Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0153470 (Spleen)
 4,015 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Spleen cells of C57BL/6J mice bearing a poorly immunogenic syngeneic tumor T241 have been shown to suppress the mitogen-induced proliferative responses of normal spleen cells. However, no suppressive effect of these cells was observed on the generation of cytotoxic cells following immunization in vitro against H-2 histocompatibility antigens. The suppressor activity disappeared rapidly after the removal of the primary tumor. Spleen cells of tumor-bearing mice also suppressed the mitogen-induced stimulation of normal spleen cells of mice of different H-2 loci. Removal of phagocytic cells with carbonyl iron treatment had very little effect on the suppressor activity. Suppressor activity was enhanced following fractionation of cells through nylon wool columns. The suppressor population was found to resist anti-immunoglobulin serum and complement treatment, but treatment with anti-thymocyte serum and complement drastically reduced the suppressor activity. These results indicate that cells with suppressor activity have characteristics of T-lymphocytes.
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PMID:Presence of suppressor cells in spleens of mice bearing a weakly immunogenic syngeneic tumor. 31 43

The cell-mediated immune response against a transplantable syngeneic metastatic solid tumor in mice was studied. The immune reactivity of spleen cells from tumor-bearing mice was found to vary during development of the tumor. For about a week after tumor transplantation, the spleen cells were able to protect recipient mice against challenge with tumor cells. Subsequently, the protective activity was replaced by an enhancing activity. Recipient mice that received tumor cells together with spleen cells from mice bearing tumors for about two or three weeks had a higher incidence of tumor takes and larger tumors than controls. This enhancement of tumor development was correlated with the size of the local tumor or metastases in the donors. The enhancing activity was found to be mediated by T lymphocytes and appeared to suppress the protective immune response of the recipients. We devised a system to strengthen the immune response of the host against the development of tumor metastases. In the tumor model used, removal of the local tumor after s.c. transplantation failed to prevent the development of lung metastases and death in most of the mice. However, syngeneic spleen cells which had been sensitized in vitro against tumor cells were found to serve as immunotherapeutic agents. Injection of such spleen cells into mice from which primary tumor implants had been removed surgically led to a markedly increased survival. Spleen cells from both normal and tumor-sensitized donors were effective, but splenocytes from mice bearing large tumors did not reduce metastatic development after sensitization in vitro. Thus, protection against the development of lethal metastases can be achieved with certain types of lymphocytes sensitized in vitro.
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PMID:A syngeneic metastatic tumor model in mice: the natural immune response of the host and its manipulation. 108 80

Different spleen and tumor cell factors modifying tumoral and metastatic growth were studied. Spleen cell culture supernatants (SCS) from small and large tumor-bearing mice enhanced tumor growth. After tumor surgery, tumor enhancement was only mediated by supernatants from large tumor resected mice. Tumor facilitation and angiogenic response were mediated by the same supernatants; different fractions for these two activities were characterized. T and non-T cells, depending on tumor burden, were responsible for the enhancing activity; but angiogenesis depended only on T cells. While augmentation of metastatic spread was produced by tumor antigens (soluble tumor extracts, tumor-cell supernatants, formolized tumor cells), primary tumor development was not modified by tumor-cell supernatants. Increased incidence of metastases was also mediated by SCS from tumor resected mice which had previously been inoculated with tumor antigens. Immune status of tumor-resected mice was evaluated by delayed-type hypersensitivity reaction. Tumor cell membranes enriched with cholesterol-hemisuccinate were able to increase anti-tumor immune response.
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PMID:[Immunoregulation of tumor growth in a murine model]. 248 20

Intracameral inoculation of allogeneic P815 mastocytoma cells (DBA/2) into BALB/c mice resulted in progressively growing intraocular tumors. Intraocular tumor cells disseminated rapidly to the spleen and cervical lymph nodes, yet extraocular nests of tumor cells never developed into fulminant tumors. Further experiments showed that tumor cells were continuously seeded from the primary intraocular tumor and were rapidly cleared from extraocular sites. Hosts harboring intraocular P815 mastocytomas rejected tumorigenic doses of P815 cells inoculated subcutaneously or even into the contralateral anterior chamber. This systemic tumor immunity was found to be radiosensitive and T cell dependent. Spleen cells from animals with progressively growing intraocular tumors protected recipient mice challenged with intracamerally inoculated tumor cells and thus suggests that a cell-mediated mechanism is the underlying basis for this form of tumor immunity. The data indicate that mice harboring progressively growing intraocular tumors develop a potent state of "concomitant immunity," that prevents the development of metastases, yet is ineffective in controlling the primary tumor.
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PMID:Intracamerally induced concomitant immunity: mice harboring progressively growing intraocular tumors are immune to spontaneous metastases and secondary tumor challenge. 641 74

