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 Previous Article | Table of Contents | Next Article 
Blood, Vol. 91 No. 12 (June 15), 1998:
pp. 4457-4463
Frequent Dysregulation of the c-maf Proto-Oncogene at 16q23 by
Translocation to an Ig Locus in Multiple Myeloma
By
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.
 |
ABSTRACT |
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.
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INTRODUCTION |
DYSREGULATION OF oncogenes by
translocation to an IgH (14q32) or IgL (, 2p11 or , 22q11) locus
is a seminal event in the pathogenesis of B-cell tumors.1
We and others have shown recently that translocations to the IgH locus
occur in most multiple myeloma (MM) tumors even though the
translocations often are not detected by conventional
karyotypes.2,3 Many nonrandom chromosomal partners (and
oncogenes) are involved in these translocations.3-9 Two
loci (cyclin D1 at 11q13 and FGFR3 at 4p16.3) are involved frequently, with each occuring at an incidence of about 20% to 25%.
Several other loci are involved recurrently but at a much lower
frequency (eg, IRF4 at 6p25, c-myc at 8q24, and
bcl-2 at 18q21), and 10 or more other loci have been identified
only once. However, in the majority of tumors that have an apparent IgH
translocation by conventional karyotypic analysis, the partner locus
has not been identified (14q+). We report here karyotypic and molecular characterization of a novel t(14;16)(q32;q23) translocation that causes
overexpression of the c-maf oncogene and appears to occur at an
incidence of about 25% in MM.
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MATERIALS AND METHODS |
Cell culture.
The human MM cell lines, as described in detail
previously,3 were grown in Petri dishes in RPMI 1640 medium
supplemented with 10% fetal calf serum The LP-1 MM cell line was
obtained from DSMZ (Braunschweig, Germany).10
Translocation breakpoint fragments.
The cloned chromosome 16 translocation breakpoint fragments in ZAP
Express (Stratagene, La Jolla, CA) included 6.9-kb
EcoRI (JJN3) and 3.5-kb EcoRI (ANBL6) fragments
detected with a 3 Sµ probe, 3.5-kb (KMS11) and 7.7-kb (MM.1)
HindIII fragments detected with a 3 S probe, and
4.1-kb Bgl II-EcoRI (ANBL6) and 4.9-kb HindIII
(MM.1) fragments detected with a 5Sµ probe.
Isolation and characterization of overlapping YAC, BAC and P1
clones.
A number of YAC and BAC clones were obtained from N. Doggett, C.M.
Aldaz, and A. Bednareck. Additional P1 and BAC human genomic library
clones (Genome Systems, St Louis, MO) were identified with PCR
reactions using primers corresponding to sequences determined from the
translocation breakpoint fragments, from the ends of BAC or P1 genomic
clones, and from c-maf.
Somatic cell hybrid mapping.
Non-Ig sequences from translocation breakpoint clones were mapped to
specific human chromosomes using hamster hybrids containing one or a
limited number of human chromosomes, as described
previously.3 In addition the Stanford high resolution TNG3
radiation hybrid panels (Research Genetics, Huntsville, AL) were used
for more precise mapping of polymerase chain reaction (PCR) markers to specific chromosome regions.
Primers and probes.
Switch region probes upstream (eg, 5Sµ) and downstream (eg,
3Sµ) of the repetitive sequences in each switch region were as
described previously.3,5 The c-maf probe used in
the Northern blot assay was a 1.2-kb fragment that contained 5
untranslated and coding sequences that were PCR-amplified from cDNA.
The primers used to amplify the Mnl I polymorphism are
5-CTTCAGTTCATGAACTGGTGT and 5-GTTTGCCAGGTTAAATGTGTA.
Information regarding the oligonucleotides used for other PCR reactions
is available by request.
Fluorescence in situ hybridization (FISH).
Preparation of metaphase chromosomes, chromosome 14 and 22 painting
probes, c-maf and JJN3 breakpoint P1 clone probes, and hybridization and detection protocols are described
elsewhere.5
Other procedures.
