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The t(1;19)(q23;p13) results in consistent fusion of E2A and PBX1 coding
sequences in acute lymphoblastic leukemias
SP Hunger, N Galili, AJ Carroll, WM Crist, MP Link and ML Cleary
Department of Pathology, Stanford University School of Medicine, CA.
The t(1;19)(q23;p13) chromosomal translocation is observed cytogenetically
in 25% of children with pre-B-cell acute lymphoblastic leukemia (ALL) and
is associated with an adverse treatment outcome. The t(1;19) juxtaposes the
E2A gene from chromosome 19 with the PBX1 gene on chromosome 1, leading to
the production of fusion transcripts and resultant chimeric proteins that
contain the transcriptional-activating motif of E2A and the DNA-binding
homeodomain of PBX1. To investigate the molecular nature of E2A/PBX1 fusion
in patients with t(1;19) ALL we used an RNA-based polymerase chain reaction
(PCR) procedure to amplify a portion of the chimeric transcript. We
detected E2A/PBX1 fusion transcripts in cells from 97% (37 of 38) of cases
in which the t(1;19) had been observed cytogenetically. Molecular evidence
of E2A/PBX1 fusion transcripts was also observed in a patient in whom a
t(1;19) was not detected cytogenetically and in one patient with
subclinical levels of minimal residual disease before overt clinical
relapse. In all PCR- positive cases the junction of E2A and PBX1 coding
sequences occurred at precisely the same location as demonstrated by
hybridization of PCR products with a fusion site-specific detection
oligonucleotide. These findings demonstrate the consistent fusion of E2A
and PBX1 coding sequences resulting from t(1;19) and suggest that
site-specific fusion of E2A and PBX1 is an important pathogenic event in
t(1;19) ALL.
Volume 77,
Issue 4,
pp. 687-693,
02/15/1991
Copyright © 1991 by The American Society of Hematology
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