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The inv(11)(p15q22) chromosome translocation of de novo and therapy-
related myeloid malignancies results in fusion of the nucleoporin gene,
NUP98, with the putative RNA helicase gene, DDX10
Y Arai, F Hosoda, H Kobayashi, K Arai, Y Hayashi, N Kamada, Y Kaneko and M Ohki
Radiobiology Division, National Cancer Center Research Institute, Chuo- ku,
Tokyo, Japan.
The inv(11)(p15q22) is a recurrent chromosomal abnormality associated with
de novo and therapy-related myeloid malignancies. Here we report the
molecular definition of this chromosomal aberration in four patients.
Positional cloning showed the consistent rearrangement of the DDX10 gene on
chromosome 11q22, which encodes a putative RNA helicase. The translocation
targets the NUP98 gene on 11p15, a member of the FG peptide repeat
nucleoporin family. In DDX10 and NUP98, the inv(11) breakpoints occurred
within two introns of each gene and the two genes merged in-frame to
produce the chimeric transcripts characteristic of this translocation.
Although two reciprocal chimeric products, NUP98- DDX10 and DDX10-NUP98,
were predicted, only NUP98-DDX10 appears to be implicated in tumorigenesis.
DDX10 is predicted to be involved in ribosome assembly. NUP98 has been
identified as a nuclear pore complex protein and a target of chromosomal
translocation in acute myeloid leukemia through the t(7;11)(p15;p15)
translocation. The predicted NUP98-DDX10 fusion protein may promote
leukemogenesis through aberrant nucleoplasmic transport of mRNA or
alterations in ribosome assembly.
Volume 89,
Issue 11,
pp. 3936-3944,
06/01/1997
Copyright © 1997 by The American Society of Hematology
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