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Frequent Dysregulation of the c-maf Proto-Oncogene at 16q23 by
Translocation to an Ig Locus in Multiple Myeloma
Marta Chesi,
P. Leif Bergsagel,
Oluwatoyin O. Shonukan,
Maria
Luisa Martelli,
Leslie A. Brents,
Theresa Chen,
Evelin Schröck,
Thomas Ried, and
W. Michael Kuehl
From the Genetics Department, Medicine Branch, National Cancer
Institute, Bethesda, MD; the Department of Medicine, Division of
Hematology and Oncology, Cornell University Medical College, New York,
NY; and the Genome Technology Branch, National Institutes of
Health-National Center for Human Genome Research, Bethesda, MD.
Dysregulation of oncogenes by translocation to an IgH (14q32) or IgL
( , 2p11 or  , 22q11) locus is a frequent event in the pathogenesis
of B-cell tumors. Translocations involving an IgH locus and a diverse
but nonrandom array of chromosomal loci occur in most multiple myeloma
(MM) tumors even though the translocations often are not detected by
conventional cytogenetic analysis. In a continuing analysis of
translocations in 21 MM lines, we show that the novel, karyotypically
silent t(14;16)(q32.3;q23) translocation is present in 5 MM lines, with
cloned breakpoints from 4 lines dispersed over an approximately 500-kb
region centromeric to the c-maf proto-oncogene at 16q23.
Another line has a t(16;22)(q23;q11), with the breakpoint telomeric to
c-maf, so that the translocation breakpoints in these 6 lines
bracket c-maf. Only these 6 lines overexpress c-maf
mRNA. As predicted for dysregulation of c-maf by translocation,
there is selective expression of one c-maf allele in 2 informative lines with translocations. This is the first human tumor in
which the basic zipper c-maf transcription factor is shown to function
as an oncogene.
Blood, Vol. 91 No. 12 (June 15), 1998:
pp. 4457-4463
© 1998 by The American Society of Hematology.
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