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Ashraf Badros

Multiple myeloma (MM) is characterized by proliferation of malignant plasma cells in the bone marrow, bone destruction, extramedullary plasmacytoma, renal failure, and, late in the disease course, marrow failure manifested as anemia, leukopenia, and thrombocytopenia.1 MM is customarily portrayed as an uncommon cancer. Nevertheless, MM accounts for 10% of all hematologic malignancies and 1% of all cancers. There are an estimated 74,000 new cases of MM worldwide each year with a worldwide prevalence of over 200,000 cases. MM is responsible for 2% of all cancer deaths yearly, with an estimated 57,370 deaths worldwide.2 In the United States, there were an estimated 15,270 new MM cases in 2004 and over 11,070 yearly deaths due to MM.3 The biology of MM suggests a multistep process as illustrated by the clinical progression from monoclonal gammopathy of unknown significance (MGUS) to the symptomatic phase of the disease. A B-cell precursor cell, after immunoglobulin gene rearrangement, is presumed to be the origin of the malignant clone in MM. The events that determine the susceptibility of B cells to undergo such malignant transformation are at best speculative.4 The racial differences in the disease, the increased risk of developing MM with certain human leukocyte antigen

(HLA) types, and the clustering of MM in certain families suggest that genetic susceptibility may predispose certain populations to develop MM. In this chapter, the biological, environmental, chemical, and familial factors and their contributions to the pathogenesis of MM are discussed.

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