Download Acute Promyelocytic Leukemia: Molecular Genetics, Mouse by Pier Paolo Pandolfi (Editor), Peter K. Vogt (Editor) PDF

By Pier Paolo Pandolfi (Editor), Peter K. Vogt (Editor)

Over the last 10 years, paintings on acute promyelocytic leukemia (APL) has develop into the paradigm of translational learn that begun with the invention of a recurrent chromosomal translocation, via the id of the genes and proteins concerned, discovering their molecular capabilities in transcriptional keep an eye on, constructing mouse versions and culminating within the improvement  of specific treatment.

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Extra info for Acute Promyelocytic Leukemia: Molecular Genetics, Mouse Models and Targeted Therapy (Current Topics in Microbiology and Immunology 313)

Example text

PLZF has traditionally been thought of as a nuclear protein, as befits a transcription factor, and in fact it is localized to the nucleus [46, 67] in the distinct nuclear speckled pattern described earlier. The speckled distribution is dependent on the presence of the BTB domain [16]. The identity and function of the PLZF speckle is as yet unclear, with some data suggesting that PLZF at least partially colocalizes with PML in PML nuclear bodies [42], while other data suggest that the two proteins are in adjacent but different structures in the nucleus [68].

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.

Although SU11657 had limited effect as a single agent, the combination of SU11657 plus ATRA rapidly restored normal hematopoiesis in the bone marrow and resulted in a marked reduction in splenic involvement by the leukemic cells. A number of FLT3 inhibitors are under study in human clinical trials (Krause and Van Etten 2005). Cyclic adenosine monophosphate (cAMP) has growth suppressive and differentiative effects on myeloid leukemia cells. A RA-resistant leukemia that arose in an MRP8 PML-RARAm4 transgenic mouse was examined in engrafted histocompatible recipients (Guillemin et al.

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