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Blood, 15 August 2001, Vol. 98, No. 4, pp. 1264-1267
BRIEF REPORT
A novel gene, NSD1, is fused to NUP98 in
the t(5;11)(q35;p15.5) in de novo childhood acute myeloid
leukemia
Rina J. Jaju,
Carrie Fidler,
Oskar A. Haas,
Amanda J. Strickson,
Fiona Watkins,
Kevin Clark,
Nicholas C. P. Cross,
Jan-Fang Cheng,
Peter D. Aplan,
Lyndal Kearney,
Jacqueline Boultwood, and
James S. Wainscoat
From the LRF Molecular Haematology Unit, Nuffield
Department of Clinical Laboratory Sciences, University of Oxford; and
MRC Molecular Haematology Unit, Institute of Molecular Medicine; both
of John Radcliffe Hospital, Oxford, United Kingdom; Children's Cancer
Research Institute, St Anna Kinderspital, Vienna, Austria; Department
of Haematology, Imperial College School of Medicine, Hammersmith
Hospital, London, United Kingdom; Life Sciences Division, Lawrence
Berkeley National Laboratory, CA; and Division of Clinical Sciences,
National Cancer Institute, Gaithersburg, MD.
The recurrent translocation t(5;11)(q35;p15.5) associated with a 5q
deletion, del(5q), has been reported in childhood acute myeloid
leukemia (AML). We report the cloning of the translocation breakpoints
in de novo childhood AML harboring a cryptic t(5;11)(q35;p15.5). Fluorescence in situ hybridization (FISH) analysis demonstrated that
the nucleoporin gene (NUP98) at 11p15.5 was disrupted by this translocation. By using 3'-rapid amplification of complementary DNA ends (3'-RACE) polymerase chain reaction, we identified a chimeric
messenger RNA that results in the in-frame fusion of NUP98
to a novel gene, NSD1. The NSD1 gene has 2596 amino acid residues and a 85% homology to the murine Nsd1
with the domain structure being conserved. The NSD1 gene
was localized to 5q35 by FISH and is widely expressed. The reciprocal
transcript, NSD1-NUP98, was also detected by reverse
transcriptase-polymerase chain reaction. This is the first report in
which the novel gene NSD1 has been implicated in human malignancy.
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