Genomic library construction and screening, isolation and sequencing of
recombinant clones, and Southern and Northern blot analysis were
described elsewhere.3 An 8226 oligo-dT primed cDNA library
was constructed with EcoRI linkers and cloned into ZAPII
(Stratagene), and a directional H929 oligo-dT primed cDNA library was
prepared in UniZAP (Stratagene).
GenBank accession numbers for c-maf and translocation
breakpoint sequences.
The GenBank accession no. for JJN3 breakpoint sequence is U73670; for
KMS11 3S, AF055379; for ANBL6 5Sµ and 3Sµ breakpoint sequences, AF055380 and AF055381, respectively; for MM.1
5Sµ and 3Sµ, AF055382 and AF055383, respectively; for
human c-maf, AF055376; for the long form of c-maf,
AF055377; and for the intronic sequence separating the two exons of the long form of c-maf, AF055378.
| |
RESULTS |
As described elsewhere, our Southern blot assay identifies candidate
translocation breakpoints as rearranged restriction enzyme fragments
that hybridize with either a 5 or a 3 probe directed against sequences that flank IgH switch regions.3
Figure 1a shows how this assay identifies
the derivative chromosomes resulting from 2 patterns of IgH switch
translocation in MM. In 1 case, there is a translocation involving only
Sµ, so that the 5Sµ probe detects the der(16) breakpoint and
the 3Sµ detects the der(14) breakpoint. In the other case, the
translocation involves Sµ and S, so that the 5Sµ probe
again detects the der(16) breakpoint, whereas a 3S probe
detects the der(14) breakpoint. Figure 1B shows translocation
breakpoint fragments for both the first kind (ANBL6) and the second
kind (MM.1) of IgH switch translocation. Using this approach, we cloned
6 translocation breakpoint fragments involving chromosome 16 from 4 MM
cell lines: (1) a 3Sµ fragment from JJN3; (2) 5 and
3Sµ fragments from ANBL6; (3) 5Sµ and 3S
fragments from MM.1; and (4) a 3S fragment from KMS11. For
each MM line, the non-Ig sequences at one end of each breakpoint fragment identify chromosome 16 in a panel of somatic cell hybrids. A
P1 clone that includes the chromosome 16 sequences from the JJN3
breakpoint maps to 16q23 by FISH analysis of normal metaphase chromosomes (see Fig 4A). Noting that the c-maf proto-oncogene also maps to 16q23,11 we isolated a P1 clone containing
c-maf and demonstrated colocalization of c-maf and the
JJN3 chromosome 16 breakpoint sequences by two-color FISH experiments
analyzing normal metaphase chromosome spreads and interphase nuclei
(see Fig 4A). We also localized c-maf on the der(14) by FISH
analysis of metaphase chromosomes from JJN3 cells (not shown), thus
showing that c-maf is telomeric to the JJN3 chromosome 16 breakpoint sequences. Mapping of P1, BAC, and YAC clones demonstrated
physical linkage at 16q23 of c-maf with the t(14;16)
breakpoints in the 4 MM lines (Fig 1C). The ANBL6 and JJN3 chromosome
16 breakpoint sequences are present within a single BAC. The KMS11 and
MM.1 breakpoints are more centromeric, with all of the cloned t(14;16)
translocation breakpoints dispersed over an approximately 500-kb
region. As shown in Fig 1C, c-maf and the chromosome 16 breakpoints from the 4 MM lines map in the order:
cen KMS11MM.1JJN3ANBL6c-maftel.
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| Fig 1.
