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Predictability of the t(1;19)(q23;p13) from surface antigen phenotype:
implications for screening cases of childhood acute lymphoblastic leukemia
for molecular analysis: a Pediatric Oncology Group study
MJ Borowitz, SP Hunger, AJ Carroll, JJ Shuster, DJ Pullen, CP Steuber and ML Cleary
Duke University Medical Center, Durham, NC.
The t(1;19)(q23;p13) translocation occurs in approximately 5% of B-
precursor acute lymphoblastic leukemias (ALLs) occurring in children. Its
presence has been associated with a poor prognosis, which may be overcome
with more intensive therapy. Although leukemic cells from cases of
t(1;19)-ALL frequently express cytoplasmic mu heavy chains, their complete
antigenic profile remains undefined. Among 697 consecutive cases of
B-precursor ALL with complete phenotypic studies using a panel of
monoclonal antibodies, 22 cases were found to carry the t(1;19). Twenty of
22 cases had an identical, complex phenotype characterized by homogeneous
expression of CD19, CD10, and CD9; complete absence of CD34; and at least
partial absence of CD20. Overall, this phenotype was seen in only 8.0% (56
of 697) of childhood B-precursor ALL. One of the two remaining
t(1;19)-carrying cases conformed to this phenotype, but was lacking data
for CD9. The other case differed by virtue of expression of CD34 and was
also hyperdiploid with 55 chromosomes. Molecular studies showed E2A-PBX1
abnormalities in all examined cases (12 of 12) with the t(1;19), including
the case lacking CD9 data. In contrast, no E2A-PBX1 abnormalities were
detected in the sole t(1;19)-ALL with CD34 expression. Seventeen cases with
the characteristic phenotype and uninformative cytogenetics were also
molecularly analyzed and 5 of 17 (including 4 of 8 with unsatisfactory
cytogenetics and 1 of 9 with a normal karyotype) contained E2A gene
rearrangements and E2A-PBX1 fusion mRNAs. Our results show that all cases
of t(1;19)-ALL with concomitant E2A-PBX1 fusion invariably express a
characteristic but uncommon profile of surface antigens. These observations
suggest that selective molecular analysis of a small subset of patients
(those with uninformative cytogenetics and the characteristic phenotype)
can identify a significant number of additional cases of ALL with E2A-PBX1
fusion that might benefit from more intensive therapy.
Volume 82,
Issue 4,
pp. 1086-1091,
08/15/1993
Copyright © 1993 by The American Society of Hematology
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