Advances in biology of multiple myeloma: clinical applications

DOI PDF 被引用文献8件
  • Teru Hideshima
    From the Jerome Lipper Multiple Myeloma Center, Department of Medical Oncology, Dana-Farber Cancer Institute and Harvard Medical School, Boston, MA; Weill Medical College of Cornell University, New York, NY; and the Genetics Branch, National Cancer Institute, Bethesda, MD.
  • P. Leif Bergsagel
    From the Jerome Lipper Multiple Myeloma Center, Department of Medical Oncology, Dana-Farber Cancer Institute and Harvard Medical School, Boston, MA; Weill Medical College of Cornell University, New York, NY; and the Genetics Branch, National Cancer Institute, Bethesda, MD.
  • W. Michael Kuehl
    From the Jerome Lipper Multiple Myeloma Center, Department of Medical Oncology, Dana-Farber Cancer Institute and Harvard Medical School, Boston, MA; Weill Medical College of Cornell University, New York, NY; and the Genetics Branch, National Cancer Institute, Bethesda, MD.
  • Kenneth C. Anderson
    From the Jerome Lipper Multiple Myeloma Center, Department of Medical Oncology, Dana-Farber Cancer Institute and Harvard Medical School, Boston, MA; Weill Medical College of Cornell University, New York, NY; and the Genetics Branch, National Cancer Institute, Bethesda, MD.

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<jats:title>Abstract</jats:title><jats:p>There appear to be 2 pathways involved in the early pathogenesis of premalignant monoclonal gammopathy of undetermined significance (MGUS) and malignant multiple myeloma (MM) tumors. Nearly half of these tumors are nonhyperdiploid and mostly have immunoglobulin H (IgH) translocations that involve 5 recurrent chromosomal loci, including 11q13 (cyclin D1), 6p21 (cyclin D3), 4p16 (fibroblast growth factor receptor 3 [FGFR3] and multiple myeloma SET domain [MMSET]), 16q23 (c-maf), and 20q11 (mafB). The remaining tumors are hyperdiploid and contain multiple trisomies involving chromosomes 3, 5, 7, 9, 11, 15, 19, and 21, but infrequently have IgH translocations involving the 5 recurrent loci. Dysregulated expression of cyclin D1, D2, or D3 appears to occur as an early event in virtually all of these tumors. This may render the cells more susceptible to proliferative stimuli, resulting in selective expansion as a result of interaction with bone marrow stromal cells that produce interleukin-6 (IL-6) and other cytokines. There are 5 proposed tumor groups, defined by IgH translocations and/or cyclin D expression, that appear to have differences in biologic properties, including interaction with stromal cells, prognosis, and response to specific therapies. Delineation of the mechanisms mediating MM cell proliferation, survival, and migration in the bone marrow (BM) microenvironment may both enhance understanding of pathogenesis and provide the framework for identification and validation of novel molecular targets.</jats:p>

収録刊行物

  • Blood

    Blood 104 (3), 607-618, 2004-08-01

    American Society of Hematology

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