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A Novel Fusion Between MOZ and the Nuclear Receptor
Coactivator TIF2 in Acute Myeloid Leukemia
Melina Carapeti,
Ricardo C.T. Aguiar,
John M. Goldman, and
Nicholas C.P. Cross
From the Department of Haematology, Imperial College School of
Medicine, Hammersmith Hospital, London, UK; and the Division of
Hematologic Malignancies, Dana Farber Cancer Institute, Boston, MA.
Chromosomal abnormalities of band 8p11 are associated with a
distinct subtype of acute myeloid leukemia with French-American-British M4/5 morphology and prominent erythrophagocytosis by the blast cells.
This subtype is usually associated with the t(8;16)(p11;p13), a
translocation that has recently been shown to result in a fusion between the MOZ and CBP genes. We have
cloned the inv(8)(p11q13), an abnormality associated with the same
leukemia phenotype, and found a novel fusion between MOZ and
the nuclear receptor transcriptional coactivator
TIF2/GRIP-1/NCoA-2. This gene has not previously been implicated in the pathogenesis of leukemia or other malignancies. MOZ-TIF2 retains the histone acetyltransferase homology domains of both
proteins and also the CBP binding domain of TIF2. We speculate that the
apparently identical leukemia cell phenotype observed in cases with the
t(8;16) and the inv(8) arises by recruitment of CBP by MOZ-TIF2,
resulting in modulation of the transcriptional activity of target genes
by a mechanism involving abnormal histone acetylation.
Blood, Vol. 91 No. 9 (May 1), 1998:
pp. 3127-3133
© 1998 by The American Society of Hematology.
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