1. 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):
September 26, 2013
©2013 by American Society of Hematology

2. 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:
©2013 by American Society of Hematology

3. 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:
©2013 by American Society of Hematology

4. 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:
©2013 by American Society of Hematology