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Consistent involvement of the bcr gene by 9;22 breakpoints in pediatric
acute leukemias
K Suryanarayan, SP Hunger, S Kohler, AJ Carroll, W Crist, MP Link and ML Cleary
Department of Pathology, Stanford University School of Medicine, CA
94305-5324.
To investigate the relationship of bcr-abl fusion mRNAs with childhood
acute lymphoblastic leukemias (ALL), we examined 27 pediatric Philadelphia
chromosome (Ph1)-positive acute leukemias using a reverse polymerase chain
reaction (PCR) procedure. In cells from 24 leukemias, single bcr-abl PCR
products were detected that corresponded to breakpoints in the minor
breakpoint cluster region (mbcr in intron 1 of the bcr gene) associated
with production of the P190 fusion protein. Cells from the three remaining
leukemias contained breakpoints in the major breakpoint cluster region
(Mbcr) as shown by PCR and Southern blot analyses. These three leukemias
also contained low levels of the mbcr PCR product that may have resulted
from alternative splicing of the bcr-abl precursor RNA. A screen of 35
additional leukemias from patients who failed therapy before day 180
(induction failures or early relapses) found one case with unsuccessful
cytogenetics to express Mbcr- abl RNA. All four children with Mbcr
breakpoints had white blood cell levels in excess of 250,000 at
presentation (compared with 2 of 24 with mbcr breakpoints) and two had
hematologic and clinical features suggestive of chronic myelogenous
leukemias (CML) in lymphoid blast crisis. Our results indicate that in
Ph1-positive pediatric leukemias, all 9;22 breakpoints occur in one of the
two known breakpoint cluster regions in the bcr gene on chromosome 22. The
reverse PCR reliably detected all patients with cytogenetic t(9;22) and is
capable of detecting additional Ph1-positive leukemias that are missed by
standard cytogenetics. Furthermore, the Mbcr-type breakpoint, associated
with production of p210, can be seen in childhood leukemias presenting
either as clinical ALL or as apparent lymphoid blast crisis of CML,
suggesting that t(9;22) breakpoint locations do not exclusively determine
the biologic and clinical features of pediatric Ph1-positive ALL.
Volume 77,
Issue 2,
pp. 324-330,
01/15/1991
Copyright © 1991 by The American Society of Hematology
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