Thursday, October 18, 2012
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Mouse studies suggest
suppressing NOTCH1 signaling could help
treat intrahepatic cholangiocarcinomas (ICCs). In mice with labeled
hepatocytes and chondrocytes, chemically induced ICC was traced to biliary
lineage cells that were derived from hepatocytes rather than from
chondrocytes. In mice, expression of a constitutively active Notch1 fragment
in hepatocytes increased hepatocyte conversion to biliary lineage cells and
malignant progression of ICC compared with no expression of the Notch1
fragment. In a separate study, overexpression of the NOTCH1 receptor
intracellular domain in the livers of wild-type mice and delivery of a protein
kinase B (PKB;
vector resulted in tumors with ICC features. Fluorescence labeling showed
that hepatocytes formed biliary lineage cells and ultimately differentiated
into the tumors. Next steps include determining whether NOTCH
inhibitors could suppress conversion of hepatocytes to biliary lineage cells.
Therapeutics Inc. has a stapled peptide NOTCH1 inhibitor in
preclinical testing to treat acute lymphoblastic leukemia (ALL).
Pharmaceuticals Inc.'s AV-232,
a mAb targeting NOTCH1, is in preclinical testing to treat cancer.
Pharmaceuticals Inc.'s OMP-52M51,
an anti-NOTCH1 antibody, is in preclinical testing to treat solid tumors.
SciBX 5(41); doi:10.1038/scibx.2012.1079
Published online Oct. 18, 2012
Findings in first study
unpatented; unavailable for licensing
Patent and licensing status unavailable for findings in second study
Sekiya, S. & Suzuki, A.
J. Clin. Invest.; published online Oct. 1, 2012;
Contact: Atsushi Suzuki, Kyushu University, Fukuoka, Japan
Fan, B. et. al. J. Clin. Invest.; published online July 17, 2012;
Contact: Holger Willenbring, University of California, San
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