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Query: UMLS:C0155339 (Brown)
 12,436 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Transplantable Brown-Pearce carcinoma was adapted successfully in the rabbit anterior chamber. Regression of tumor growth was attained on tri-weekly perfusion of the AC with 10 micromolar of methotrexate. Tumor cyclic nucleotide phosphodiesterase (PDE) and protein activator were found to be markedly depressed during the course of chemotherapy and the PDE cAMP/cGMP ratio was similarly altered. Corroborative light and electron-microscopic studies showed specific alterations of intracellular organelles in relation to MTX and tumor cell death. These findings suggest that metabolic pathways of cyclic nucleotides are important biochemical modulators of neoplastic cells. The method of intraocular perfusion precludes systemic toxic effects and avoids compromising the animals' immunocompetence.
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PMID:Experimental intraocular malignancy: the effect of intracameral perfusion. 23 85

Brown Norway and Lewis rats were challenged with a Brown Norway Moloney sarcoma tumor, MST-1, admixed with nonimmune peritoneal exudate macrophages syngeneic to the host; or admixed with nonimmune peritoneal exudate macrophages and hyperimmune anti-MST-1 antibodies. In vivo growth of MST-1 in BN and Lewis rats was inhibited by admixing Brown Norway or Lewis macrophages, respectively, with BN anti-MST-1 antibodies. The inhibiting BN antibodies were of the IgG2 class, lacking IgG2a antibodies. Brown Norway anti-MST-1 of IgG2 class without macrophages did not affect growth of MST-1. Brown Norway and Lewis anti-MST-1 antibodies of IgG2a class enhanced tumor growth, whether admixed with macrophages or not. Anti-MST-1 antibodies of IgM and IgG1 classes did not influence tumor growth. Peritoneal exudate macrophages removed from Lewis donors 8 to 10 days after inoculation of MST-1 inhibited completely growth of the challenge tumor; macrophages of Brown Norway origin were inhibitory only when harvested from hyperimmune donors, that is, 40 or more days after inoculation of MST-1. Macrophages from hyperimmune donors were specifically cytotoxic to MST-1 and did not inhibit an unrelated syngeneic BN tumor of chemical origin.
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PMID:Effect of macrophages and antibodies on in vivo growth of Moloney sarcoma in the rat. 30 84

In animals with Brown--Pearce carcinoma electric stimulation of the hypothalamus makes it possible to model an increased corticosterone level in blood at early stages of the tumor growth, which conditions more active development of antitumor reactions and consequently an enhanced tumor resorption. The increased level of free corticosterone seems to be essential for "triggering" and an active mode of proceeding of antitumor immune reactions.
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PMID:[Effect of hypothalamic electrostimulation on the 11-hydroxy-corticosteroid content in the blood and on the immunological indices in rabbits with Brown-Pearce carcinoma]. 46 51

Thirty-one cervical carcinomas have been studied immunohistochemically to determine tumor growth fraction by using the monoclonal antibody Ki-67, which reacts with a nuclear antigen expressed only by proliferating cells. The growth fraction of individual tumor is estimated as the percentage of stained nuclei in a population of 1000 tumor cells. There is a good correlation of the growth fraction measured by Ki-67 with mitotic index and high histological grade of cervical carcinoma. This study, together with that of D. C. Brown, D. Cole, K. C. Gatter, and D. Y. Mason [Brit. J. Cancer 57(2), 178-181 (1988)], shows the usefulness of Ki-67 in the evaluation of growth fraction in cervical carcinoma.
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PMID:Tumor growth fraction in cervical carcinoma. 198 15

