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Interplay between Notch Signaling and Epigenetic Silencers in Cancer

Instituto de Neurociencias, Consejo Superior de Investigaciones Cientificas-Universidad Miguel Hernández, Campus de Sant Joan, Alicante, Spain

Requests for reprints: Maria Dominguez, Instituto de Neurociencias, Consejo Superior de Investigaciones Cientificas-Universidad Miguel Hernández, Campus de Sant Joan, Apto. 18, 03550 Alicante, Spain. Phone: 34-96591-9390; Fax: 34-96591-9561; E-mail: m.dominguez{at}umh.es.

Given its role in the development and self-renewal of many tissues, it is not surprising that a prominent role has recently been proposed for the Notch signal transduction pathway in tumor development. However, exactly how Notch hyperactivation promotes oncogenesis is poorly understood. Recent findings in Drosophila melanogaster have linked the Notch pathway to epigenetic silencing and the tumor suppressor gene Rb during tumorigenesis. Because aberrant epigenetic gene silencing contributes to the pathogenesis of most human cancers, these findings may provide a new focal point to understand how Notch is associated with cancers, and to help develop better selective cancer therapies. (Cancer Res 2006; 66(18): 8931-4)