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Blood, Vol. 92 No. 4 (August 15), 1998:
pp. 1125-1130
RAPID COMMUNICATION
ABI-1, a Human Homolog to Mouse Abl-Interactor 1, Fuses the
MLL Gene in Acute Myeloid Leukemia With t(10;11)(p11.2;q23)
Tomohiko Taki,
Noriko Shibuya,
Masafumi Taniwaki,
Ryoji Hanada,
Kazuhiro Morishita,
Fumio Bessho,
Masayoshi Yanagisawa, and
Yasuhide Hayashi
From the Department of Pediatrics, Faculty of Medicine, University of
Tokyo, Bunkyo-ku, Tokyo, Japan; the 3rd Department of Internal
Medicine, Kyoto Prefectural University of Medicine,
Kawaramachi-Hirokoji, Kamigyo-ku, Kyoto, Japan; the Division of
Hematology/Oncology, Saitama Children's Medical Center, Iwatsuki,
Japan; and the Biology Division, National Cancer Center Research
Institute, Chuo-ku, Tokyo, Japan.
Recurrent translocation t(10;11) has been reported to be associated
with acute myeloid leukemia (AML). Recently, two types of chimeric
transcripts, MLL-AF10 in t(10;11)(p12;q23) and
CALM-AF10 in t(10;11)(p13;q14), were isolated. t(10;11) is
strongly associated with complex translocations, including
invins(10;11) and inv(11)t(10;11), because the direction of
transcription of AF10 is telomere to centromere. We analyzed a
patient of AML with t(10;11)(p11.2;q23) and identified ABI-1 on
chromosome 10p11.2, a human homolog to mouse Abl-interactor 1 (Abi-1),
fused with MLL. Whereas the ABI-1 gene bears no
homology with the partner genes of MLL previously described,
the ABI-1 protein exhibits sequence similarity to protein of homeotic
genes, contains several polyproline stretches, and includes a
src homology 3 (SH3) domain at the C-terminus that is required
for binding to Abl proteins in mouse Abi-1 protein. Recently, e3B1, an
eps8 SH3 binding protein 1, was also isolated as a human homolog to
mouse Abi-1. Three types of transcripts of ABI-1 gene were
expressed in normal peripheral blood. Although e3B1 was
considered to be a full-length ABI-1, the MLL-ABI-1
fusion transcript in this patient was formed by an alternatively
spliced ABI-1. Others have shown that mouse Abi-1 suppresses
v-ABL transforming activity and that e3B1, full-length ABI-1, regulates
cell growth. In-frame MLL-ABI-1 fusion transcripts combine the
MLL AT-hook motifs and DNA methyltransferase homology region with the
homeodomain homologous region, polyproline stretches, and SH3 domain of
alternatively spliced transcript of ABI-1. Our results suggest
that the ABI-1 gene plays a role in leukemogenesis by
translocating to MLL.
© 1998 by The American Society of Hematology.
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