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Query: UMLS:C0079731 (B-cell lymphoma)
 16,671 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

SJL/J mice are a genetically low-NK strain, and their cytotoxic activity cannot be augmented with conventional NK inducers. In contrast, effector cells taken from the lymphoid tissues of SJL mice bearing a syngeneic B cell lymphoma (RCS) show variable, but significant levels of cytotoxic activity against NK-susceptible targets, such as YAC-1. Previous results suggested that the RCS cells themselves contributed to this cytotoxicity. However, results presented here indicate the most, if not all of the activity present within the lymphoid tissues of RCS-bearing mice is mediated by RCS-activated, host NK cells. These results were confirmed by in vitro studies, which demonstrate that both gamma irradiated (gamma-) RCS cells and gamma-allogeneic spleen cells induce cytotoxic activity in SJL spleen cells against YAC targets. However, the cytotoxicity induced by gamma-allogeneic cells is mediated largely by lymphokine-activated killer (LAK) cells, since these effectors also lyse NK-resistant target cells, such as L1210. In contrast, the cytotoxic effector cells that are induced by syngeneic gamma-RCS cells cause lysis of YAC targets, but not L1210 target cells. These data indicate that the syngeneic B cell lymphomas of SJL mice are a unique stimulus for host NK cells in this strain. Since activated NK cells produce a variety of lymphokines, RCS stimulation of host NK cells in SJL mice may provide some of the growth-promoting lymphokines that are known to be necessary for progressive growth of these lymphoma cells.
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PMID:Syngeneic B lymphoma cells provide a unique stimulus to natural killer (NK) cells in genetically low-NK SJL/J mice. 198 85

The spontaneously arising B-cell lymphoma (la+ reticulum cell sarcoma, RCS) in SJL/J mice has been shown to depend on host CD4 T cells for proliferation and growth. Treatment of mice with CD4 monoclonal antibody (mAb) prior to or after inoculation of a lethal dose of RCS tumor cells inhibits cell growth and the mice survive. The mechanism of tumor growth inhibition was studied by adoptively transferring cells from CD4 mAb treated tumor bearers into naive syngeneic mice. The recipient mice developed tumors and died. Tumor growth was dependent on the concentration of the adoptively transferred tumor cells. These results suggested that a state of tumor dormancy was established in the treated mice. Tumor dormancy was long lasting, as cells transferred as late as 11 weeks after the initial RCS inoculation still developed tumors in the recipient. The maintenance of dormancy was not due to failure of the recipient mice to mount an anti-tumor response or to the induction of suppressor cells. These results suggest that in the absence of CD4 cells, the RCS tumor remains dormant and this state of dormancy persists for long periods after total recovery of the CD4 cell subpopulation. Thus, it appears that RCS proliferation and growth is dependent on host CD4 cells but maintenance is under the influence of other cells or factors. Further characterization of this tumor dormant system and its regulation by the host may reveal novel mechanisms of tumor dormancy.
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PMID:Regulation of B-cell lymphoma growth in syngeneic SJL/J mice. establishment of tumor dormancy following administration of anti-CD4 monoclonal antibody into tumor-bearing mice. 823 Dec 49

Spontaneous germinal center (GC)-derived B cell lymphomas of SJL mice (RCS) transcribe a 1.8-kb Mtv-29 mRNA under control of the META-env promoter. The encoded vSAg29 stimulates syngeneic Vbeta16(+) CD4(+) T cells, thereby acquiring T cell help necessary for RCS growth. Other strains of B cell lymphoma-prone mice include Mtv29(+) C57L and MA/MyJ, and the Mtv29(-) Mtv7(+)-recombinant inbred strain, SW x J-1. The lymphomas of these mice produce similar mouse mtv-vSAg-encoding mRNA, as characterized by Northern blotting, PCR, and RNase protection. A 1.8-kb mRNA in C57L/J and MA/MyJ lymphomas hybridized with an Mtv29-specific oligonucleotide, whereas SW x J-1 lymphomas produced 1.8-kb transcripts hybridizing with an Mtv7-specific oligonucleotide. Similar META-env-initiated transcripts were absent from LPS-activated B cells from any strain examined but were detected in Peyer's patch RNA from SJL mice. Like typical SJL-derived RCS, all these lymphomas stimulated syngeneic CD4(+) T cells and Vbeta16(+) T hybridoma cells. Immunohistochemical staining of primary tumors showed the presence of peanut agglutinin binding (PNA(+)) highly mitotic lymphoblasts, suggesting their GC derivation. The findings indicate that this novel mRNA for Mtv29 is present in B cell lymphomas from several Mtv29(+) mouse strains. Additionally, this is the first description of the ability of Mtv7 to produce transcripts that are controlled and spliced identically to those of Mtv29 and that are expressed in SW x J-1, I-A(s+), lymphomas that also stimulate Vbeta16(+) T cells. Our results suggest an important role for mouse mtv-vSAgs and Vbeta16 T cell stimulation in the development of GC-derived murine B cell lymphomas.
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PMID:META-controlled env-initiated transcripts encoding superantigens of murine Mtv29 and Mtv7 and their possible role in B cell lymphomagenesis. 1131 79