p300, which was originally cloned as a nuclear binding target of the a
denovirus E1A oncoprotein, forms a family with cyclic-AMP response ele
ment binding protein (CREB)-binding protein (CBP), p300/CBP are consid
ered to be transcriptional coactivators that connect the basal transcr
iptional machinery to various DNA-binding transcriptional factors. p30
0/CBP are implicated in both cell differentiation and regulation of ce
ll-cycle. We identify here that the p300 gene is fused to the MLL gene
and that in-frame MLL-p300 fusion protein is generated in acute myelo
id leukemia (AML) with t(11;22)(q23;q13). These findings suggest that
the basis for the leukemogenesis of t(11;22)-AM L is the inability of
p300 to regulate cell-cycle and cell differentiation after fusion with
MLL. (C) 1997 by The American Society of Hematology.