Chemotherapy-induced metastasis: mechanisms and translational opportunities.

Chemotherapy-induced metastasis: mechanisms and translational opportunities.
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DOI:
10.1007/s10585-017-9870-x
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发表时间:
2018-04
影响因子:
4
通讯作者:
Oktay MH
Oktay MH
中科院分区:
医学3区
文献类型:
--
作者:
Karagiannis GS;Condeelis JS;Oktay MH

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肿瘤通常通过获得性或环境介导的耐药性来克服化疗的细胞毒效应。此外,来自微环境的信号混淆了化疗的有益效果,并可能促进进展和转移。在化疗诱导的转移中,精液介质似乎是一系列来自骨髓的造血祖细胞、间充质细胞和免疫祖细胞。这些细胞的实际用途是协调对化疗的细胞毒性损伤的修复反应。然而,这些修复反应在转移级联的每一步都被肿瘤细胞利用,从肿瘤细胞的侵袭、血管内和血源性扩散到转移部位的外渗和有效定植。更好地了解化疗诱导转移的机制基础将使我们能够更好地预测哪些患者更有可能对化疗表现出促转移反应,并将有助于开发新的治疗策略来中和化疗引起的促转移改变。
Tumors often overcome the cytotoxic effects of chemotherapy through either acquired or environment-mediated drug resistance. In addition, signals from the microenvironment obfuscate the beneficial effects of chemotherapy and may facilitate progression and metastatic dissemination. Seminal mediators in chemotherapy-induced metastasis appear to be a wide range of hematopoietic, mesenchymal and immune progenitor cells, originating from the bone marrow. The actual purpose of these cells is to orchestrate the repair response to the cytotoxic damage of chemotherapy. However, these repair responses are exploited by tumor cells at every step of the metastatic cascade, ranging from tumor cell invasion, intravasation and hematogenous dissemination to extravasation and effective colonization at the metastatic site. A better understanding of the mechanistic underpinnings of chemotherapy-induced metastasis will allow us to better predict which patients are more likely to exhibit pro-metastatic responses to chemotherapy and will help develop new therapeutic strategies to neutralize chemotherapy-driven prometastatic changes.
替代性的11A序列改变了MENA对肌动蛋白细胞骨架组织和细胞行为的影响。
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