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Query: UMLS:C0027651 (tumor)
 685,946 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Nb rat prostatic adenocarcinomas, previously induced by the administration of testosterone and estrogen, have been serially studied as heterotransplants into congenitally athymic (nude) mice and into groups of Nb rats. This animal system has been used to evaluate the chemotherapeutic efficacy of 5-fluorouracil and Ftorafur. The use of both species was to determine if there would be any significant difference in relative tumor growth in nude mice which lack functional T cells as opposed to intact Nb rats. The autonomous tumor, 102 Pr, is the subject of the thesis presented herein. One donor Nb rat bearing 102 Pr prostatic adenocarcinoma served as the donor for this experiment. The nude mice and Nb rats received the transplant on the same date and were subjected to the chemotherapies outlined above and were treated after there was sufficient increase in tumor volume from the 2 mm3 wedge to assure growth and neovascularity (greater than 60 mm3). Statistically significant data was presented revealing 5-fluorouracil to be efficacious in the treatment of these tumors. Also presented is data revealing differences in growth versus time in the respective recipient animal hosts. It is suggested herein that this combination animal model system could be used for screening potential cytotoxic chemotherapeutic agents.
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PMID:Immunobiology and therapeutic manipulation of heterotransplanted Nb rat prostatic adenocarcinoma. Chemotherapy of autonomous tumor, 102 Pr, heterotransplanted into congenitally athymic (nude) mice and syngeneic Nb rats. 11 27

The involvement of peritoneal macrophages in rejection of mastocytoma cells in the C57BL/6 mice was examined in comparison to similar cell responses in susceptible DBA/2 mice. By means of scanning and transmission electron microscopy it was found that macrophages constituted the major cell class responding to the mastocytoma cells in the peritoneum of both mouse strains. However, in the resistant mouse strain macrophages formed the predominant cell type during the course of tumor growth. Furthermore, tissue culture of peritoneal exudate cells from this resistant mouse strain injected with mastocytoma cells five days earlier failed to grow out tumor cells. On the other hand, macrophages decreased in number in the susceptible DBA/2 mouse strain and tumor cells did grow readily in vitro when peritoneal cells containing tumor cells and macrophages were cultured in vitro. These results indicate that macrophages constitute an important cell class in resistance of a mouse strain which is now susceptible to mastocytoma cells. The ultrastructural study provided some insight into the nature of the cell types involved and their interaction with the tumor cell.
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PMID:Involvement of peritoneal macrophages in cellular responses to mastocytoma in resistant and susceptible mice. 12 Oct 34

The R3230AC mammary adenocarcinoma was not dependent on insulin; tumor growth was equal to or greater in diabetic rats than in intact animals. However, tumor growth was reduced when daily doses of insulin were administered. Treatment with estrogen inhibited growth of the R3230AC carcinoma, either in diabetic rats or in intact animals simultaneously treated with insulin. The effects of insulin plus estrogen treatment appeared to be additive in causing inhibition of tumor growth. Tumors from diabetic rats showed few metabolic alterations as reflected by little or no changes in the activities of selected glycolytic enzymes, pyruvate kinase, phosphofructokinase, and hexokinase, nor any striking changes in the activities of glucose-6-phosphate dehydrogenase and 6-phosphogluconate dehydrogenase, representing the pentose phosphate pathway. A modest reduction in the ratio of utilization of (1-14C)glucose: (6-14C)glucose was seen in vitro by tumors from diabetic rats. It was concluded that insulin, along with estrogen and prolactin, should be considered as a hormonal factor that influences growth of this automonous, hormone-responsive adenocarcinoma.
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PMID:Influence of insulin on estrogen-induced responses in the r3230ac mammary carcinoma. 12 68

