fig1

Drug targets and resistance mechanisms in multiple myeloma

Figure 1. Overview of the MM cell interaction with its microenvironment and overview of MM drug targets. Red dashed arrows show targets. Bone-marrow stromal cells support growth and survival of MM cells via various cytokines. MM cells secrete dikkopf homolog 1 (DKK1) which inhibits the differentiation of osteoblastic precursors. Bone marrow stromal cells induce angiogenesis through secretion of VEGF. OPG produced by bone marrow stromal cells and osteblasts inhibits osteoclasts. BAFF-receptor: human B-cell-activating factor receptor; Cdk: cycline dependent kinase; DKK1: Dickkopf-1; HDACi: histone deacetylase inhibitor; HGF: hepatocyte growth factor; IL-6: interleukin-6; IL-6R: IL-6 receptor; JAK: Janus kinase; IMiD: immunomodulatory imide drug; MTA: microtubules targeting agents; mTOR: mammalian target of rapamycin; NF-κB: nuclear factor-κB; OPG: osteoprotegerin; PI: proteasome inhibitor; RANKL: receptor activator of NF-kappaB ligand; STAT: signal transducer and activator of transcription; TNFα: tumor necrosis factor-alpha; VEGF: vascular endothelial growth factor; WNT: wingless pathway

Cancer Drug Resistance
ISSN 2578-532X (Online)

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