Several genetic mechanisms underlying the pathogenesis of multiple myeloma have been
elucidated in the past decade. In particular, the presence of two distinct karyotypic
patterns, that identify two patient groups and drive different pathogenetic and prognostic
paths in the development of myeloma, have been identified, and the role of reciprocal
chromosomal translocations and cyclin dysregulation have been identified. Despite
this progress, several questions of critical importance remain to be addressed for
the understanding of the pathogenesis of multiple myeloma. For example, little is
known about the role of the primary events, including cyclin D overexpression and
multiple myeloma set domain activity in the early pathogenesis of the disease. The
additional lesions that promote the evolution of monoclonal gammopathy of undetermined
significance to multiple myeloma (MM) and, within MM, the progression toward a more
aggressive and proliferative disease is only starting to emerge. The heterotypic relationship
between the stroma and the MM plasma cells also has not been fully explored. The understanding
of the biology of MM cancer stem cells and of the pathways driving their maintenance,
proliferation, and differentiation is still in its infancy. Recent and ongoing high-resolution
genomic studies are leading the way toward a more refined and conclusive understanding
of this disease.
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Article info
Footnotes
This work was supported by the International Myeloma Foundation (Brian D. Novis Research Award) and by the Fund to Cure Myeloma. Giovanni Tonon is a Special Fellow of the Leukemia and Lymphoma Society.
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© 2007 Elsevier Inc. Published by Elsevier Inc. All rights reserved.
