Journal article
Therapeutic inhibition of jak activity inhibits progression of gastrointestinal tumors in mice
E Stuart, M Buchert, T Putoczki, S Thiem, R Farid, J Elzer, D Huszar, PM Waring, TJ Phesse, M Ernst
Molecular Cancer Therapeutics | AMER ASSOC CANCER RESEARCH | Published : 2014
Abstract
Aberrant activation of the latent transcription factor STAT3 and its downstream targets is a common feature of epithelial-derived human cancers, including those of the gastrointestinal tract. Mouse models of gastrointestinal malignancy implicate Stat3 as a key mediator of inflammatory-driven tumorigenesis, in which its cytokine/gp130/Janus kinase (Jak)-dependent activation provides a functional link through which the microenvironment sustains tumor promotion. Although therapeutic targeting of STAT3 is highly desirable, such molecules are not available for immediate clinical assessment. Here, we investigated whether the smallmolecule Jak1/2 inhibitor AZD1480 confers therapeutic benefits in tw..
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Awarded by NHMRC
Funding Acknowledgements
This work was generously supported by the Ludwig Institute for Cancer Research, the Victorian State Government Operational Infrastructure Support, the Independent Research Institutes Infrastructure Support Scheme of the National Health and Medical Research Council Australia (NHMRC), and NHMRC grants #487922 (to M. Ernst and M. Buchert), #433617 (to M. Ernst), #603122 (to M. Ernst), and #603127 (to T.J. Phesse and M. Buchert). M. Ernst is a NHMRC Senior Research Fellow (#331004).