Disease relevance of Plasmacytoma

• Point mutations in the c-Myc transactivation domain are common in Burkitt's lymphoma and mouse plasmacytomas [1].
• The IgH 3' enhancer could therefore play a part in the activation of the translocated c-myc genes in rat immunocytomas, mouse plasmacytomas and Burkitt lymphomas [2].
• A major effect of indomethacin treatment was a reduction in the appearance of microscopic plasmacytomas that appear in the oil granuloma before plasmacytomas can be detected by routine sampling of the peritoneal exudate [3].
• Rapid induction of IgM-secreting murine plasmacytomas by pristane and an immunoglobulin heavy-chain promoter/enhancer-driven c-myc/v-Ha-ras retrovirus [4].
• An activity has been purified 350-fold from extracts of mouse plasmacytoma cells that forms 5-hydroxymethyluracil (alpha-hydroxythymine) and apyrimidinic sites with phage SPO1 DNA, which contains this base in place of thymine [5].

Psychiatry related information on Plasmacytoma

• A retroviral vector, RIM, containing murine c-myc under the control of immunoglobulin heavy-chain gene promoter and enhancer elements and v-Ha-ras driven by a Moloney murine leukemia virus long terminal repeat induced IgM-secreting plasmacytomas in 28% of adult and 83% of 3-week-old pristane-conditioned mice with mean latency periods of 60-70 days [4].

High impact information on Plasmacytoma

• Chromosome translocations between c-myc and immunoglobulin (Ig) are associated with Burkitt's lymphoma in humans and with pristane- and IL6-induced plasmacytomas in mice [6].
• The context of C mu sequences in DNA from a plasmacytoma secreting IgM differed from that in embryo DNA, as did C alpha sequences in two IgA- and several IgG-secreting plasmacytomas [7].
• Nonrandom chromosome changes involving the Ig gene-carrying chromosomes 12 and 6 in pristane-induced mouse plasmacytomas [8].
• Mouse plasmacytoma (MOPC) 460 cells contain two chromatographic forms of RNA polymerase III (IIIA and IIIB) in addition to the major class I and II RNA polymerases [9].
• In contrast, an analogous myc transgene, designed to mimic the myc-Igh translocation product typical of Burkitt's lymphoma and rodent plasmacytoma, promotes B lymphoid cell proliferation and predisposes mice to malignancy in pre-B and B lymphoid cells [10].

Chemical compound and disease context of Plasmacytoma

• The growth of primary plasmacytomas in transplant that is dependent on the pristane-conditioned peritoneal environment was not inhibited by indomethacin treatment [3].
• The many binding studies of monoclonal immunoglobulin (Ig) produced by plasmacytomas have found no universally common binding properties, but instead, groups of plasmacytomas with specific antigen-binding activities to haptens such as phosphorylcholine, dextrans, fructofuranans, or dinitrophenyl [11].
• The role of indomethacin in inhibiting plasmacytoma development was not established; two possibilities are that it inhibits production of mutagenic and tissue destructive oxidants by inflammatory cells, and it inhibits prostaglandin synthesis and intracellular production of oxidant biproducts [3].
• The present study deals with the identification of effector-cytotoxic cells that may be developed as a result of chemotherapy-induced tumor regression and their possible potentiation by active, specific immunization with melphalan- and glutaraldehyde-treated MOPC-315 plasmacytoma cells [12].
• BALB/c mice with the plasmacytoma MOPC 104E were cured of palpable tumors (6-15x10(7) cells) with a single injection of cyclophosphamide (10 mg/kg) [13].

Biological context of Plasmacytoma

• A rearranged c-myc oncogene was cloned from murine plasmacytoma ABPC17 in the expectation that it would reflect the t(6;15) chromosome translocation carried by this tumor [14].
• With these results in mind, we have determined the precise breakpoints within c-myc for two plasmacytoma lines in order to search for any common features that may shed some light on the mechanism of chromosomal translocation [15].
• These results suggest that HS1234 may function as a locus control region (LCR), deregulating c-myc expression in t(15;12) plasmacytomas, as well as potentially contributing to aspects of normal IgH chain expression [16].
• Restricted immunoglobulin variable region (Ig V) gene expression accompanies secondary rearrangements of light chain Ig V genes in mouse plasmacytomas [11].
• DNA rearrangement and constitutive expression of the interleukin 6 gene in a mouse plasmacytoma [17].

Anatomical context of Plasmacytoma

• The level of c-myc RNA in the fibroblast tumors was similar to that found in mouse plasmacytomas [18].
• In this report we describe rearrangement of c-mos in a second mouse plasmacytoma, NSI, and in two hybridomas [19].
• Molecular cloning of the complementary DNA predicts that BSF-2 is a protein of relative molecular mass (Mr) 26,000 similar or identical to interferon beta 2, hybridoma plasmacytoma growth factor and hepatocyte stimulating factor [20].
• The transcription factor Pax5 activated endogenous mb-1 transcription in a plasmacytoma cell line, but could not when the promoter was methylated [21].
• CD19 transcripts are restricted to members of the B cell lineage, being most abundant in pre-B cell lines and least abundant in plasmacytomas [22].

Gene context of Plasmacytoma

• Since IL-6 functions as a potent growth factor for murine plasmacytomas, over-expression of abnormal IL-6-R may function as a positive selection element for the development of certain plasmacytomas [23].
• Oncostatin M, leukemia inhibitory factor, and interleukin 6 induce the proliferation of human plasmacytoma cells via the common signal transducer, gp130 [24].
• These results demonstrate that mast cell-derived Ang-1 promotes the growth of plasmacytomas by stimulating neovascularization and provide further evidence supporting a causal relationship between inflammation and tumor growth [25].
• Rapamycin, a specific inhibitor of FRAP, did not inhibit growth of plasmacytoma cell lines [26].
• However, the kappaB binding complex in the plasmacytomas that were examined lacked c-Rel and instead contained only a p50-related protein [27].

Analytical, diagnostic and therapeutic context of Plasmacytoma

• The IgG1 fractions of C3H and CBA anti-BALB/c globulins were tested for their effect on growth of the BALB/c plasmacytomas MOPC-315 and MOPC-460 in C3H and CBA mice by incubation with the tumor cells before transplantation and by injection periodically thereafter into the hosts [28].
• Cloning, restriction mapping, heteroduplex analyses, and sequence analyses of the nonproductively rearrange C alpha genes from two plasmacytomas, M603 and M167, have demonstrated that the nonproductive rearrangement occurs within the alpha switching region, S alpha [29].
• The IAP elements expressed in plasmacytoma MPC11 were characterized by sequence analysis of 22 cDNA clones [30].
• We describe the purification to apparent homogeneity of the murine immunoglobulin heavy-chain (IgH) enhancer-binding protein mu EBP-E from murine plasmacytoma cells by ion exchange and affinity chromatography [31].
• Conversely, of the 4 pRB(+) HCLs and 3 pRB(+) plasmacytomas, only 1 of each was cyclin D1(+). pRB appeared to exist primarily in the underphosphorylated (fastest migrating) form on Western blot, despite the fact that cyclin D1 was complexed to CDK4, a form in which it normally phosphorylates pRB [32].

References