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本帖最后由 细胞海洋 于 2010-12-20 17:56 编辑 6 R" l; H% o3 _3 ]9 r& S& |
3 l n( `+ n6 O# q主题：通过抑制Wnt、Notch和Hedgehog途径靶向攻击癌症干细胞
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3 S4 y6 G0 _( a' A1 O1 v说明：原文来源自Nature Reviews Clinical Oncology，由干细胞之家新闻小组成员deron翻译（转帖请注明）9 q" B. w D3 x' b" [
$ _" U" O; L, | P翻译内容：肿瘤复发与转移依然是肿瘤患者总的生存的主要障碍，这至少可以部分归咎于肿瘤干细胞（CSC）的存在。CSCs具有致瘤性和自我更新的能力，形成分化的子细胞以对抗外界的肿瘤治疗。CSCs利用很多与正常干细胞相同的信号途径——比如Wnt、Notch和Hh。CSCs的起源仍没有完全了解，但是数据显示它们起源于正常干细胞或者祖细胞，或者可能是其它癌细胞。对CSCs和主体肿瘤群的靶向治疗可能提供了一种抑制肿瘤再生的策略。信号交互作用复杂化了Wnt、Notch和Hh途径中靶向性关键步骤的能因发展。这篇综述概括了CSCs功能中胚胎信号途径的作用、新的抗CSC治疗动因的发展以及潜在的CSC信号交互的复杂作用。6 g, m% R2 v; A$ U3 Y
原摘要：Tumor relapse and metastasis remain major obstacles for improving overall cancer survival, which may be due at least in part to the existence of cancer stem cells (CSCs). CSCs are characterized by tumorigenic properties and the ability to self-renew, form differentiated progeny, and develop resistance to therapy. CSCs use many of the same signaling pathways that are found in normal stem cells, such as Wnt, Notch, and Hedgehog (Hh). The origin of CSCs is not fully understood, but data suggest that they originate from normal stem or progenitor cells, or possibly other cancer cells. Therapeutic targeting of both CSCs and bulk tumor populations may provide a strategy to suppress tumor regrowth. Development of agents that target critical steps in the Wnt, Notch, and Hh pathways will be complicated by signaling cross-talk. The role that embryonic signaling pathways play in the function of CSCs, the development of new anti-CSC therapeutic agents, and the complexity of potential CSC signaling cross-talk are described in this Review.6 J o; E0 a+ Z% B& w5 O3 r$ V0 l
B4 l% x4 H2 X' n原文：抱歉无法提供全文，只有摘要链接。 http://www.nature.com/nrclinonc/ ... inonc.2010.196.html* r @. P% k9 I0 q- e' u
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说明：因没有接触过信号通路方面，所以这次翻译得实在是心里没底，希望大家指正文中的不妥之处。尤其“signaling cross-talk”，不知译成“信号交互作用”是否妥帖。 |
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发表于 2010-12-18 12:15
发表于 2010-12-20 14:24
发表于 2010-12-20 15:41
