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Receptor-interacting serine-threonine kinase 4 (RIPK4; RIP4)

Studies in cell culture, mice and human tissue samples suggest inhibiting RIPK4 could help treat cancers driven by increased wingless-type MMTV integration site (WNT) signaling. In human cells, RIPK4 overexpression increased WNT signaling compared with no overexpression. In a xenograft mouse model for cancer with WNT pathway activation, RIPK4 depletion suppressed tumor growth. In patient tissue samples, RIPK4 mRNA was increased in some ovarian, skin and colorectal tumors compared with matched healthy tissue. Next steps include testing whether inhibiting RIPK4 would have efficacy in tumors with WNT pathway activation that lack downstream activating mutations.

SciBX 6(8); doi:10.1038/scibx.2013.189
Published online Feb. 28, 2013

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Huang, X. et al. Science; published online Jan. 31, 2013;
Contact: Vishva M. Dixit, Genentech Inc., South San Francisco, Calif.