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首页> 外文期刊>Seminars in cancer biology >Adhesion molecules--The lifelines of multiple myeloma cells.
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Adhesion molecules--The lifelines of multiple myeloma cells.

机译：粘附分子-多发性骨髓瘤细胞的生命线。

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Multiple myeloma is an incurable hematological malignancy of terminally differentiated immunoglobulin-producing plasma cells. As a common presentation of the disease, the malignant plasma cells accumulate and proliferate in the bone marrow, where they disrupt normal hematopoiesis and bone physiology. Multiple myeloma cells and the bone marrow microenvironment are linked by a composite network of interactions mediated by soluble factors and adhesion molecules. Integrins and syndecan-1/CD138 are the principal multiple myeloma receptor systems of extracellular matrix components, as well as of surface molecules of stromal cells. CD44 and RHAMM are the major hyaluronan receptors of multiple myeloma cells. The SDF-1/CXCR4 axis is a key factor in the homing of multiple myeloma cells to the bone marrow. The levels of expression and activity of these adhesion molecules are controlled by cytoplasmic operating mechanisms, as well as by extracellular factors including enzymes, growth factors and microenvironmental conditions. Several signaling responses are activated by adhesive interactions of multiple myeloma cells, and their outcomes affect the survival, proliferation and migration of these cells, and in many cases generate a drug-resistant phenotype. Hence, the adhesion systems of multiple myeloma cells are attractive potential therapeutic targets. Several approaches are being developed to disrupt the activities of adhesion molecules in multiple myeloma cells, including small antagonist molecules, direct targeting by immunoconjugates, stimulation of immune responses against these molecules, and signal transduction inhibitors. These potential novel therapeutics may be incorporated into current treatment schemes, or directed against minimal residual malignant cells during remission.
机译：多发性骨髓瘤是终末分化的产生免疫球蛋白的浆细胞的不可治愈的血液系统恶性肿瘤。作为该疾病的常见表现，恶性浆细胞在骨髓中积累和增殖，在骨髓中它们破坏正常的造血功能和骨骼生理。多发性骨髓瘤细胞和骨髓微环境通过可溶性因子和粘附分子介导的相互作用的复合网络相连。整联蛋白和syndecan-1 / CD138是细胞外基质成分以及基质细胞表面分子的主要多发性骨髓瘤受体系统。 CD44和RHAMM是多发性骨髓瘤细胞的主要透明质酸受体。 SDF-1 / CXCR4轴是将多发性骨髓瘤细胞归巢至骨髓的关键因素。这些粘附分子的表达和活性水平受细胞质操作机制以及细胞外因子（包括酶，生长因子和微环境条件）的控制。多发性骨髓瘤细胞的粘附相互作用激活了几种信号反应，它们的结果影响这些细胞的存活，增殖和迁移，并在许多情况下产生耐药表型。因此，多发性骨髓瘤细胞的粘附系统是有吸引力的潜在治疗靶标。正在开发几种方法来破坏多发性骨髓瘤细胞中粘附分子的活性，包括小的拮抗剂分子，通过免疫缀合物直接靶向，刺激针对这些分子的免疫应答以及信号转导抑制剂。这些潜在的新型疗法可被纳入当前的治疗方案，或针对缓解期间残留的最小恶性细胞。

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