Thursday, November 7, 2013
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(CTNNB1); interferon regulatory factor 8
mouse studies suggest simultaneously increasing IRF8 expression and
inhibiting CTNNB1 could help treat CML. In Irf8-/- mice,
which develop CML, enhanced activation of Ctnnb1 caused disease progression
to fatal blast crisis. In a BCR-ABL tyrosine kinase mouse
model of CML, combined Irf8 knockout and Ctnnb1 activation increased Gleevec imatinib resistance
compared with wild-type Irf8 expression and normal Ctnnb1 activation.
Next steps include testing Gleevec in combination with Irf8 activation
and Ctnnb1 inhibition as a triple therapy at the initiation of blast crisis
in models of CML.
Novartis AG markets
Gleevec, a BCR-ABL tyrosine kinase inhibitor, to treat gastrointestinal
stromal tumors (GISTs), acute lymphoblastic leukemia (ALL) and CML.
Prism Pharma Co. Ltd. and Eisai Co. Ltd. have the
CTNNB1 inhibitor PRI-724 in Phase I/II
testing to treat CML and other cancers.
Marina Biotech Inc.'s CEQ508, an oral RNAi
targeting CTNNB1, is in Phase I/II testing to treat colorectal cancer.
Published online Nov. 7, 2013
Patent and licensing status
Scheller, M. et al. J.
Exp. Med.; published online Oct. 7, 2013;
Contact: Achim Leutz, Max Delbrueck Center for Molecular
Contact: Marina Scheller, same affiliation as above
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