Identification and characterization of t(14;16)(q32;q23)
translocation breakpoints. (A) Diagram of der(14) and der(16)
breakpoints from translocations involving Sµ and S. The centromere
is to the left. Structural elements include enhancers (3E and
5E), switch region (S), and coding segments (rectangles). Thick
horizontal lines depict hybridization probes. Vertical lines represent
restriction enzyme sites. H, HindIII; Ba, BamHI; Bg,
Bgl II. (B) Southern blots of MM cell line genomic DNAs
digested with HindIII. Probes flanking switch regions are
indicated at the bottom of each lane. For the ANBL6 line, 17-kb and
16.5-kb rearranged fragments are detected with the 5 and
3Sµ probes, respectively. For the MM.1 line, 4.9-kb and 7.7-kb
rearranged fragments are detected with the 5Sµ and
3S probes, respectively. The MM.1 4.0-kb fragment(s) that
cohybridizes with 5S and 3S probes represents an
unrearranged, germline fragment containing a switch region. (C) Map
of region at 16q23 that contains c-maf and sequences present in
the cloned t(14;16) breakpoint fragments. For the BAC clones
(designated by number within box), the T7 (T) and SP6 (S) ends are
shown when the orientation has been defined. Mapping was performed by
using PCR reactions to detect sequences derived from the ends of BAC/P1 clones, translocation breakpoint fragments, and c-maf, plus 5 other chromosome 16 markers28. The composite map is not to
scale but is fully consistent with analysis of additional clones and
markers that are not shown. The dashed arrow indicates that the
t(16;22) breakpoint in 8226 is telomeric to c-maf by FISH
analysis.
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| Fig 4.
Two-color FISH analysis of normal lymphocytes and 2 MM
cell lines. (A) P1 clones containing the c-maf gene (red
signal) and chromosome 16 sequences from the JJN3 MM t(14;16)
breakpoint (green signal) were hybridized to metaphase chromosomes
(counterstained blue) and interphase nuclei from normal lymphocytes.
The signals colocalize at chromosome band 16q23. (B) A chromosome 14 painting probe (red signal) and a c-maf P1 clone (green signal)
were hybridized to metaphase chromosomes from the OCI-My5 MM cell line.
There are no normal copies of chromosome 14 or 16. One copy of
c-maf (arrowhead) has been translocated to the telomeric end of
chromosome 14 at band q32, consistent with a t(14;16)(q32;q23)
translocation, involving the IgH locus and c-maf, respectively. A
second copy of c-maf (arrow) is translocated to a structurally
altered, unidentified chromosome. (C) A chromosome 22 painting probe
(red signal) and a c-maf P1 clone (green signal) were hybridized to
metaphase chromosomes from the 8226 MM cell line. There are 4 copies of
the c-maf gene, 2 of which have chromosome 22 sequences
translocated telomeric to c-maf (arrowhead), whereas 2 are on a
normal chromosome 16 (arrow). The breakpoint on chromosome 22 is
consistent with a t(16;22)(q23;q11) translocation near the
c-maf and IgL, loci, respectively.
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Hypothesizing that c-maf is the oncogene dysregulated by the
t(14;16)(q32;q23) translocation, we screened our panel of 21 MM lines
for c-maf expression using a reverse transcription-PCR (RT-PCR) assay. We found high levels of expression in the
4 MM lines with t(14;16) (MM.1, JJN3, KMS11, and ANBL6) plus 2 additional lines (OCI-My5 and 8226) and lower levels in several other
lines after a limited number of PCR cycles (data not shown). To obtain a more quantitative estimate of c-maf mRNA expression, we did a
Northern blot using total RNA from the 14 lines for which expression was detected by the RT-PCR assay. As shown in
Fig 2A, there is a high level of expression
of 4.4- and 2.3-kb c-maf mRNAs in the 6 lines mentioned above. The
other lines show either no detectable expression or a level of
expression that is approximately 10-fold lower. The same 4.4-and 2.3-kb
mRNAs are expressed in most human tissues, some examples of which are
shown in Fig 2B. In view of the unexplained finding of two sizes of
mRNA for c-maf and the fact that human c-maf had not
been well characterized, we decided to look more carefully at the
structure of human c-maf. Previously, using a subtractive cDNA
approach, we identified c-maf expression in the H929 and 8226 MM lines, whereas c-maf expression was not detected in the pair
