Expression of the ABL-BCR fusion gene in Philadelphia-positive acute
lymphoblastic leukemia
JV Melo, DE Gordon, A Tuszynski, S Dhut, BD Young and JM Goldman
Department of Haematology, Royal Postgraduate Medical School, London, UK.
We have previously shown that the chimeric gene ABL-BCR, formed on the
derivative chromosome 9q+ as a result of the t(9;22) translocation, is
transcriptionally active in 65% of chronic myeloid leukemia patients. We
have now used the same technique, reverse transcription/polymerase chain
reaction amplification of ABL-BCR transcripts, to study nine patients with
Philadelphia (Ph) chromosome-positive acute lymphoblastic leukemia (ALL);
seven expressed the P190 and two the P210 type of BCR- ABL fusion protein.
All seven patients with P190 had ABL-BCR transcripts containing a junction
between ABL exon Ib and BCR exon 2 (Ib-e2); in two cases, ABL-BCR
transcripts with the Ia-e2 junction type were also present. Of the two P210
ALL patients, one had a Ib-b4 ABL- BCR transcript and the other showed no
detectable ABL-BCR expression. Although the BCR-ABL gene is probably
fundamental in the pathogenesis of the Ph+ leukemias, differential
expression of the ABL-BCR gene could contribute to the biologic
heterogeneity of the disease.
Volume 81,
Issue 10,
pp. 2488-2491,
05/15/1993
Copyright © 1993 by The American Society of Hematology
