The protein phosphatase 2A (PP2A) tumor suppressor is inactivated in different leukemias through the activity of its endogenous inhibitors (e.g., SET), which are aberrantly regulated by oncogenic tyrosine kinases. Like other effective and nontoxic PP2A-activating drugs (PAD), OP449 inhibits SET and impairs leukemogenesis. This further supports the immediate use of PADs in patients with leukemia.
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http://dx.doi.org/10.1158/1078-0432.CCR-14-0166 | DOI Listing |
Endocr Relat Cancer
October 2017
Division of EndocrinologyDiabetes and Bone Diseases, Department of Medicine, Icahn School of Medicine at Mount Sinai, New York, USA
Hyperinsulinemia is associated with a decrease in breast cancer recurrence-free survival and overall survival. Inhibition of insulin receptor signaling is associated with glycemic dysregulation. SET is a direct modulator of PP2A, which negatively regulates the PI3K/AKT/mTOR pathway.
View Article and Find Full Text PDFClin Cancer Res
April 2014
Authors' Affiliations: The Ohio State University Comprehensive Cancer Center, Columbus, Ohio; and Department of Medicine, The Greenebaum Cancer Center, University of Maryland School of Medicine, Baltimore, Maryland.
The protein phosphatase 2A (PP2A) tumor suppressor is inactivated in different leukemias through the activity of its endogenous inhibitors (e.g., SET), which are aberrantly regulated by oncogenic tyrosine kinases.
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