of lymphoblastoid cell lines used for the subtraction.12
Using sequence analysis of c-maf cDNAs isolated from 8226 and
H929, we determined the full sequence of alternatively processed human
c-maf mRNAs (Fig 3). The 4.4-kb
mRNA species encodes a predicted c-maf basic zipper transcription
factor protein of 373 amino acids that is highly homologous to reported
amino acid sequences for avian (86% identity) and murine (95%
identity) c-maf.13 The 2.3-kb mRNA encodes a predicted
c-maf protein of 403 amino acids, although the 5 untranslated
and coding sequence is identical to the 4.4-kb mRNA through amino acid
372. Noting a potential donor splice site at codon 373 in the 4.4-kb
mRNA (Fig 3B), we proceeded to PCR-amplify from genomic DNA a 2.1-kb
fragment that started just upstream of the polyadenylation site in the
4.4-kb mRNA species and ended in the unique coding region in the 2.3-kb mRNA species. Sequence analysis of the downstream end of this fragment
demonstrated the presence of an acceptor splice signal within codon 373 of the 2.3-kb mRNA (Fig 3B), indicating that the 2.3-kb mRNA results
from the removal of an approximately 4-kb intron that includes the
3 untranslated region of the 4.4-kb mRNA species. The additional
30 amino acids in the predicted 403 residue protein contain no known
sequence motifs and have no obvious homologies to other proteins, so
that the significance of alternatively spliced forms of c-maf is
presently unclear.
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| Fig 2.
Expression of c-maf mRNA in myeloma cell lines and some
normal human tissues. (A) A Northern blot containing 15 µg of total RNA from each of 14 MM lines was probed for c-maf, with the
horizontal lines indicating the position of 5.0- and 2.0-kb ribosomal
RNAs. Ethidium bromide staining is shown in the lower panel. (B) A
Northern blot containing 2 µg of poly (A)+ RNA from each of several
normal tissues was assessed for c-maf expression. (C) Genomic
DNA, cDNA, and RNA from 2 MM cell lines was subjected to PCR
amplification using appropriate oligonucleotides from the 3
untranslated region of c-maf. The amplified products were
digested with Mnl I and fractionated by electrophoresis on a
2% acrylamide gel. The positions of Mnl I sites, including the
polymorphic (*) Mnl I site, in the amplified fragments are
shown.
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| Fig 3.
Sequence of short and long c-maf proteins generated by
alternative RNA processing of transcripts from the c-maf gene.
(A) A single letter code indicates the two sequences, with the long form identical to residues 1 through 372 of the short form. The basic
region is underlined as a block, and individual residues that
contribute to a presumptive leucine zipper are individually underlined.
(B) This diagram summarizes the genome organization and codon sequences
that account for the alternative RNA processing that generates the 2 forms of c-maf mRNA. The exon unique to the long form of the c-maf
protein is located about 2.1 kb downstream of the polyadenylation
signal used to generate the 4.4-kb mRNA that encodes the short form of
the c-maf protein. The sequences of the exon-intron boundaries for the
short mRNA are indicated, with the exon sequences in capital letters.
The homology of the 4.4-kb mRNA to the avian c-maf genomic
sequence indicates that the coding region and 3 untranslated
region are contained within a single exon.
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Two MM lines (8226 and OCI-My5) that overexpress c-maf had no
candidate IgH switch translocation breakpoint fragments by our Southern
blot assay, which could represent a failure of the assay to detect a
switch-mediated translocation or could represent an example of a VDJ
recombinase-mediated translocation into or near a JH or JL segment. The
8226 MM line has a t(1;14)(p13;q32) translocation as determined by
conventional cytogenetic analysis,14 which we confirmed by
two-color FISH analysis of metaphase chromosomes with chromosome 1 and
14 painting probes (data not shown), whereas there is no published
karyotype for the OCI-My5 line. A metaphase FISH analysis with a
c-maf probe and a chromosome 14 painting probe demonstrated
that c-maf has been translocated to the telomere of the long
arm of 14, ie, a t(14;16 )(q32;q23) translocation in OCI-My5
(Fig 4B) but not in 8226 (not shown).
