Abstract

Multiple Myeloma (MM) is a progressive and debilitating B-cell disorder typified by the accumulation and dissemination of malignant plasma cells in the bone marrow which subsequently induce osteolytic lesions.Despite recent advancement of new therapies for MM, patients ultimately develop drug resistanceand succumb to the disease. This highlights the need to increase our understanding of the disease and to identify new myeloma targets for drug development.

Highlights

  • Multiple Myeloma (MM) is a progressive and debilitating B-cell disorder typified by the accumulation and dissemination of malignant plasma cells in the bone marrow which subsequently induce osteolytic lesions [1]

  • Evidence for the MET receptor signaling pathway being an important contributor to the pathogenesis of this disease has been mounting. Both MET and its ligand, hepatocyte growth factor (HGF), are expressed in an autocrine loop in most myeloma cell lines and primary patient samples, as discerned at both the mRNA and protein level [7,8,9,10]. This is compounded by the high expression of the proteoglycan, syndecan 1 (CD138), on plasma cells as it binds HGF and boosts HGF-mediated signaling [11,12]

  • HGF levels are increased in patients with extensive bone lesions, and correlates with increases in cytokines, interleukin-6 (IL-6) and tumor necrosis factor-alpha, involved in osteoclast stimulation [24]

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Summary

Introduction

Multiple Myeloma (MM) is a progressive and debilitating B-cell disorder typified by the accumulation and dissemination of malignant plasma cells in the bone marrow which subsequently induce osteolytic lesions [1]. The growth and progression of myeloma is multifaceted and signaling through several cytokine/receptor pathways have been shown to be vital for the pathobiology of this disease [3,4,5,6]. Both MET and its ligand, hepatocyte growth factor (HGF), are expressed in an autocrine loop in most myeloma cell lines and primary patient samples, as discerned at both the mRNA and protein level [7,8,9,10].

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