Cellular and Molecular Mediators of Bone Metastatic Lesions.

Cellular and Molecular Mediators of Bone Metastatic Lesions.
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DOI:
10.3390/ijms19061709
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发表时间:
2018-06-08
影响因子:
5.6
通讯作者:
Del Fattore A
Del Fattore A
中科院分区:
生物学2区
文献类型:
--
作者:
Battafarano G;Rossi M;Marampon F;Del Fattore A

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骨是乳腺和前列腺肿瘤的优先转移部位。癌细胞与宿主组织建立紧密的关系,分泌刺激或抑制骨细胞的因子,接收骨重塑活动产生的信号,并显示骨细胞的一些特征。肿瘤和骨细胞之间的这种相互作用改变了生理性骨重塑,导致产生促进骨转移生长的恶性循环。为了预防与骨转移相关的骨骼相关事件(SRE),报道了抑制破骨细胞骨吸收的方法。双膦酸盐和狄诺塞麦目前用于治疗骨病变患者。它们的作用是预防或抵消 SRE,包括病理性骨折、脊髓压迫和与骨转移相关的疼痛。然而,它们对肿瘤细胞的主要作用仍然存在争议。在这篇综述中,描述了导致骨转移发生的机制以及治疗骨转移的临床方法。
Bone is the preferential site of metastasis for breast and prostate tumor. Cancer cells establish a tight relationship with the host tissue, secreting factors that stimulate or inhibit bone cells, receiving signals generated from the bone remodeling activity, and displaying some features of bone cells. This interplay between tumor and bone cells alters the physiological bone remodeling, leading to the generation of a vicious cycle that promotes bone metastasis growth. To prevent the skeletal-related events (SRE) associated with bone metastasis, approaches to inhibit osteoclast bone resorption are reported. The bisphosphonates and Denosumab are currently used in the treatment of patients affected by bone lesions. They act to prevent or counteract the SRE, including pathologic fractures, spinal cord compression, and pain associated with bone metastasis. However, their primary effects on tumor cells still remain controversial. In this review, a description of the mechanisms leading to the onset of bone metastasis and clinical approaches to treat them are described.
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