocations t(4;14), t(14;16), t(14;20), t(6;14) and t(11;14). A unifying event in the pathogenesis of multiple myeloma is the dysregulated expression of a cyclin D gene, either directly by juxtaposition to an immunoglobulin enhancer, as a result of ectopic expression of a MAF family transcription factor, or indirectly by as yet unidentified mechanisms. Secondary genetic events include rearrangements of MYC, activating mutations of NRAS, KRAS or BRAF, a promiscuous array of mutations that activate NFkB and deletions of 17p. Among the poor-risk genetic features are t(4;14), t(14;16), t(14;20), del 17p and gains of 1q. Available evidence supports the use of a risk-stratified approach to the treatment of patients with multiple myeloma, with the early and prolonged use of bortezomib particularly in patients with t(4;14) and del 17p.

PMID:
23456262
PMCID:
PMC3962846
DOI:
10.1007/s12185-013-1291-2
[Indexed for MEDLINE]
Free PMC Article

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