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The t(15;17) breakpoint in acute promyelocytic leukemia cluster within two
different sites of the myl gene: targets for the detection of minimal
residual disease by the polymerase chain reaction
KS Chang, JF Lu, G Wang, JM Trujillo, E Estey, A Cork, DT Chu, EJ Freireich and SA Stass
Hematopathology Program, University of Texas M.D. Anderson Cancer Center,
Houston 77030.
The retinoic acid receptor alpha (RAR alpha) and the myl gene are involved
in the translocation breakpoint t(15;17)(q22;q21) in acute promyelocytic
leukemia (APL). The majority of the breakpoint sites have been mapped
within the second intron of the RAR alpha gene; however, the breakpoint
sites on the myl gene are variable. Using primer sets derived from exon 2
or exon 3 of the RAR alpha gene and a primer derived from the myl cDNA, we
were able to amplify the breakpoint sites of the fusion transcripts of all
six APL RNA samples by the reverse transcriptase-polymerase chain reaction
(RT-PCR). A DNA fragment of 290 bp (breakpoint A) was amplified using RNA
samples from three patients, whereas two DNA fragments of 630 and 774 bp
(breakpoint B) were amplified using RNA samples from the other three APL
patients. DNA sequence analysis of the amplified fragments suggests that
the APL breakpoints clustered within two different introns of the myl gene.
Northern blot analysis demonstrated that fusion transcripts RAR alpha/myl
and myl/RAR alpha of varying sizes were detected in patients with different
breakpoint sites on the myl gene. In addition, we analyzed five APL samples
in complete remission and detected t(15;17)- positive cells. We conclude
that the t(15;17) breakpoints in APL can be amplified by PCR using a single
primer set and that minimal residual disease can be demonstrated in APL
using RT-PCR.
Volume 79,
Issue 3,
pp. 554-558,
02/01/1992
Copyright © 1992 by The American Society of Hematology
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