Chlorozotocin, 2-(3-(2-chloroethyl)-3-nitrosoureido)-D-glucopyranose, is a newly synthesized, water-soluble nitrosourea antitumor agent that is active against L1210 leukemia in mice. A 701% and a 401% increase in life-span were attained with a dose that was lethal to 10% of the animals (15 to 20 mg/kg, i.p.) in mice treated on Day 2 or Day 6 of L1210 tumor growth, respectivley. Sixity % of Day 2-treated mice and 30% of Day 6-treated mice survived for 90 days. At the maximally effective dose against L1210, chlorozotocin produced no significant depression in normal bone marrow DNA synthesis nor in peripheral neutrophil count, in contrast to a sustained greater than 90% inhibition in L1210 ascites cell DNA synthesis. If the antitumor activity and reduced bone marrow toxicity of chlorozotocin are confirmed in man the use of this compound would facilitate treatment of patients with neoplastic disease who have preexisting abnormal bone marrow function or would allow for the more effective use of a nitrosourea agent in combination with anticancer agents possessing more potent myelosuppressive properties.
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PMID:Chlorozotocin, 2-(3-(2-chloroethyl)-3-nitrosoureido)-D-glucopyranose, an antitumor agent with modified bone marrow toxicity. 12 70

Component levels of the fibrinolysin system in the plasma and ascitic fluid of Swiss mice bearing Ehrlich ascites tumor cells were determined during a 15-day tumor growth time phase. During tumor growth, the concentration of plasminogen in the ascitic fluid decreased inversely to the total packed cell volume. Free plasmin was not present in the ascitic fluid nor was there any measurable plasminogen activator activity. Both antiplasmin activity and fibrinogen levels present in the fluid decreased during tumor growth. The nuclear and mitochondrial-microsomal subcellular fractions of the tumor cell exhibited plasminogen activator activity. No significant changes in the above parameters occurred in the plasma during the tumor growth period we studied.
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PMID:Proteases during the growth of Ehrlich ascites tumor. I. The fibrinolysin system. 12 66

The addition of deoxyuridine (UDR) to fluorouracil (FU) or floxuridine (5-fluoro-2' deoxyuridine) (FUDR) produced a substantial increase in their toxicity in BDF1 mice. Antitumor assays using sarcoma 180 tumor-bearing mice showed a concomitant increase in tumor growth inhibition for the nucleoside-drug combination over identical doses of the single drug. However, no significant increase in antitumor activity with the combination treatment was demonstrated when equitoxic doses were given. Additional support for the therapeutic equality of the single and combination drug regimens was the similarity of the therapeutic indexes for each treatment regimen involving either fluorouracil or floxuridine. The results suggested that any therapeutic benefit achieved with the combination therapy could be duplicated with either fluorouracil or floxuridine at a higher dose.
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PMID:Effect of deoxyuridine coadministration on toxicity and antitumor activity of fluorouracil and floxuridine. 12 47

During growth of Ehrlich ascites tumor cells in vivo, the proportion of cells in the S phase of the proliferative cell cycle decreases in a manner analogous to the decreasing growth fraction often associated with the growth of solid tumors. An examination of biochemical parameters that might regulate the growth fraction of Ehrlich ascites tumors by causing accumulation of cells in G1-G0 shows that (a) the tumor progresses from an aerobic to an anerobic state as it approaches the plateau phase of growth, as indicated by lactate dehydrogenase content, but cellular adenosine triphosphate content remains constant; (b) tumor-specific growth inhibitors (chalones) are not detectable in cell-free ascites fluid from plateau-phase tumors; (c) electrophoretically identifiable soluble proteins isolated from tumor cells that have been exposed to labeled amino acids in vivo are qualitatively identical during early and late tumor growth; and (d) ornithine decarboxylase activity increases in a bimodal fashion in the first 10 hr after transplantation of 10(7) cells and then declines rapidly during the first few days of growth. The second (and larger) of the two ornithine decarboxylase increases coincides with the surge of cells from G1-G0 into S phase, suggesting that this enzyme, or the polyamines that it synthesizes, may play a role in controlling the growth fraction of this cell population.
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PMID:The role of adenosine triphosphate, chalones, and specific proteins in controlling tumor growth fraction. 12 98

