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Chronic myelogenous leukemia (CML)

IL-1 receptor-like 1 (IL1RL1; ST2); IL-33 (NF-HEV)

Mouse and cell culture studies suggest inhibiting IL-33 signaling could help treat Gleevec imatinib-resistant CML. CD34+ cells from patients with CML had surface expression of ST2 and greater proliferation in response to IL-33 than CD34+ cells from healthy subjects. IL-33 is an activating ligand for ST2. In patient-isolated CD34+ cells, IL-33 blocked the effect of Gleevec on proliferation. Next steps could include evaluating IL-33 inhibitors in combination with Gleevec in models of Gleevec-resistant CML.
Novartis AG markets Gleevec, a BCR-ABL tyrosine kinase inhibitor, to treat CML, acute lymphoblastic leukemia (ALL) and gastrointestinal stromal tumors (GISTs).
AnaptysBio Inc.'s ANB020, an anti-IL-33 antibody, is in discovery for various inflammatory conditions.

SciBX 7(17); doi:10.1038/scibx.2014.488
Published online May 1, 2014

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Levescot, A. et al. Cancer Res.; published online March 27, 2014;
Contact: Andre Herbelin, Institut National de la Santé et de la Recherche Médicale (INSERM), Poitiers, France