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      Ectopic Expression of MAFB Gene in Human Myeloma Cells Carrying (14;20)(q32;q11) Chromosomal Translocations

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          Abstract

          Chromosome 14q+, which represents a chromosomal rearrangement involving the immunoglobulin heavy chain gene ( IgH) locus, is a genetic hallmark of human multiple myeloma (MM). Here, we report the identification of (14;20)(q32;qll) chromosomal translocations found in MM cells. Double color fluorescence in situ hybridization analyses pinpointed the breakpoints at the 20qll locus in two MM cell lines within a length of at most 680 kb between the KIAA0823 and MAFB gene loci. Among the transcribed sequences in the vicinity of the breakpoints, an ectopic expression of the MAFB gene, which is located at 450‐680 kb telomeric to one of the breakpoints and encodes a member of the MAF family basic region/leucine zipper transcription factor, was demonstrated to be associated with t(14;20). This finding, together with that of a previous study describing its transforming activity, suggests that the MAFB gene may be one of the targets deregulated by regulatory elements of the IgH gene as a result of t(14;20).

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          Frequent translocation t(4;14)(p16.3;q32.3) in multiple myeloma is associated with increased expression and activating mutations of fibroblast growth factor receptor 3.

          P Bergsagel, E Nardini, M Chesi … (1997)
          Dysregulation of oncogenes by translocation to the IgH locus (14q32) is a seminal event in the pathogenesis of B-cell tumours. In multiple myeloma (MM), translocations to the IgH locus have been reported at an incidence of 20-60%. For most translocations, the partner chromosome is unknown (14q+); for the others, a diverse array of chromosomal partners have been identified, with 11q13 (cyclin D1) the only chromosome that is frequently involved. Recently, we developed a Southern-blot assay that detects translocation breakpoint fragments in most MM tumours, including those with no translocation detected by conventional karyotyping. In a continuing analysis of translocation in 21 myeloma cell lines and primary tumours, we show that the novel, karyotypically silent translocation t(4;14)(p16.3;q32.3) is present in five lines and at least three of ten primary tumours. The chromosome-4 breakpoints are clustered in a 70-kb region centromeric to the fibroblast growth factor receptor 3 gene (FGFR3), the apparent dysregulated oncogene. Two lines and one primary tumour with this translocation selectively express an FGFR3 allele containing activating mutations identified previously in thanatophoric dwarfism. We propose that after the t(4;14) translocation, somatic mutation during tumour progression frequently generates in FGFR3 protein that is active in the absence of ligand.
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            Diverse karyotypic abnormalities of the c-myc locus associated with c-myc dysregulation and tumor progression in multiple myeloma.

            G Dewald, I R Kirsch, P Bergsagel … (2000)
            Translocations involving c-myc and an Ig locus have been reported rarely in human multiple myeloma (MM). Using specific fluorescence in situ hybridization probes, we show complex karyotypic abnormalities of the c-myc or L-myc locus in 19 of 20 MM cell lines and approximately 50% of advanced primary MM tumors. These abnormalities include unusual and complex translocations and insertions that often juxtapose myc with an IgH or IgL locus. For two advanced primary MM tumors, some tumor cells contain a karyotypic abnormality of the c-myc locus, whereas other tumor cells do not, indicating that this karyotypic abnormality of c-myc occurs as a late event. All informative MM cell lines show monoallelic expression of c-myc. For Burkitt's lymphoma and mouse plasmacytoma tumors, balanced translocation that juxtaposes c-myc with one of the Ig loci is an early, invariant event that is mediated by B cell-specific DNA modification mechanisms. By contrast, for MM, dysregulation of c-myc apparently is caused principally by complex genomic rearrangements that occur during late stages of MM progression and do not involve B cell-specific DNA modification mechanisms.
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              MafB is an inducer of monocytic differentiation.

              L Kelly, U Englmeier, I Lafon … (2000)
              The bZip transcription factor MafB is expressed specifically in the myeloid lineage of the hematopoietic system and is up-regulated successively during myeloid differentiation from multipotent progenitors to macrophages. Here we report that this induction reflects an essential role of MafB in early myeloid and monocytic differentiation. We observed that the expression of MafB in transformed chicken hematopoietic precursors dramatically increases the proportion of myeloid colony formation at the expense of multipotent progenitor-type colonies. In addition, the overexpression of MafB in transformed myeloblasts stimulates the rapid formation of macrophages, as judged by morphology, surface marker expression and functional criteria. MafB-induced macrophages exhibit typical levels of phagocytic activity and nitric oxide release after activation by lipopolysaccharide. By contrast, overexpression of the myeloid transcription factor PU.1 in these cells does not induce macrophage differentiation. Furthermore, a dominant-negative allele of MafB inhibits both myeloid colony formation and the differentiation of myeloblasts into macrophages. Taken together, our results indicate that MafB induction is a specific and essential determinant of the monocytic program in hematopoietic cells.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Jpn J Cancer Res
                Journal ID (iso-abbrev): Jpn. J. Cancer Res
                Journal ID (doi): 10.1111/(ISSN)1349-7006a
                Journal ID (publisher-id): CAS
                Title: Japanese Journal of Cancer Research : Gann
                Publisher: Blackwell Publishing Ltd (Oxford, UK )
                ISSN (Print): 0910-5050
                ISSN (Electronic): 1876-4673
                Publication date (Print): June 2001
                Volume: 92
                Issue: 6 ( doiID: 10.1111/cas.2001.92.issue-6 )
                Pages: 638-644
                Affiliations
                [ 1 ]Second Department of Internal Medicine, Nagoya City University Medical School, 1 Kawasumi, Mizuho‐chou, Mizuho‐ku, Nagoya 467‐8601
                [ 2 ]Aichi Blood Disease Research Foundation, 13‐2 Machikita, Moriyama‐ku, Nagoya 463‐0074
                [ 3 ]Third Department of Internal Medicine, Kyoto Prefectural University of Medicine, 465 Kawaramachi‐Hirokoji, Kamigyo‐ku, Kyoto 602‐0841
                [ 4 ]Department of Infectious Diseases, Nagoya University School of Medicine, 65 Tsuruma‐chou, Showa‐ku, Nagoya 466‐8560
                [ 5 ]Shimane Prefectural Central Hospital, 116 Imaichi‐chou, Izumo, Shimane 693‐8555
                [ 6 ]Department of Genetics, Institute for Developmental Research, Aichi Human Service Center, 713‐8 Kamiya‐chou, Kasugai, Aichi 480‐0392
                [ 7 ]Second Department of Internal Medicine, Aichi Medical University, 21 Karimata, Nagakute‐chou, Aichi‐gun, Aichi 480‐1195
                Author notes
                [*] [* ] To whom correspondence should be addressed. E‐mail: iida@ 123456med.nagoya-cu.ac.jp
                Article
                Publisher ID: CAE638
                DOI: 10.1111/j.1349-7006.2001.tb01142.x
                PMC ID: 5926752
                PubMed ID: 11429052
                SO-VID: 29b618b7-dd8a-4c98-b3e2-c99f407c55cc
                History
                Page count
                References: 21, Pages: 7
                Categories
                Subject: Article
                Custom metadata
                source-schema-version-number 2.0
                cover-date June 2001
                details-of-publishers-convertor Converter:WILEY_ML3GV2_TO_NLMPMC version:4.6.9 mode:remove_FC converted:04.11.2015

                Keywords: multiple myeloma,t(14;20)(q32;qll),mafb,ectopic expression
                Data availability:
                Keywords: multiple myeloma, t(14;20)(q32;qll), mafb, ectopic expression

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