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1 Children's Memorial Research Center, Cancer Biology and Epigenomics Program, Robert H. Lurie Comprehensive Cancer Center, Northwestern University Feinberg School of Medicine, Chicago, Illinois and 2 The Schulich School of Medicine, University of Western Ontario, London, Ontario, Canada
Requests for reprints: Mary J.C. Hendrix, Northwestern University Feinberg School of Medicine, 2300 Children's Plaza, Box 222, Chicago, IL 60614. Phone: 773-755-6528; Fax: 773-755-6534; E-mail: MJChendrix{at}childrensmemorial.org.
Aggressive tumor cells express a plastic, multipotent phenotype similar to embryonic stem cells. However, the absence of major regulatory checkpoints in these tumor cells allows aberrant activation of embryonic signaling pathways, which seems to contribute to their plastic phenotype. Emerging evidence showing the molecular cross-talk between two major stem cell signaling pathways Nodal and Notch suggests a promising therapeutic strategy that could target aggressive tumor cells on the basis of their unique plasticity, and provide new insights into the mechanisms underlying the re-emergence of developmental signaling pathways during tumor progression. [Cancer Res 2009;69(18):7131–4]
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Correction: Development and Cancer: At the Crossroads of Nodal and Notch Signaling Cancer Res., November 1, 2009; 69(21): 8526 - 8527. [Full Text] [PDF] |
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G. C. Prendergast Stromal Mutations and Notch/Nodal Signaling in Cancer Cancer Reviews Online Content, January 1, 2009; 2009(10): 19 - 19. [Full Text] [PDF] |
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