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癌症中的融合:非整倍体、转移形成和耐药性的解释模型。

Fusion in cancer: an explanatory model for aneuploidy, metastasis formation, and drug resistance.

作者信息

Mohr Marieke, Zaenker Kurt S, Dittmar Thomas

机构信息

Institute of Immunology and Experimental Oncology, Centre for Biomedical Education and Research, University of Witten/Herdecke, Stockumer Str. 10, 58448, Witten, Germany,

出版信息

Methods Mol Biol. 2015;1313:21-40. doi: 10.1007/978-1-4939-2703-6_2.

DOI:10.1007/978-1-4939-2703-6_2
PMID:25947654
Abstract

Aneuploidy, metastasis formation, and drug resistance are major issues to overcome in most cancers. If there exists common underlying proceedings for the formation of these phenomena is still unknown. The searching and thereby better understanding of causal mechanisms could promote the generation of drugs targeting the ultimate cause of these cancer promoting events. The merging of a cancer cell with another cancer cell or normal cell could be one explanation how cancer cells could gain advantageous properties and escape eliminating cell fates thereby foster cancer progression. This chapter summarizes how cell-cell fusion could directly be involved in the pathogenesis of cancer and which often cancer associated mechanisms, like viral infections or chronic inflammation, are hitherto proposed to trigger cell fusion in cancer context.

摘要

非整倍体、转移形成和耐药性是大多数癌症中需要克服的主要问题。这些现象的形成是否存在共同的潜在过程仍然未知。寻找并更好地理解其因果机制可能会促进针对这些癌症促进事件根本原因的药物研发。癌细胞与另一个癌细胞或正常细胞的融合可能是癌细胞如何获得有利特性并逃避消除细胞命运从而促进癌症进展的一种解释。本章总结了细胞间融合如何直接参与癌症的发病机制,以及迄今为止提出的哪些与癌症相关的机制,如病毒感染或慢性炎症,在癌症背景下触发细胞融合。

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