作者: Joost H.A. Martens , Henk G. Stunnenberg
DOI: 10.1016/J.FEBSLET.2010.04.002
关键词:
摘要: Acute myeloid leukemia (AML) associated translocations often cause gene fusions that encode oncofusion proteins. Although many of the breakpoints involved in chromosomal have been cloned, most cases role chimeric proteins tumorigenesis is not elucidated. Here we will discuss fusion 4 common with AML as well molecular mechanisms these four and other utilize to transform progenitor cells. Intriguingly, although individual partners within represent a wide variety cellular functions, at level commodities can be found.