Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0027651 (tumor)
 685,946 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

L-Asparagine synthetase appears in serum approximately 7 days after the s.c. implantation of 1 X 10(5) cells of Leukemia 5178Y/AR (resistant to L-asparaginase) and increases in activity as the neoplasm grows and metastasizes. The principal source of the enzyme is the primary tumor. After intravranial inoculation of tumor, the rate of leakage of the enzyme is more pronounced than when the subcutaneous, intramuscular, or intraperitoneal routes are used. 1-(2-Chloroethyl)-3-cyclohexyl-1-nitrosourea (NSC 79037), a nitro-sourea effective in the palliation of L5178Y/AR, temporarily halts the influx of enzyme into the blood stream, as does surgical excision of the s.c. tumor nodules. Treatment of mice with L-asparaginase within 24 hr of inoculation of the tumor markedly augments both tumor growth and the rate of penetration of L-asparagine synthetase into the circulation. Several other L-asparagine synthetase into the circulation. Several other L-asparaginase-resistant tumors also were found to spill L-asparagine synthetase into the serum, but the correlation between this phenomenon and the specific activity of the enzyme in homogenates of the tumor was imperfect.
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PMID:L-Asparagine synthetase in serum as a marker for neoplasia. 1 81

The growth of an ascitic murine plasmacytoma, MOPC 315, can be retarded in CAF1 hybrid host mice by the i.p. injection of donor lymphoid cells. The graft-vs-host reaction can be established by a variety of donor cells, including parental BALB/c and A/J and congenic inbred B10.D2 which share the major histocompatibility locus with BALB/c(H-2d). Optimal results are consistently obtained when parental BALB/c spleen cells are injected before tumor inoculation, and a second dose of donor spleen cells injected 1 week later. This aloogeneic effect on tumor growth is manifested by delayed appearance of the tumor and prolonged host survival. Pathologic studies on the ascites tumor indicated that the allogeneic effect suppresses the initial appearance and early growth of the plasmacytoma. However, once established, MOPC 315 grows rapidly and fatally in both control mice and recipients of donor lymphoid cells. Further, a subcutaneous implant of MOPC 315 is suppressed by an allogeneic effect established either i.v. with BALB/c spleen cells before tumor inoculation or by BALB/c spleen cells administered subcutaneously at the time of MOPC 315 implant. Thirty percent of mice treated by i.v. or subcutaneous donor lymphoid cells were tumor free at 150 days after tumor inoculation.
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PMID:The allogeneic effect on tumor growth. II. Suppression of both ascitic and solid MOPC 315 plasmacytoma by the graft-vs-host reaction, with pathologic correlation. 1 35

In DA X Wistar F1 rats, growth of 10(4) Wistar-specific Sp 1 carcinoma cells s.c. was commonly prevented by a mild subclinical graft=versus-host reaction produced by injecting 50 X 10(6) Wistar spleen cells i.p. either concurrently with the tumor or 7 to 14 days previously, Spleen cells alone had no effect on established tumor, but their injection on Day 14 significantly reduced the recurrence rate after excision of tumor on Day 21. In vitro tests in tumor-bearing rats with graft-versus-host reactions showed increased spleen lymphocyte and serum cytotoxicity; these mechanisms may inhibit tumor growth in vivo. Because Wistar lymphocytes and Sp 1 cells are syngeneic, inhibition of tumor cannot be due to allograft rejection but is probably an effect of increased host immunoreactivity during the graft-versus-host reaction.
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PMID:Effects of graft-versus-host reaction on inhibition of tumor growth in vivo and on tumor cytotoxicity in vitro. 1 23

We tested the cyclophosphamide effects against the growth of adenovirus-transformed cells and the subsequent tumor development in the syngeneic host. Cyclophosphamide did not show any effect on the tumor evolution when injected 24 and 6 hours before cell implantation. Cyclophosphamide injected 24 or 39 hours after cell implantation prevented or retarded the tumor growth. In mice bearing palpable tumors, it induced their complete regression in 85,7% of the animals, but did not effect the development of the homograft immunity.
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PMID:Effect of cyclophosphamide on syngeneic transplantation of adenovirus 12-transformed tumor cells in C3H/he mice. 2 Sep 3

A significant tumor damaging effect (growth inhibition) on transplanted syngeneic sarcoma in mouse was obtained by means of pH-dependent activation of a transport form of a cancerostatic drug by an enzyme foreign to the organism. This effect was achieved by combined administration of 8-0-(alpha-L-arabinofuranosyl)beta-peltatin-A as a transport form of beta-peltatin-A and the exogenous enzyme alpha-L-arabinofuranosidase from Aspergillus niger and additional increase of the acidity of the tumor by injection of glucose. The combined application of the transport form plus enzyme showed a more favorable effect on selectivity than free peltatin when a quantitative comparison was made between the tumor growth inhibition and the damage to the blood picture.
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PMID:Experiments to increase the selectivity of tumor chemotherapy by means of in vivo activation of transport forms of cancerostatics by exogenous enzymes. 2 45

The effects of dietary-induced acidosis on the growth and rates of complete regression of Sarcoma 180 in mice have been studied. The experiments here reported have demonstrated that mineral acidification of laboratory food produces a late decrease in tumor growth and significantly increases the rates of complete tumor regression. Blood acid-base studies also demonstrate the effects of these diets in altering the acid-base balance, and seemingly, this is independent of starvation and/or ketosis. The relationships of such in vivo acid-base metabolic changes to the control of tumor metabolism are briefly discussed. A therapeutic potential for this preliminary approach is considered.
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PMID:Effects of systemic acidification of mice with Sarcoma 180. 4 Jun 91

