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 examine that started with the invention of a recurrent chromosomal translocation, by way of the id of the genes and proteins concerned, discovering their molecular features in transcriptional keep watch over, constructing mouse versions and culminating within the improvement of detailed treatment.
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Additional info for Acute Promyelocytic Leukemia: Molecular Genetics, Mouse Models and Targeted Therapy (Current Topics in Microbiology and Immunology 313)
J. McConnell · J. D. Licht PLZF-null mice do not exhibit an obvious hematopoietic phenotype, nor do they develop leukemia or other tumors. However, this does not rule out a role for PLZF in hematopoiesis. A second PLZF-like gene exists, which is expressed in a similar pattern during differentiation of hematopoietic progenitor cells. 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.
These ﬁndings also imply that PLZF and the related FAZF gene may be important for the proper control of growth and homeostasis of multiple tissues. Unresolved questions in regard to PLZF include its exact mode of repression, and key transcriptional targets and physiological stimuli that lead to its posttranslational modiﬁcation and subsequent regulation of transcriptional function. References 1. 2. 3. 4. 5. 6. Ball HJ, Melnick A, Shaknovich R, Kohanski RA, Licht JD (1999) The promyelocytic leukemia zinc ﬁnger (PLZF) protein binds DNA in a high molecular weight complex associated with cdc2 kinase.
Furthermore, animal models of APL are equally important for assessing ideas regarding the value of novel therapies. As we learn more about APL, added questions are raised. Among the areas that animal models will be used for in the coming years are: 1. Developing a better understanding of the cells from which relapses arise in APL and other AMLs. ) 2. Identifying the critical transcriptional targets repressed by X-RARα proteins. 3. Elucidating effects on PML and its interaction partners that facilitate leukemic transformation.
Acute Promyelocytic Leukemia: Molecular Genetics, Mouse Models and Targeted Therapy (Current Topics in Microbiology and Immunology 313) by Pier Paolo Pandolfi (Editor), Peter K. Vogt (Editor)