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Blood, 15 February 2002, Vol. 99, No. 4, pp. 1428-1433
NEOPLASIA
Single-translocation and double-chimeric transcripts: detection
of NUP98-HOXA9 in myeloid leukemias with
HOXA11 or HOXA13 breaks of the chromosomal
translocation t(7;11)(p15;p15)
Takashi Fujino,
Akitaka Suzuki,
Yoshikazu Ito,
Kazuma Ohyashiki,
Yoshiaki Hatano,
Ikuo Miura, and
Takuro Nakamura
From the Department of Carcinogenesis, The Cancer
Institute, Japanese Foundation for Cancer Research, Tokyo, Japan; the
Department of Pathology and Immunology, Aging and Developmental
Sciences, Division of Gerontology and Gerodontology, Graduate School,
Tokyo Medical and Dental University, Japan; the First Department of
Internal Medicine, Tokyo Medical University, Japan; and the Third
Department of Internal Medicine, Akita University School of Medicine,
Japan.
It has been demonstrated that the chromosomal translocation
t(7;11)(p15;p15) in patients with human acute myelogenous leukemia (AML) and chronic myelogenous leukemia (CML) invariably involves fusion
of the nucleoporin gene, NUP98, on chromosome 11 and the class 1 HOX gene, HOXA9, on chromosome 7, and
that the fusion gene NUP98-HOXA9 is an
important gene in myeloid leukemogenesis. Here are reported 2 novel
chromosome 7p15 targets of the t(7;11)(p15;p15) chromosomal
translocation in 2 patients with CML and myelodysplastic syndrome
(MDS). Southern blot and polymerase chain reaction (PCR) analyses of
leukemia cell DNA failed to show rearrangement of HOXA9,
whereas NUP98 was found to be rearranged in both cases. Reverse transcription-PCR analysis using a NUP98 primer and
a degenerate primer corresponding to the third helix of the homeodomain of HOXA demonstrated that NUP98 was fused
in-frame to HOXA11 in the patient with CML and to
HOXA13 in the patient with MDS. The chromosomal breakpoints
on 7p15 were located within introns of HOXA11 or
HOXA13 genes. In both patients chimeric
NUP98-HOXA9 transcripts were also observed. These findings
suggest that AbdB-type HOXA genes are common targets of
t(7;11)(p15;p15) chromosomal translocations and that a single
translocation can produce more than one
NUP98-HOXA fusion gene, presumably because of
altered splicing.
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