by Wolfgang Warsch, Christoph Walz, and Veronika Sexl

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by Wolfgang Warsch, Christoph Walz, and Veronika Sexl JAK of all trades: JAK2-STAT5 as novel therapeutic targets in BCR-ABL1+ chronic myeloid leukemia by Wolfgang Warsch, Christoph Walz, and Veronika Sexl Blood Volume 122(13):2167-2175 September 26, 2013 ©2013 by American Society of Hematology

The BCR-ABL1-JAK2-PP2A network. The BCR-ABL1-JAK2-PP2A network. The scheme depicts how the BCR-ABL1-JAK2–mediated up-regulation of the phosphatase SET helps to maintain BCR-ABL1 activity, BCL2 expression, and MYC stability. Wolfgang Warsch et al. Blood 2013;122:2167-2175 ©2013 by American Society of Hematology

CML progenitor cell treatment with BCR-ABL1 TKIs leads to an abrogation of STAT5 signaling essential for survival and proliferation of the cell. CML progenitor cell treatment with BCR-ABL1 TKIs leads to an abrogation of STAT5 signaling essential for survival and proliferation of the cell. Wolfgang Warsch et al. Blood 2013;122:2167-2175 ©2013 by American Society of Hematology

Leukemic stem cell. Leukemic stem cell. The presence of a cytokine-enriched microenvironment leads to a BCR-ABL1–independent activation of STAT3 and STAT5 via JAK2. Targeting both pathways via BCR-ABL1 and JAK2 TKIs would interfere with these essential survival signals. Wolfgang Warsch et al. Blood 2013;122:2167-2175 ©2013 by American Society of Hematology