Please use this identifier to cite or link to this item: https://doi.org/10.1016/j.ccr.2010.03.022
Title: Accelerated Leukemogenesis by Truncated CBFβ-SMMHC Defective in High-Affinity Binding with RUNX1
Authors: Kamikubo, Y.
Zhao, L.
Hyde, R.K.
Kundu, M.
Compton, S.
Liu, P.P.
Garrett, L.
Wunderlich, M.
Mulloy, J.C.
Corpora, T.
Wolff, L.
Bushweller, J.
Paul, T.A.
Huang, G.
Ito, Y. 
Keywords: CELLCYCLE
Issue Date: 2010
Source: Kamikubo, Y., Zhao, L., Hyde, R.K., Kundu, M., Compton, S., Liu, P.P., Garrett, L., Wunderlich, M., Mulloy, J.C., Corpora, T., Wolff, L., Bushweller, J., Paul, T.A., Huang, G., Ito, Y. (2010). Accelerated Leukemogenesis by Truncated CBFβ-SMMHC Defective in High-Affinity Binding with RUNX1. Cancer Cell 17 (5) : 455-468. ScholarBank@NUS Repository. https://doi.org/10.1016/j.ccr.2010.03.022
Abstract: Dominant RUNX1 inhibition has been proposed as a common pathway for CBF leukemia. CBFβ-SMMHC, a fusion protein in human acute myeloid leukemia (AML), dominantly inhibits RUNX1 largely through its RUNX1 high-affinity binding domain (HABD). However, the type I CBFβ-SMMHC fusion in AML patients lacks HABD. Here, we report that the type I CBFβ-SMMHC protein binds RUNX1 inefficiently. Knockin mice expressing CBFβ-SMMHC with a HABD deletion developed leukemia quickly, even though hematopoietic defects associated with Runx1-inhibition were partially rescued. A larger pool of leukemia-initiating cells, increased MN1 expression, and retention of RUNX1 phosphorylation are potential mechanisms for accelerated leukemia development in these mice. Our data suggest that RUNX1 dominant inhibition may not be a critical step for leukemogenesis by CBFβ-SMMHC. © 2010 Elsevier Inc. All rights reserved.
Source Title: Cancer Cell
URI: http://scholarbank.nus.edu.sg/handle/10635/26839
ISSN: 15356108
DOI: 10.1016/j.ccr.2010.03.022
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