Another FISH analysis on metaphase chromosomes from line 8226 using the
c-maf probe and a chromosome 22 painting probe showed
translocation of chromosome 22 telomeric to c-maf on chromosome
16 (Fig 4C). The position of the breakpoint on chromosome 22 is
consistent with a t(16;22)(q23;q11) translocation that would
dysregulate c-maf by juxtaposition to the IgL locus.
A chromosomal translocation involving 1 of the Ig loci typically
results in cis dysregulation of an oncogene located on the chromosomal
partner involved in the translocation, whereas the allelic oncogene on
the chromosome not involved in the translocation is not dysregulated.
By comparison of our c-maf sequences and expressed sequence
tags deposited in GenBank, we identified an apparent Mnl I
polymorphism in the 3 untranslated region of c-maf and
confirmed that two MM lines contain c-maf alleles distinguished by the polymorphism at this site (Fig 2C). As predicted, the KMS11 line, which has a t(14;16) translocation, selectively expresses 1 of
the 2 c-maf alleles. By contrast, the LP1 MM line, which has a
t(4;14) translocation (unpublished data), expresses a very low level of c-maf, with equal levels of expression from each allele. In addition, we screened other lines for polymorphic markers in
c-maf and identified two c-maf alleles distinguished by
a T>C polymorphism at nucleotide 3626 in the 3 untranslated
region in the 8226 MM line. Again, one c-maf allele is
selectively expressed (data not shown), consistent with the variant
t(16;22) translocation causing dysregulation and overexpression of the
c-maf allele involved in the translocation.
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DISCUSSION |
Although the translocation t(14;16)(q32.3;q23) has not been identified
by conventional cytogenetic analysis, presumably because of the
telomeric positions of both loci, our finding that 16q23 is
translocated to an Ig locus in 6 of 21 MM lines suggests that translocation of 16q23 to 1 of the Ig loci occurs with an incidence of
about 25% in MM, ie, an incidence similar to what we have observed for
t(4;14) (FGFR3) and t(11;14) (cyclin D1). This translocation is
not restricted to cell lines. First, tumor cells from the 1 cell line
(JJN3) for which we were able to examine the primary tumor cells
contained the translocation breakpoint as determined by Southern
blot.3 Second, two labs reported recently that FISH
analysis detects a t(14;16)(q32;q23) translocation in primary MM
tumors.2,15 Finally, 7 of 22 primary intramedullary MM tumor samples express c-maf mRNA at a level comparable to the lines
documented here to have a t(14;16) or t(16;22) translocation, whereas 4 samples from patients with monoclonal gammopathy of undetermined
significance (MGUS) and the other tumor samples express low or
nondetectable levels of c-maf (data not shown).
