Abstract
Primary genetic abnormalities in myeloma (MM) such as trisomies of chromosomes 3, 5, 7, 9, 11, 15, 19 and 21 associated with hyperdiploid MM and translocations involving the immunoglobulin heavy chain (IgH) locus on chromosome 14q32 and three main recurrent partners: MMSET/FGFR3, CCND1 and c-MAF are already present in the pre-malignant monoclonal gammopathy of undetermined significance (MGUS) stage.1 Some patients with these genetic abnormalities may remain as MGUS for many years without transforming to MM, suggesting that they are involved in clonal initiation but do not mediate malignant transformation.
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