Understanding multiple myeloma pathogenesis in the bone marrow to identify new therapeutic targets

By T. Hideshima, C. Mitsiades, G. Tonon, P. Richardson, K. Anderson. Nature Reviews. Cancer, 2007

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Heterogeneity of genomic evolution and mutational profiles in multiple myeloma (2014, positive): “These chromosomal abnormalities are, however, insufﬁcient for malignant transformation, as they are also observed in monoclonal gammopathy of unknown signiﬁcance, a premalignant syndrome that precedes virtually every MM case 2,3 .”
Targeting interleukin-6 in inflammatory autoimmune diseases and cancers. (2014, background): “Anti-IL-6 antibody inhibited the proliferation of myeloma cells in vitro and in vivo (Kishimoto et al., 1992; Hideshima et al., 2007).”
Lenalidomide after Stem-Cell Transplantation for Multiple Myeloma (2012, neutral): “Neutropenia 74 (32) 30 (13) 27 (12) 7 (3) <0.”
BET bromodomain inhibition as a therapeutic strategy to target c-Myc (2011, positive): “As interaction of MM cells with BMSCs is widely recognized to confer resistance to numerous therapeutic agents (Hideshima et al., 2007; McMillin et al., 2010), we sought to characterize the effect of BMSCs on MM cell sensitivity to BET inhibition.”