ZME-018 monoclonal antibody (MAb, IgG2a subclass, 0.04 mg), recombinant human tumor necrosis factor-alpha (rHuTNF-alpha, 10(4) units), and recombinant human interferon-gamma (rHuIFN-gamma, 10(6) units) were injected intravenously into athymic nude mice bearing human malignant melanoma (Brown C5513) xenografts. Sixty-four animals were injected subcutaneously with 0.2 ml tumor chunks 4 days prior to administration of one or more of the treatments. The mice were randomized into eight groups so that mean tumor volume/group before initiation of treatment was similar (212-360 mm3); (a) saline, 2X; (b) rHuTNF-alpha, 1X; (c) rHuIFN-gamma, 1X; (d) ZME-018, 1X; (e) rHuIFN-gamma + rHuTNF-alpha, 1X each; (f) rHu-IFN-gamma + ZME-018 + rHuTNF-alpha, 1X each; (g) rHuTNF-alpha + ZME-018, 2X each; (h) rHuTNF-alpha + ZME-018, 3X each. The order of administration of the agents in those groups given more than one modality is as shown above and each injection was separated by a 24 h period. Tumor volume was measured daily for 9 days after the beginning of treatment. Compared to control mice, minimal suppression of tumor growth was noted when ZME-018, rHuTNF-alpha, or rHuIFN-gamma was used singly, but significantly (p less than or equal to 0.05) slower tumor progression occurred in animals given rHuIFN-gamma + rHuTNF-alpha or ZME-018 + rHuTNF-alpha when compared to controls. Histopathologic analyses of tumor biopsies obtained at 1 and 4 days after the last treatment for each group indicated that 15-95% necrosis was present. Necrosis was most striking in the animals given rHuIFN-gamma + rHuTNF-alpha or the ZME-018 MAb alone. However, the group receiving all three agents exhibited a tumor growth rate similar to that seen in the controls and demonstrated minimal necrosis. These results suggest that ZME-018, rHuIFN-gamma, and rHuTNF-alpha may be useful in the treatment of human melanoma. However, the effects of administration of all three of these agents in a single host needs to be evaluated further.
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PMID:Effects of monoclonal antibody, recombinant interferon-gamma, and tumor necrosis factor-alpha in the treatment of human melanoma xenografts. 251 78

At -1, 0, +1 weeks from tumor inoculation, carrageenan-impregnated cotton sponges were subcutaneously implanted. Tumor BN472, a malignant adenocarcinoma, was transplanted in syngeneic Brown Norway female rats, either subcutaneously or intravenously. Plasma eicosanoid values (prostaglandin-E2, thromboxane-B2 and 6-keto-prostaglandin-F1 alpha) were determined as well as the cellular immune response (natural killer activity, concanavalin-A and phytohemagglutinin stimulation of spleen lymphocytes). Primary tumor growth and the number of tumor foci in the lungs were measured as parameters of tumor growth and dissemination. No statistically significant differences were observed in primary tumor growth. However, the number of metastatic foci in the lungs of rats in which the tumor was implanted subcutaneously, as well as those in which the tumor was inoculated intravenously, was significantly reduced in those that had carrageenan implanted one week after tumor inoculation. In all other carrageenan-treated groups only slightly reduced numbers of metastatic foci were seen. In those rats with a decreased number of tumor metastatic foci in the lungs, no correlation could be shown with either altered plasma prostaglandin levels, or cellular immune response.
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PMID:Inhibition of tumor metastasis by carrageenan-induced granulomas. 290 26

The effect of 13-cis-retinoic acid (13-cis-RA) on 1,2-dimethylhydrazine (DMH)-induced colon cancer in male, random bred, Sprague-Dawley (S-D) and inbred Wister/Furth (W/Fu) rats and on isograft tumor growth and metastases in a Brown Norwegian (BN) X W/Fu F1 rat was studied. 13-cis-RA (300 mg/kg diet) was administered to S-D rats 1 week before commencing DMH injections and for the duration of the experiment. W/Fu rats received 13-cis-RA (10 mg/kg weight X 5 days) 6 weeks after DMH injection had begun and monthly thereafter. Primary tumors were detected by serial laparotomy under ether anesthesia in both strains. The time to tumor onset was significantly delayed in treated groups, S-D and W/Fu, P = 0.0339 and 0.0322, respectively (Mantel-Haenszel test), compared with placebo-treated controls. 13-cis-RA (15 mg/kg weight) administered 2 days before and for the duration of isograft tumor growth (DMH 2054, a well-differentiated mucin-producing colon adenocarcinoma that spontaneously metastasized to lung) had no effect on tumor growth or metastasis in the BN X W/Fu F1 rat. The findings suggest that the role of 13-cis-RA is in colon cancer prevention and not in its treatment either in an adjuvant or established setting.
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PMID:Effect of 13-cis-retinoic acid on tumor prevention, tumor growth, and metastasis in experimental colon cancer. 348 Mar 91

