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Cloning of several species of MLL/MEN chimeric cDNAs in myeloid leukemia
with t(11;19)(q23;p13.1) translocation
K Mitani, Y Kanda, S Ogawa, T Tanaka, J Inazawa, Y Yazaki and H Hirai
Third Department of Internal Medicine, Faculty of Medicine, University of
Tokyo, Japan.
The t(11;19)(q23;p13.1) translocation is thought to play an important role
in pathogenesis of myeloid leukemias in older patients. The MLL gene
involved in other 11q23 abnormalities was also rearranged by this
translocation. Screening of cDNA libraries of the t(11;19)(q23;p13.1)-
carrying leukemic cells resulted in the isolation of several species of
fusion cDNAs between the MLL gene and an unknown gene on 19p13.1, named MEN
(myeloid eleven-nineteen translocation), which is ubiquitously expressed.
Although the MLL gene was alternatively spliced, the fusion protein should
contain an N-terminal half of the MLL, including AT hook motifs, that is
fused to the MEN protein with a lysine-rich sequence, suggesting that the
MLL/MEN fusion protein could be a chimeric transcription factor. The
MLL/MEN fusion transcripts of 8.0 kb were detected in leukemic cells of two
cases with the translocation. The MLL/MEN fusion was consistent in all
three cases of the t(11;19)(q23;p13.1)-carrying leukemia examined by
RNA-based polymerase chain reaction. These findings strongly suggest that
the t(11;19)(q23;p13.1) results in the fusion formation encoding a new
class of potential chimeric transcription factor that contributes to
leukemogenesis of myeloid lineage.
Volume 85,
Issue 8,
pp. 2017-2024,
04/15/1995
Copyright © 1995 by The American Society of Hematology
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