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Involvement of the putative hematopoietic transcription factor SCL in T-
cell acute lymphoblastic leukemia
PD Aplan, DP Lombardi, GH Reaman, HN Sather, GD Hammond and IR Kirsch
National Cancer Institute/Navy Medical Oncology Branch, National Naval
Medical Center, Bethesda, MD 20889.
The SCL gene, initially discovered at the site of a translocation
breakpoint associated with the development of a stem cell leukemia, encodes
a protein that contains the highly conserved basic helix-loop- helix (bHLH)
motif found in a large array of eukaryotic transcription factors. Recently,
we have described a nonrandom, site-specific SCL rearrangement in several
T-cell acute lymphoblastic leukemia (ALL) cell lines that juxtaposes SCL
with a distinct transcribed locus, SIL. The SIL/SCL rearrangement was found
in leukemic blasts from 11 of 70 (16%) newly diagnosed T-cell ALL patients,
a prevalence substantially higher than that of the t(11;14) translocation,
which has previously been reported as the most frequent nonrandom
chromosomal abnormality in T- cell ALL. We did not detect the SIL/SCL
rearrangement in the leukemic blasts from 30 patients with B-cell precursor
ALL, indicating that the rearrangement was specific for T-cell ALL.
Analysis of RNA from these patients indicated that an SIL/SCL fusion mRNA
was formed, joining SIL and SCL in a head-to-tail fashion. The fusion
occurs in the 5' untranslated region (UTR) of both genes, preserving the
SCL coding region. The net result of this rearrangement is that SCL mRNA
expression becomes regulated by the SIL promoter, leading to inappropriate
SCL expression. The resultant inappropriate expression of this putative
transcription factor may then contribute to leukemic transformation in
T-cell ALL.
Volume 79,
Issue 5,
pp. 1327-1333,
03/01/1992
Copyright © 1992 by The American Society of Hematology
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