The proteinase activity was assayed in the leukemia cells L 1210 and in the ascites fluid with [3H] acetylated haemoglobin as a substrate. The proteinase activity at pH 4.1 increased in cells and in the ascites fluid with age of the tumor. The proteinase activity at pH 7.8 was low, but the enzyme activity in the cell homogenate increased between 5th and 7th day of the tumor growth and it was also present in the ascites fluid. It was observed that the leukemia cells aggregate in vivo and in vitro at pH values of the ascites fluid above pH 7.0. It was suggested, that the aggregation of leukemia cells is due to the tumor cell proteinase activity released to the ascites fluid.
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PMID:Proteinase activity and agglutination of leukemia cells. 4 19

A 53 year old woman presented with diabetes mellitus, hyperglucagonemia (600 to 1,500 pg/ml), clinical hyperparathyroidism and an abdominal mass diagnosed on biopsy as an islet cell carcinoma. Glucagon content of the tumor was 0.78 mug/g wet weight. Hourly blood samples during a 24 hour period revealed a direct correlation between plasma glucose and glucagon. The oral administration of glucose paradoxically increased whereas the intravenous administration decreased plasma glucagon. Circulating glucagon levels were markedly increased with arginine and epinephrine infusion. Both short- and long-term administration of alpha adrenergic blockade depressed the glucagon response to epinephrine infusion. In contrast, long-term alpha adrenergic blockade increased glucagon secretion despite improved glucose tolerance during a second 24 hour study. Although the patient demonstrated overt clinical and chemical findings of hyperparathyroidism, parathyroid hormone (PTH) was not detected in her plasma. The pattern of tumor growth was consistent with an origin from pancreatic islets. We conclude that (1) the tumor was responsive to physiologic stimuli known to affect glucagon secretion; (2) elevations of plasma glucagon levels with oral and dietary glucose suggest regulation of secretion by intestinal factors; and (3) improvement of glucose tolerance with alpha adrenergic blockade may be related to increased insulin secretion.
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PMID:Uncontrolled diabetes mellitus and hyperglucagonemia associated with an islet cell carcinoma. 4 4

In vitro lymphocyte stimulation by mitomycin-C-blocked tumor cells has been used to demonstrate tumor-specific antigens in syngeneic murine systems and to follow the evolution of tumor immunity with the tumor-bearing state. Mitomycin-blocked tumor cells stimulated syngeneic lymphocytes from normal mice, from those bearing small tumors (less than 1 cm in diameter) and from tumor-immune mice, sensitized by tumor-cell inoculation and subsequent tumor removal, to undergo increased DNA synthesis as measured by the incorporation of tritiated thymidine. However, lymph-node cells from mice bearing tumors over 1 cm in diameter appeared to be maximally stimulated in vivo and incapable of further stimulation by the same tumor cells in vitro. This was reflected by the progressively increasing background levels of nucleic acid synthesis with the length of tumor-bearing and the size of the tumor. Although lymph-node cells from mice with large tumors did not respond to the same tumor cells in vitro, they did have normal responses to PHA. Within 7-14 days of surgical removal of the tumor, specific lymphocyte responsiveness and background activity returned to previous normal levels, but reinoculation with 10-6 tumor cells resulted in progressive tumor growth and loss of specific in vitro responsiveness when the second tumor had reached the critical size of 1 cm in diameter. Brief exposure of tumor-immune lymph-node cells to a soluble antigen extract of the same tumor resulted in a marked increase in DNA synthetic activity compared to that obtained after exposure to a different tumor extract, muscle extract or medium alone underwent stimulation when cultured with mitomycin-blocked tumor cells. However, normally responsive tumor-immune lymph-node cells, after brief exposure to a soluble antigen extract of the same tumor, initially underwent increased DNA synthesis, but were incapable of further stimulation by mitomycin-blocked tumor cells. Tumor antigen, alone or complexed with antibody, was also demonstrated in the sera of mice bearing large tumors and is thought to be responsible for the refractoriness of lymph-node cells from these mice to further stimulation in vitro. These experiments demonstrate that tumor size and the consequent antigen load to which the tumor-bearing animals is subjected have a profound effect on tumor-specific lymphocyte responsiveness.
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PMID:Refractoriness of lymph-node cells from tumour-bearing animals. 4 43

A steroid, 6-chloro-17-hydroxypregna-1,4,6-triene-3,20-doine (CHP) that exhibits selective activity in several models of cellular immunity including an apparent inhibitory action on the elicitation of delayed hypersensitivity, was examined in a new, simple experimental model for assessing aspects of host-cell-mediated immunological competence. This model is based upon the capacity of the adult mouse to prevent the progressive growth of tumors induced by the Moloney sarcoma virus. Two steroids reported to have immunosuppressive activity in other assay systems, namely, cortisol and progesterone, were also studied. Control mice and those injected with CHP maintained their capacity to reject the tumor. In contrast, significant numbers of mice receiving a single large injection of cortisol or progesterone succumbed to progressive tumor growth under the experimental conditions used. The data indicate that CHP, while influencing selected parameters of cellular immunity, e.g., the elicitation of delayed hypersensitivity, does not decrease the capacity of the host to mount a defense against the progressive growth of the Moloney virus-induced sarcoma. The results indicate that CHP may be useful in modulating specific aspects of cellular immunity without altering others. In addition, the experimental model described provides a simple method of assessing the possible immunosuppressive effects of naturally occurring and synthetic agents on viral-induced tumor growth.
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PMID:Selective immunosuppressive activity of steroids in mice inoculated with the Moloney Sarcoma virus (38503). 4 58


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