Adenocarcinomas were induced in the prostate-seminal vesicle complex of Lobund-Wister (L-W) rats by a single IV inoculation of N-methyl-N-nitrosourea. This was followed by three slow-release S.C. implants of testosterone propionate, each at intervals of 2 months. Small (0.5 cm diameter) palpable tumors developed which enlarged during the following month to 3-4 cm diameter. At the latter stage, tumor cells spread via lymphatics to the lungs and/or by direct extension into the peritoneal cavity. Rats with small palpable tumors were inoculated IV with viable Bacillus Calmette-Guerin (BCG). One month later, the rats were killed and examined. Untreated rats with large tumors served as controls. Comparison of the two groups revealed that body weights and tumor sizes were similar and most of them had developed metastatic tumors in the peritoneal cavity. However, lung metastases were rare in the BCG-inoculated rats compared to controls. Spleen and liver weights were significantly heavier in the BCG-treated rats. It is speculated that an intra-vascular mechanism(s), engendered by BCG, immobilized the circulating tumor cells, but not those tumor cells that spread by direct extension from the primary tumor into the peritoneal cavity.
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PMID:The antimetastatic effect of IV-inoculated BCG on adenocarcinomas in the prostate-seminal vesicle complex of L-W rats. 807 91

Spleen cells from mice bearing late-stage methylcholanthrene-induced tumor did not show any tumor activity when mixed with tumor cells in Winn's assay. Treatment of these mice with cyclophosphamide (CY) induced a tumor-inhibitory activity in spleen, occurring on day 7 after treatment, reaching its maximum on day 11 and disappearing by day 21. This antitumor activity could not be induced in control, tumor-free or T-deficient tumor-bearing mice. CY-induced tumor-inhibitory activity was immunologically specific, and mediated by Thy-1+, L3T4-, Ly-2+ cells. Contrary to spleen cells from untreated tumor-bearing mice, spleen cells from CY-treated tumor-bearing mice did not suppress the antitumor activity of immune spleen cells in Winn's assay. However, in contrast to immune spleen cells, CY-induced tumor-inhibitory cells did not manifest antitumor activity when transferred systemically (i.v.) into T-cell-deficient tumor-bearing mice. Even more, spleen cells from CY-pretreated mice, harvested 7-15 days after the drug administration, partially suppressed the antitumor activity of concomitantly transferred spleen cells from specifically immune mice. Nevertheless, CY-pretreated mice manifested concomitant immunity, i.e. these mice exhibited higher resistance to a second inoculum of the same tumor than did nontreated mice or even mice with excised primary tumor.
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PMID:The influence of cyclophosphamide on antitumor immunity in mice bearing late-stage tumors. 809 55

We investigated possible mechanisms of the antitumor action of gamma-(9H-purine-6-yl) thiomethyl L-glutamate (6-MPG), a water-soluble derivative of 6-MP. In the double grafted tumor system, BALB/c mice were inoculated intradermally with 10(6) cells of MethA fibrosarcoma at the right inguinal region on day 0 (the primary tumor) and later with 3 x 10(6) cells at the left on day 10 (the secondary tumor). Intraperitoneal administration of 6-MPG at a dose of 100 mg/kg/day from day 3 through 7 completely prevented growth of the secondary tumor. 6-MPG showed no effect on growth of colon 26 adenocarcinoma cells inoculated in place of the secondary MethA cells (antigen specificity). 6-MPG did not inhibit the secondary MethA growth in the BALB/c (nu/nu) mouse. The inhibitory effect of 6-MPG on the secondary tumor growth was diminished by prior treatment of the primed animals with cyclosporin A and anti-Thy antibody. Spleen cells from the tumor-bearing mice treated with 6-MPG showed a tumor-neutralizing activity (Winn assay). Treatment of the spleen cells with anti-CD8 antibody plus complement diminished the tumor-neutralizing effect but that with anti-CD4 antibody plus complement did not, indicating that CD8-positive cells are responsible for potentiation of the tumor immunity. These results suggest that the antitumor effect of 6-MPG against the secondary tumor is elicited by augmenting tumor specific T-cell production.
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PMID:Study on the mechanism of immunopotentiating antitumor effect of 6-MPG, a water-soluble derivative of 6-mercaptopurine. 928 48