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Identification of a breakpoint cluster region 3' of the ribophorin I gene
at 3q21 associated with the transcriptional activation of the EVI1 gene in
acute myelogenous leukemias with inv(3)(q21q26)
K Suzukawa, E Parganas, A Gajjar, T Abe, S Takahashi, K Tani, S Asano, H Asou, N Kamada and J Yokota
Biology Division, National Cancer Center Research Institute, Tokyo, Japan.
Structural alterations occur in the long arm of chromosome 3 in
approximately 2% of patients with acute myelogenous leukemia (AML) or
myelodysplastic syndrome (MDS). The major alterations are inv(3)(q21q26)
and t(3:3)(q21;q26) and are often classified as the 3q21q26 syndrome. We
previously reported that the EVI1 gene is transcriptionally activated in
AMLs with t(3;3)(q21;q26) and inv(3)(q21q26) and that the chromosomal
breakpoints at 3q26 in the translocations were 5' of the EVI1 gene, whereas
the breakpoints in the inversion cases were 3' of the gene. In these
studies, four additional cases of AML with inv(3)(q21q26) are shown to
express the EVI1 gene and to have breakpoints 3' of the gene. To
characterize the 3q21 breakpoint region, cosmid and phage clones were
isolated that cover approximately 100 kb. At 3q21, the breakpoints for both
AMLs with t(3;3)(q21;q26) and inv(3)(q21q26) were found to cluster over a
region of approximately 50 kb downstream of the Ribophorin I gene. The
results indicate a common mechanism for the translocations and inversions
and support the hypothesis that the transcriptional activation of the EVI1
gene is mediated by enhancer elements associated with the Ribophorin I
gene.
Volume 84,
Issue 8,
pp. 2681-2688,
10/15/1994
Copyright © 1994 by The American Society of Hematology
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