[Molecular pathogenesis of myeloma for the therapeutic targets].
Multiple myeloma(MM) is a neoplasia of plasma cells in bone marrow. High dose chemotherapy followed by stem cell transplantation and new drugs such as thalidomide and bortezomib have improved the survival in MM. However, most of patients with myeloma are incurable so there is a need for the new therapeutic approaches that have been developed against molecular targets and pathway. It has been reported that activation of NF-kappaB pathway was required to survival of myeloma cells and this pathway was the potential target for anti -MM therapy. Recently we reported diverse genetic aberrations that activated NF-kappaB signaling in MM. In this section, the molecular pathogenesis of myeloma, especially the new findings related with NF-kappaB activation, will be reviewed in Japanese.
Hanamura
Ichiro
I
Department of Hematology, Division of Internal Medicine, Aichi Medical University.
D015894:Genome, Human / Q000235:genetics; D006801:Humans; D009101:Multiple Myeloma / Q000235:genetics* / Q000628:therapy*; D009154:Mutation; D016328:NF-kappa B / Q000235:genetics* / Q000276:immunology / Q000502:physiology*; D017346:Protein Serine-Threonine Kinases / Q000235:genetics / Q000502:physiology; D015398:Signal Transduction / Q000235:genetics / Q000502:physiology; D048008:TNF Receptor-Associated Factor 3 / Q000235:genetics / Q000502:physiology; D000097782:NF-kappaB-Inducing Kinase
D016328:NF-kappa B; D017346:Protein Serine-Threonine Kinases; D048008:TNF Receptor-Associated Factor 3; D000097782:NF-kappaB-Inducing Kinase