Induction of Plasmacytomas With Silicone Gel Genetically Susceptible Strains of Mice

Potter, M; Morrison, Susan; Wiener, Francis; Zhang, Xiaokui K.; Miller, Frederick W.

doi:10.1093/jnci/86.14.1058

Cited by 87 publications

(38 citation statements)

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“…administration of small fragments of a silicone gel. 4 All mice were bred and maintained at our conventional mouse facility (PerImmune, Rockville, MD, USA) under NCI contract N01-BC-21075. Plasmacytomas were diagnosed by finding 10 or more hyperchromatic, atypical plasma cells in cytofuge specimens of ascitic cells that were obtained by abdominal paracentesis and stained with Wright-Giemsa.…”

Section: Induction and Diagnosis Of Plasmacytomasmentioning

confidence: 99%

“…1 In previous work we showed that the T(12;15) translocation comprises a very early and, most likely, initiating oncogenic event in the development of inflammation-induced peritoneal plasmacytomas. 2 Furthermore, the analysis of peritoneal inflammatory granulomas, the tissue site where plasmacytomas develop, 3,4 revealed that numerous T(12;15) + clones were commonly present during tumor latency long before frank malignant growth was observed. [5][6][7] These results suggested that translocated cells residing in inflammatory granulomata constitute a remarkably large and diverse pool of tumor precursor cells from which plasmacytomas could evolve.…”

Section: Introductionmentioning

confidence: 99%

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Clonal diversification of primary BALB/c plasmacytomas harboring T(12;15) chromosomal translocations

2000

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DNA sequence analysis of PCR amplified Igh/c-myc junction fragments of T(12;15) chromosome translocations and immunohistochemical determination of immunoglobulin isotype production were employed to study the clonal diversification of neoplastic translocated plasma cells that resided in peritoneal inflammatory granulomas of BALB/c mice harboring primary plasmacytomas. The diversity of plasma cells was found to take two major forms when the fine structure of the T(12;15) translocation was used as the clonotypic marker. First, mosaics of clones containing translocations that were apparently unrelated to each other were detected in nine out of 17 (53%) mice. Second, subclones derived from common T(12;15) + progenitors by either secondary deletions in translocation breakpoint regions or aberrant isotype switching near translocation breaksites were found in five of 17 (29.5%) mice. When Ig expression was utilized as the clonotypic marker, clonal mosaics were shown to occur in all mice. This was demonstrated by the finding that the prevalent IgA-or IgG-producing plasmacytoma clone was invariably accompanied by smaller clones of IgG-or IgA-expressing neoplastic plasma cells, respectively. These results provided new insights into the clonal diversification at the terminal stage of plasmacytomagenesis. In addition, they suggested that BALB/c plasmacytomas may be uniquely useful for studying clonal diversity during B cell oncogenesis, since clonal evolution can be evaluated in a pool of tumor and tumor precursor cells that is clearly defined by the T(12;15) chromosomal translocation and the production of monoclonal immunoglobulin. Leukemia (2000) 14, 909-921.

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Section: Induction and Diagnosis Of Plasmacytomasmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Clonal diversification of primary BALB/c plasmacytomas harboring T(12;15) chromosomal translocations

2000

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“…Plasma cell tumors arise in BALB/cAnPt mice following 5-12 months of chronic exposure to mineral oil, pristane, or silicone gels (Potter and Boyce, 1962;Potter, 1984;Potter et al, 1994a). These tumors require IL6 (Nordan and Potter, 1986;Hilbert et al, 1995), which activates the Ras/MAP kinase signal transduction pathway for growth (Ogata et al, 1997), and the JAK/STAT3 pathway for antiapoptotic survival factors (Puthier et al, 1999).…”

Section: Introductionmentioning

confidence: 99%

p16INK4a gene promoter variation and differential binding of a repressor, the ras-responsive zinc-finger transcription factor, RREB

et al. 2003

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“…Plasmacytomas arise in the peritoneal cavity of BALB/c mice upon induction by a variety of agents including chemical carcinogens such as pristane as well as oncogene containing retroviruses (Potter and Boyce, 1962;Anderson and Potter, 1969;Troppmair et al, 1989;Largaespada et al, 1992;Potter et al, 1994a). A common feature of virtually all pristane induced plasmacytomas is a transcriptionally deregulated c-myc gene (Shen-Ong et al, 1982;Adams et al, 1983;Potter and Wiener, 1992) resulting from a reciprocal chromosomal translocation which, in *90% of cases, involves chromosomes 12 and 15, (t(12;15)).…”

Section: Introductionmentioning

confidence: 99%

Chromosomal translocations deregulating c-myc are associated with normal immune responses

et al. 1997

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Plasmacytomas induced in BALB/c mice by pristane consistently evidence chromosomal translocations involving the c-myc gene and one of the Ig loci. This observation has lead to the suggestion that c-myc deregulation is a critical event in the generation of such tumors. However, it is not clear whether c-myc translocation is related to pristane treatment or occurs in normal lymphocyte populations nor whether such translocations occur normally, and at similar frequencies, in strains genetically resistant to plasmacytoma development, such as DBA/2. In order to address these questions, a Long Distance PCR assay with single copy sensitivity was employed to assess the frequency of cmyc/IgA translocations in normal and immunized mice of both plasmacytoma resistant and susceptible lineages in the absence of pristane treatment. Our data demonstrate that spontaneous translocations occur in normal DBA/2 and BALB/c mice with no signi®cant di erences in frequency. A 3 ± 5-fold increase in translocation frequency was observed in mice immunized with cholera toxin, a strong stimulator of IgA responses. We conclude that c-myc deregulation by chromosomal translocation is associated with normal physiological processes of B-cell di erentiation and, as such, can not be the determining factor leading to malignancy.

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Induction of Plasmacytomas With Silicone Gel Genetically Susceptible Strains of Mice

Cited by 87 publications

References 0 publications

Clonal diversification of primary BALB/c plasmacytomas harboring T(12;15) chromosomal translocations

Clonal diversification of primary BALB/c plasmacytomas harboring T(12;15) chromosomal translocations

p16INK4a gene promoter variation and differential binding of a repressor, the ras-responsive zinc-finger transcription factor, RREB

Chromosomal translocations deregulating c-myc are associated with normal immune responses

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