Wnt/β-catenin-pathway as a molecular target for future anti-cancer therapeutics

被引：164

作者：

Dihlmann, S ^{[1
]}

Doeberitz, MVK ^{[1
]}

机构：

[1] Heidelberg Univ, Inst Mol Pathol, D-69120 Heidelberg, Germany

来源：

INTERNATIONAL JOURNAL OF CANCER | 2005年 / 113卷 / 04期

关键词：

signaling; targeted therapy; pharmacologic inhibitor; NSAID; endostatin; proteasomal degradation; oncolytic virus;

D O I：

10.1002/ijc.20609

中图分类号：

R73 [肿瘤学];

学科分类号：

100214 ;

摘要：

Conventional chemotherapeutic drugs used for the treatment of cancer patients in advanced stages have yielded only limited benefit, regarding survival time not to mention cure of the patients. To improve the clinical outcome of cancer, agents aimed at novel molecular targets are required. Colorectal and many other cancers are caused by hyperactivity of the Wnt/beta-catenin signaling pathway that results in constitutive beta-catenin mediated transactivation of T cell factor (Tcf)-dependent genes. Accordingly, disruption of this signaling pathway holds promise for the development of new anti-cancer drugs. Our study describes recent therapeutic strategies to interfere with tumor growth by blocking the unrestricted activation of the Wnt/beta-catenin pathway. The antagonists, which may become lead compounds of new anticancer therapeutics include established drugs in new application areas, recombinant biomolecules, virus mediated selective cell killing, and small molecules, disrupting protein-protein interactions.

引用

页码：515 / 524

页数：10

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