Effect of PS-K on tumor growth and antibody production was studied in inbred C57BL/6, SL, C3H/He, and AKR mice, and in colony-bred ICR mice. (1) PS-K exhibited antitumor activity on sarcoma-180 in ICR mice, but not in AKR mice. Growth of sarcoma-180 was suppressed to the intermediate extent in other strains. (2) In ICR strain, antibody production against trinitrophenyl was depressed in mice bearing sarcoma-180 and restored by PS-K. In AKR mice, on the other hand, antibody production was not depressed in tumor-bearing state and was not augmented by PS-K. Other strains showed intermediate degrees of suppression of antibody-producing capacity by sarcoma-180 and its restoration by PS-K.CR strain, the growth of Ehrlich tumor as the challenge tumor was enhanced in mice bearing sarcoma-180 as compared to that in controls. After the treatment with PS-K in this strain, however, not only the growth of sarcoma-180 but also of Ehrlich tumor was inhibited completely. On the other hand, the growth of Ehrlich tumor in AKR strain was neither enhanced in mice bearing sarcoma-180 nor inhibited by PS-K.
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PMID:Mouse strain difference in the expression of antitumor activity of PS-K. 13 29

The inhibitory effect of the thoracic duct lymph of a patient with lung cancer on the "one-way" mixed lymphocyte reaction without cytoxicity is unequivocally demonstrated. The effect seems to be dose related. A moderate inhibition of mixed lymphocyte reaction is still observed, even if the responding cells are preincubated in the thoracic duct lymph for 1 hr only prior to the addition of stimulating cells. The inhibitory effect of thoracic duct lymph on the mixed lymphocyte reaction is no longer evident when the material is added 1-4 days after the beginning of culture. These observations suggest that the mechanism of the inhibitory effect of thoracic duct lymph may be a simple attachment of inhibitory factors to the receptor sites on the responding lymphocytes, causing interference in cell to cell interaction. The inhibitory effect of thoracic duct lymph collected 1 week after the thoracic duct drainage on mixed lymphocyte reaction is significantly lower than that of thoracic duct lymph collected at the beginning of the procedure. This indicates that the blocking effect of thoracic duct lymph can be easily removed by this technique; which is technically feasible in man. The interrelationship of the tumor-specific blocking factor, thoracic duct drainage, and tumor growth pattern are discussed with respect to the potential usefulness of this procedure as adjuvant immunotherapy in the management of patients with neoplastic diseases.
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PMID:Inhibition of mixed lymphocyte reaction by thoracic duct lymph: removal of inhibitory effect by thoracic duct drainage in lung cancer. 13 73

Synthetic aromatic analogs of retinoic acid were administered i.p. and p.o. to Fischer F344 rats bearing a transplantable chondrosarcoma. 35CO4 incorporation into glycosaminoglycans were compared for neoplastic and normal cartilage explants after removal from animals given various analogs. There was a direct relationship between [35S]glycosaminoglycan synthesis by chondrosarcoma chondrocytes and inhibition of tumor growth. The degree of inhibition of [35S]glycosaminoglycan synthesis in the neoplastic cartilage was dependent on the dose of the retinoid administered. At 20-mg/kg/day doses of retinoid for 4 weeks, 35SO4 incorporated into glycosaminoglycan by treated tumor explants was reduced as much as 95%. There was no reduction of [35S] glycosaminoglycan produced in normal costal cartilage of the same animals. Retinoid treatment of 20-mg/kg/day doses for 4 weeks resulted in a 75% reduction in glycosaminoglycan per mg of chondrosarcoma; there was no reduction in costal cartilage glycosaminoglycan. Retinoid (10- to 20-mg/kg/day doses) elevated collagen levels per mg of chondrosarcoma but had no effect on costal cartilage collagen. Combined in vitro and in vivo studies showed that retinoid administration modified neoplastic chondrocyte function but had no measurable effect on normal chondrocyte function.
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PMID:Effect of aromatic retinoids on rat chondrosarcoma glycosaminoglycan biosynthesis. 13 54


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