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Blood, Vol. 92 No. 8 (October 15), 1998:
pp. 2879-2885
CBFA2(AML1) Translocations With Novel Partner Chromosomes in
Myeloid Leukemias: Association With Prior Therapy
Diane Roulston,
Rafael Espinosa III,
Giuseppina Nucifora,
Richard
A. Larson,
Michelle M. Le Beau, and
Janet D. Rowley
From the Section of Hematology/Oncology, Department of Medicine, and
the Cancer Research Center, The University of Chicago Pritzker School
of Medicine, Chicago, IL.
CBFA2(AML1) has emerged as a gene critical in hematopoiesis;
its protein product forms the DNA-binding subunit of the heterodimeric core-binding factor (CBF) that binds to the transcriptional regulatory regions of genes, some of which are active specifically in
hematopoiesis. CBFA2 forms a fusion gene with ETO and
MDS1/EVI1 in translocations in myeloid leukemia and with
ETV6(TEL) in the t(12;21) common in childhood pre-B acute
lymphoblastic leukemia. We have analyzed samples from 30 leukemia
patients who had chromosome rearrangements involving 21q22 by using
fluorescence in situ hybridization (FISH). Our analysis showed that 7 of them involved CBFA2 and new translocation partners. Two
patients had a t(17;21)(q11.2;q22), whereas the other 5 had
translocations involving 1p36, 5q13, 12q24, 14q22, or 15q22. Five of
these novel breakpoints in CBFA2 occurred in intron 6; this
same intron is involved in the t(3;21). One breakpoint mapped to the
t(8;21) breakpoint region in intron 5, and 1 mapped 5 to that
region. All 7 CBFA2 rearrangements resulted from balanced translocations. All 7 patients had myeloid disorders (acute myeloid leukemia or myelodysplastic syndrome); 2 were de novo and 5 had treatment histories that included topoisomerase II targeting agents. The association of therapy-related disorders with translocations involving CBFA2 was significant by Fisher's exact test
(P < .003). These results provide further evidence that this
region of CBFA2 is susceptible to breakage in cells exposed to
topoisomerase II inhibitors.
© 1998 by The American Society of Hematology.
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