We cannot exclude the possibility that other genes are dysregulated by
the t(14;16) translocation in MM, but we have identified the
c-maf proto-oncogene as at least one oncogene that is
dysregulated by these translocations involving 16q23. First, the
breakpoints are dispersed over an approximately 500-kb region
centromeric to c-maf, so that it is located on the der(14)
chromosome that contains the strong 3 IgH enhancer(s) but not
the weaker intronic enhancer (Fig 1A). This dispersion of breakpoints
hundreds of kilobases centromeric to an oncogene is similar to the
situation for cyclin D1 and FGFR3, which are dysregulated in
mantle cell lymphoma and MM when widely dispersed translocation
breakpoints involving the IgH locus are localized as far as several
hundred kilobases centromeric to these genes.4,5,16,17
Second, the translocation breakpoint for a variant (IgL) t(16;22)
translocation is telomeric to c-maf. It is well established for
c-myc, bcl-2, and cyclin D1 that IgH translocation breakpoints and
variant (IgL) translocation breakpoints, which usually are located
centromeric or telomeric, respectively, bracket the
oncogene.18-20 Third, c-maf is overexpressed only
in the 6 MM lines for which we have identified a translocation
involving 16q23. Fourth, 2 informative MM lines (KMS11 and 8226)
contain 2 genetically distinguishable c-maf alleles, but each
selectively expresses 1 allele, as predicted if the translocation is
responsible for dysregulation of c-maf. By contrast, another MM
line (LP1) without an apparent t(14;16) translocation expresses both
genetically distinguishable alleles to a similar extent. Finally, it is
important to emphasize that v-maf is a classical oncogene
identified in an avian transforming virus21 and that studies by others have shown that overexpression of wild type c-maf
is capable of contributing to transformation of fibroblasts in a
model system.22 As indicated above, c-maf is a member of a
large family of basic zipper transcription factors, eg, jun, fos,
NF-IL6, and small maf proteins, many of which form heterodimers with
one another. This family of transcription factors is involved in many
basic cellular processes, including proliferation, differentiation, and
responsiveness to interleukin-6, a cytokine that has a central role in
normal plasma cell differentiation and in pathogenesis of
MM.23
As stated at the outset, it is clear that translocations involving 1 of
the Ig loci are present in most, if not all, MM tumors, including at
least 20 lines in our panel of 21 MM lines. Curiously, in 2 of our MM
lines with translocations involving 16q23, there is a second
translocation involving an IgH locus, ie, a t(1;14)(p13;q32) translocation (but lacking an identified oncogene at present) in 8226 and a t(4;14)(p16.3;q32.3) translocation that dysregulates FGFR3 in KMS11. Despite the difficulty of identifying
translocations from conventional cytogenetic analysis of MM tumors and
cell lines, others have also reported the coincidence of 2 IgH
translocations, or an IgH translocation plus a variant translocation,
in a number of MM lines and tumors.2,8,24-26 Obviously, the
presence of 2 independent translocations in a single MM tumor is not a
rare event. We note a recent report suggesting a similar incidence of
IgH translocations in premalignant MGUS and frankly malignant MM.2 Thus, it seems likely that translocations in MGUS and MM occur during normal plasma cell development as a consequence of
errors resulting from reactivated VDJ recombination in germinal centers27 or perhaps more often as a consequence of errors
in physiological IgH switch recombination. Tumor progression beyond 1 or 2 translocations clearly involves a variety of additional genetic
changes, including activating mutations in ras or
FGFR3, the latter occurring in MM tumors with a
t(4;14)(p16.3;q32.3) translocation, including the KMS11 cell
line5 that also has a t(14;16)(q32.3;q23) translocation and
overexpresses c-maf.
| |
FOOTNOTES |
Submitted February 4, 1998;
accepted March 26, 1998.
Address reprint requests to W. Michael Kuehl, MD, NCI Medicine Branch,
Genetics Department, Naval Hospital, Bldg 8, Room 5101, Bethesda, MD
20889-5105; e-mail: wmk{at}helix.nih.gov.
The publication costs of this article were defrayed in part by page charge payment. This article must therefore be hereby marked "advertisement" is accordance with 18 U.S.C. section 1734 solely to indicate this fact.
| |
ACKNOWLEDGMENT |
The authors thank Norman Doggett for providing probes and YAC clones,
plus the initial mapping of the JJN3 breakpoint and c-maf
sequences to his YAC clones. In addition, we are grateful to C. Marcelo
Aldaz and Andrezj Bednareck for generously providing us with BAC and
YAC DNAs at 16q23.
| |
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P. J. Ho, R. D. Brown, G. J. Pelka, A. Basten, J. Gibson, and D. E. Joshua
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W. S. Dalton, P. L. Bergsagel, W. M. Kuehl, K. C. Anderson, and J. L. Harousseau
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Abstract
Introduction
Abstract