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Additional resources for Acute Leukemias IX: Basic Research, Experimental Approaches and Novel Therapies
Et al. (1997). A complex containing N-CoR, mSin3 and histone deacetylase mediates transcriptional repression [see comments], Nature 387,43-8. Hiebert, S. , Davis, I. , Downing, I. , Roussell, M. E, Gilliland, D. , et al. (1996). The t(12;21) translocation converts AML-l B from an activator to a re- 24 pressor of transcription, Molecular & Cellular Bio· logy 16, 1349-55. , Bae, S. , and Ito, Y. (1998). Cytoplasmic sequestration of the polyomavirus enhancer binding protein 2 (PEBP2)/core binding factor alpha (CBFalpha) subunit by the leukemia- related PEBP2ICBFbeta-SMMHC fusion protein inhibits PEBP2/CBF-mediated transactivation, Mol Cell BioI 18, 4252-61.
Disturbed Differentiation of AMl1lETO Transduced Human (034+ Progenitors J. BASECKEt, CH. BAUM 2 , O. PFAHLERT l , G. BRITTINGERt, B. WORMANN3, and F. GRIESINGER l Introduction Material and Methods The translocation t( 8;21) (q22;q22), AMLl/ETO, one of the most frequent genetic aberrations in acute myelogenous leukemia is detectable in 40% of AML FAB M2. This entity is characterized by myeloblasts with a tendency towards differentiation and a comparably good prognosis (Mitelmann and Heim, 1998).
In each case the ability of the transcription factor to bind an AML-1 DNA binding site is retained. , 1995). , 1998a). , 1999). Here, the mechanisms of transcriptional repression for these Department of Biochemistry, Vanderbilt-Ingram Cancer Center, Vanderbilt University School of Medicine Room 512 Medical Research Building II, 23'" and Pierce Avenue, Nashville, TN 37232 USA 21 important chromosomal translocation fusion proteins will be addressed. , 1998a). Therefore, a candidate approach was taken to search for potential corepressors that might interact with the domains required for repression in ETO.