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Mouse Models To Determine The Cause Of Aggressive Leukemia

rface of lymphocytes, which triggers the activity of the JAK kinases. This later stimulates cell growth through a signaling pathway that operates alongside the one controlled by the Bcr-Abl kinase. The investigators used a chemical inhibitor of JAK kinases to block the effect of IL-7 on leukemic cells in culture which restored the ALL cells’ sensitivity to imatinib. In conclusion the team said that the study has provided unexpected insights into how factors in the mice and potentially in humans might contribute to imatinib resistance.
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