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Turk J Haematol. 2022 Dec 1;39(4):245-253. doi: 10.4274/tjh.galenos.2022.2022.0046. Epub 2022 Aug 15.
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Blocking glycine utilization inhibits multiple myeloma progression by disrupting glutathione balance.阻断甘氨酸利用通过破坏谷胱甘肽平衡来抑制多发性骨髓瘤的进展。
Nat Commun. 2022 Jul 11;13(1):4007. doi: 10.1038/s41467-022-31248-w.
3
Armored BCMA CAR T Cells Eliminate Multiple Myeloma and Are Resistant to the Suppressive Effects of TGF-β.装甲 BCMA CAR T 细胞能消除多发性骨髓瘤,并能抵抗 TGF-β的抑制作用。
Front Immunol. 2022 Feb 9;13:832645. doi: 10.3389/fimmu.2022.832645. eCollection 2022.
4
Deciphering spatial genomic heterogeneity at a single cell resolution in multiple myeloma.在单细胞分辨率下解析多发性骨髓瘤中的空间基因组异质性。
Nat Commun. 2022 Feb 10;13(1):807. doi: 10.1038/s41467-022-28266-z.
5
The Exosomes Containing LINC00461 Originated from Multiple Myeloma Inhibit the Osteoblast Differentiation of Bone Mesenchymal Stem Cells via Sponging miR-324-3p.外泌体来源的 LINC00461 通过海绵吸附 miR-324-3p 抑制骨髓间充质干细胞成骨分化。
J Healthc Eng. 2022 Jan 25;2022:3282860. doi: 10.1155/2022/3282860. eCollection 2022.
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Pharmacol Res. 2021 Dec;174:105967. doi: 10.1016/j.phrs.2021.105967. Epub 2021 Nov 3.
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DKK1 activates noncanonical NF-κB signaling via IL-6-induced CKAP4 receptor in multiple myeloma.DKK1 通过 IL-6 诱导的 CKAP4 受体激活多发性骨髓瘤中的非经典 NF-κB 信号通路。
Blood Adv. 2021 Sep 28;5(18):3656-3667. doi: 10.1182/bloodadvances.2021004315.
8
Elevation of miR-302b prevents multiple myeloma cell growth and bone destruction by blocking DKK1 secretion.miR-302b水平升高通过阻断DKK1分泌来抑制多发性骨髓瘤细胞生长和骨质破坏。
Cancer Cell Int. 2021 Mar 31;21(1):187. doi: 10.1186/s12935-021-01887-y.
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Characterization and Function of Tumor Necrosis Factor and Interleukin-6-Induced Osteoclasts in Rheumatoid Arthritis.肿瘤坏死因子和白细胞介素 6 诱导的破骨细胞在类风湿关节炎中的特征和功能。
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10
Hypoxia-induced CREB cooperates MMSET to modify chromatin and promote DKK1 expression in multiple myeloma.缺氧诱导的CREB与MMSET协同作用,修饰染色质并促进多发性骨髓瘤中DKK1的表达。
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多发性骨髓瘤骨病发病机制的研究进展。

Advances in the pathogenesis of multiple myeloma bone disease.

机构信息

Institute of Oncology, School of Basic Medicine, Central South University, Changsha 410078, China.

出版信息

Zhong Nan Da Xue Xue Bao Yi Xue Ban. 2023;48(9):1403-1410. doi: 10.11817/j.issn.1672-7347.2023.220534.

DOI:10.11817/j.issn.1672-7347.2023.220534
PMID:38044652
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10929876/
Abstract

Multiple myeloma (MM) is a clonal proliferative malignant tumor of plasma cells in bone marrow. With the aging of population in China, the incidence of MM is on the rise. Multiple myeloma bone disease (MBD) is one of the common clinical manifestations of MM, and 80%-90% of MM patients are accompanied by osteolytic lesions at the time of their first visit to the clinic. MBD not only increases the disability rate of patients, but also severely reduces the physical function of patients due to skeletal lesions and bone-related events. Currently available drugs for treating of MBD are ineffective and associated with side effects. Therefore, it is important to find new therapeutic approaches for the treatment of MBD. It is generally believed that the increased osteoclast activity and suppressed osteoblast function are the main pathologic mechanisms for MBD. However, more and more studies have suggested that soluble molecules in the bone marrow microenvironment, including cytokines, extracellular bodies, and metabolites, play an important role in the development of MBD. Therefore, exploring the occurrence and potential molecular mechanisms for MBD from multiple perspectives, and identifying the predictive biomarkers and potential therapeutic targets are of significance for the clinical treatment of MBD.

摘要

多发性骨髓瘤(MM)是骨髓中浆细胞的克隆性增生性恶性肿瘤。随着中国人口老龄化,MM 的发病率呈上升趋势。多发性骨髓瘤骨病(MBD)是 MM 的常见临床表现之一,80%-90%的 MM 患者在首次就诊时就伴有溶骨性病变。MBD 不仅增加了患者的残疾率,还因骨骼病变和与骨骼相关的事件严重降低了患者的身体功能。目前用于治疗 MBD 的药物疗效不佳且存在副作用。因此,寻找治疗 MBD 的新治疗方法很重要。一般认为,破骨细胞活性增加和成骨细胞功能受抑制是 MBD 的主要病理机制。然而,越来越多的研究表明,骨髓微环境中的可溶性分子,包括细胞因子、细胞外体和代谢物,在 MBD 的发展中起重要作用。因此,从多个角度探讨 MBD 的发生及潜在分子机制,鉴定预测生物标志物和潜在治疗靶点,对于 MBD 的临床治疗具有重要意义。