Download Acute Promyelocytic Leukemia: Molecular Genetics, Mouse by P. P. Pandolfi (auth.), Pier Paolo Pandolfi MD, Ph.D., Peter PDF

By P. P. Pandolfi (auth.), Pier Paolo Pandolfi MD, Ph.D., Peter K. Vogt Ph.D. (eds.)

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1, suggesting that it arose by duplication of the PLZF-MLL locus at 11q23. The FAZF protein also has a BTB domain, and three Kruppel-like C2 H2 zinc fingers highly homologous to the final three DNA-binding zinc fingers of PLZF. It can heterodimerize with PLZF, and can bind the same DNA sequences as PLZF in vitro [30]. FAZF is found in a pattern of nuclear foci similar to the PLZF speckles, and forced expression in a U937 cell had the same suppression of growth and induction of apoptosis as PLZF [12].

8 Additional Investigational Therapies Other agents and combinations have been tested in mouse APL models. Abnormal tyrosine kinases are an attractive target for therapy of leukemias, as evidenced by the effect of imatinib on human chronic myelogenous leukemia. SU11657 is a tyrosine kinase inhibitor that inhibits a class of receptor tyrosine kinases including FLT3, PDGFR, KIT, VEGFR1, and VEGFR2. The effect of SU11657 on leukemias that arose in cells expressing MRP8 PML-RARA plus an activated FLT3 was assessed (Sohal et al.

Elucidating effects on PML and its interaction partners that facilitate leukemic transformation. 4. Delineating how events cooperate at a molecular level to block differentiation and deregulate proliferation and survival. 5. Extending differentiation therapy to other leukemias. Acknowledgements Thanks to Dr. Galit Rosen for Fig. 1 as well as Drs. Michael Bishop, Hugues de Thé, Jeffrey Lawrence, Frank McCormick, and Kevin Shannon for their continuing interest and support. Scott Kogan is a Scholar of the Leukemia and Lymphoma Society.

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