By T. Haferlach, C. Schoch, W. Hiddemann (auth.), Prof. Dr. med. Wolfgang Hiddemann, Prof. Dr. Dr. med. phil. Torsten Haferlach, Dr. med. Michael Unterhalt, Prof. Dr. med. Thomas Büchner, Prof. Dr. med. Jörg Ritter (eds.)
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Extra info for Acute Leukemias IX: Basic Research, Experimental Approaches and Novel Therapies
AML-l binds the canonical DNA sequence TGT/cGGT in concert with core binding factor ~ to activate or repress transcription. The chromosomal translocation fusion proteins that disrupt this heterodimeric transcription factor create constitutive repressors. Our work has focused on defining the molecular mechanism of transcriptional regulation by these cancer-associated fusion proteins. We have found that the t(8;21) fusion protein makes multiple contacts with the mSin3A and NCoR co-repressors. In addition, the fusion protein also contacts histone deacetylases 1, 2, and 3 independent of the co-repressors.
1999) Patterns of care and survival for adolescents and young adults with Acute leukaemia - a populationbased study. ) et al. (2000) Incidence of Cancer in the Netherlands 1996. Utrecht: Vereniging van Integrale Kankercentra 9 Philadelphia Chromosome-Positive Mature B-cell (Burkitt cell) Leukemia G. MANN, O. A. HAAS, E. R. GRUMAYER-PANZER, M. N. DWORZAK, M. M. TREBo, and H. , 1995). , 1997). Its occurrence is not only a therapeutic challenge but also gives room to speculations about multi-step leukemiogenesis.
9% of the cases the preliminary diagnosis of AL turned out to be incorrect. 5% of the cases the diagnosis has been principally changed (preliminary diagnosis of ALL has been replaced by one of AML variants or even AL-unrelated diseases have been revealed). In 50% of all cases being referred to the Reference Laboratory the diagnosis has been defined more exactly, namely T- or non-T-cell variants of ALL or one of AML variants (MI-M7) have been delineated on the basis of the analysis of cytochemical characteristics.