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Wnt/β‐catenin‐pathway as a molecular target for future anti‐cancer therapeutics
Author(s) -
Dihlmann Susanne,
von Knebel Doeberitz Magnus
Publication year - 2004
Publication title -
international journal of cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.475
H-Index - 234
eISSN - 1097-0215
pISSN - 0020-7136
DOI - 10.1002/ijc.20609
Subject(s) - wnt signaling pathway , transactivation , colorectal cancer , cancer , cancer research , beta catenin , catenin , signal transduction , medicine , biology , bioinformatics , gene , transcription factor , microbiology and biotechnology , genetics
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/β‐catenin signaling pathway that results in constitutive β‐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/β‐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.