Advances in the understanding of myeloma bone disease and tumour growth.
Advances in the understanding of myeloma bone disease and tumour growth.
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DOI：
10.1111/j.1365-2141.2010.08141.x
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发表时间：
2010-05
影响因子：
6.5
通讯作者：
Yaccoby S
中科院分区：
文献类型：
--
作者：
Yaccoby S
多发性骨髓瘤的进展支持了这样一种观点，即相关的骨疾病，其特征在于破骨细胞生成增加和成骨细胞生成抑制，既是肿瘤进展的结果，也是肿瘤进展的必然。成骨细胞生成受到成骨细胞上分泌的抑制剂和细胞表面“偶联”因子的失调的抑制。破骨细胞生成增加是成骨细胞失活和破骨细胞活化因子产生的结果。破骨细胞表达刺激骨髓瘤生长的可溶性和细胞表面因子，而成骨细胞产生抑制依赖于微环境的骨髓瘤细胞生长的成骨因子;详细的分子机制进行了讨论。实验和临床研究结果表明，有效促进骨形成的药理学和实验性成骨细胞活化剂也减少骨髓瘤细胞在骨内的生长，似乎是通过同时刺激成骨细胞生成和抑制破骨细胞生成。解开骨髓瘤骨病的机制扩展了开发新干预措施的视野，也有助于更好地理解骨质溶解诱导与疾病进展之间的关联。
Advances in multiple myeloma support the notion that the associated bone disease, characterized by increased osteoclastogenesis and suppressed osteoblastogenesis, is both a consequence and necessity of tumour progression. Osteoblastogenesis is suppressed by secreted inhibitors and dysregulation of cell-surface “coupling” factors on osteogenic cells. Osteoclastogenesis is increased as a consequence of osteoblast deactivation and of production of osteoclast-activating factors. Osteoclasts express soluble and cell-surface factors that stimulate myeloma growth, while osteoblasts produce bone-building factors that restrain growth of myeloma cells that are dependent on the microenvironment; detailed molecular mechanisms are discussed. Experimental and clinical findings indicate that pharmacological and experimental osteoblast-activating agents that effectively promote bone formation also reduce growth of myeloma cells within bone, seemingly by simultaneously stimulating osteoblastogenesis and restraining osteoclastogenesis. Unravelling mechanisms of myeloma bone disease expands horizons for developing novel interventions and also facilitates better understanding of the association between induction of osteolysis and disease progression.
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