Indication

Target/marker/pathway

Summary

Licensing status

Publication and contact information

Cancer

Cancer

b-Catenin (CTNNB1); B cell CLL lymphoma 9 (BCL9); wingless-type MMTV integration site (WNT)

Mouse studies suggest disrupting the interaction between CTNNB1 and the WNT pathway coactivator BCL9 could help treat WNT-driven cancers. The stapled peptide SAH-BCL9 was generated by incorporating a stabilizing hydrocarbon staple into a peptide derived from the helical domain of BCL9 that interacts with CTNNB1. In xenograft mouse models of WNT-driven colorectal cancer and multiple myeloma (MM), SAH-BCL9 decreased tumor angiogenesis and primary or metastatic tumor burden compared with a control peptide. Next steps include determining the range of cancer subtypes driven by the BCL9-CTNNB1 interaction.

SciBX 5(37); doi:10.1038/scibx.2012.977
Published online Sept. 20, 2012

Patent application filed; available for licensing

Takada, K. et al. Sci. Transl. Med.; published online Aug. 22, 2012;
doi:10.1126/scitranslmed.3003808
Contact: Daniel Ruben Carrasco,
Dana-Farber Cancer Institute, Boston, Mass.
e-mail:
ruben_carrasco@dfci.harvard.edu
Contact: Loren D. Walensky,
same affiliation as above
e-mail:
loren_walensky@dfci.harvard.edu