Diets high (17.7 cal%) and low (3.3 cal%) in linoleic acid were given to groups of Brown Norway female rats before and after inoculation of syngeneic tumor models with different characteristics, with regard to tumor spread, malignancy, immunogenicity, growth rate, rat strain, and histopathological features. Despite the differences in characteristics, in most tumor models, tumor growth was identical in both experimental groups. However, in 2 tumor models, an adrenal cortical carcinoma and a myeloid leukemia, differences in growth were noted. In rats given the diet low in linoleic acid, growth of the cortical carcinoma was significantly increased, whereas the opposite effect was seen in rats with myeloid leukemia.
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PMID:Influence of the linoleic acid content of the diet on tumor growth in transplantable rat tumor models. 396 48

Circulating immune complexes (CIC) were quantitated by a Raji cell radioimmunoassay in sera from Brown Norway rats bearing progressing or regressing methylcholanthrene-induced sarcomas. Quantitative profiles of CIC over time were related to tumor dose, tumor mass, and the regressive or progressive course of tumor growth. Animals bearing progressing tumors demonstrated an initial peak of CIC levels by 7 weeks but thereafter displayed a persistent decline in quantities of CIC despite continued tumor growth. Animals bearing regressing tumors were found to have a more directly proportional relationship between the tumor mass and the levels of CIC, but the appearance and disappearance of CIC lagged slightly behind the appearance and disappearance of the tumor. These data are almost identical to data previously published detailing quantities of CIC in BN and Lewis rats bearing Moloney sarcomas and are similar to fluctuations in CIC observed in animals and humans hosting a number of disparate neoplasms.
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PMID:Consistent fluctuations in quantities of circulating immune complexes during progressive and regressive phases of tumor growth. 740 17

Estrogen treatment to rats of the Fischer 344 (F344) strain induces growth of pituitary tumors that exhibit accelerated cell proliferation, breakdown of basement membrane, and formation of hemorrhagic lakes. Estrogen-dependent pituitary growth is due to variation in a group of quantitative trait loci (QTL), called Edpm for estrogen-dependent pituitary mass, that we previously identified in an F(2) intercross of F344 and the tumor-resistant Brown Norway strain. We previously identified 5 QTL, and microsatellite markers developed since our earlier work have allowed us to scan new chromosomal regions, resulting in two new QTL for estrogen-dependent pituitary mass: Edpm9-2 and a possible QTL on the X Chromosome (Chr). Here we report evidence that these QTL differ from each other in how they affect growth. To examine the effect of the Edpm QTL on biochemical components of tumor growth, we tested their effects in 138 progeny of a backcross to the F344 strain which were given a 10-week chronic estrogen treatment. Hemoglobin/DNA ratio (a measure of blood volume relative to cell number) and total pituitary DNA (a measure of cell number) correlated only weakly, and very large pituitaries were observed which had a low hemoglobin/DNA ratio resembling a normal gland. Through QTL mapping, we found that Edpm2-1, Edpm3, Edpm5, and Edpm9-2 all had significant effects on pituitary mass, but Edpm2-1 and Edpm9-2 primarily affected DNA content, Edpm5 primarily affected hemoglobin/DNA ratio, and Edpm3 affected all traits equally.
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PMID:Different functions of QTL for estrogen-dependent tumor growth of the rat pituitary. 1100 99


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