Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0007097 (carcinoma)
 152,788 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Ehrlich ascites carcinoma growth in mice induces hypertriglyceridemia. The degree of hypertriglyceridemia found in one laboratory (Spector's) was much greater than we observed in our laboratory. Moreover, major differences were reported with respect to fasting (no effect on tumor extracellular fluid triglyceride levels in Spector's tumor-bearing mice; marked decrease in ours). We have obtained tumorous CBA mice from Spector's laboratory and have studied them simultaneously with our Swiss-Webster mice. Triglyceride levels of the above two groups and from two controlled crossover groups, included to evaluate the influence of mouse and tumor strains on hypertriglyceridemia, were determined. The CBA mice had intense hypertriglyceridemia and high triglyceride levels in tumor extracellular fluid regardless of the subline source of ascites tumor. On the other hand, only mild hyperlipidemia was induced with both strains of tumor in Swiss-Webster mice. Thus, the variations in plasma and tumor extracellular fluid triglyceride levels probably arise from the mouse strains and not from variations in the tumor subline. Fasting caused a decrease in both plasma and tumor extracellular fluid triglyceride concentrations in CBA, as well as in Swiss-Webster mice. A mouse strain difference was also evident from a significant decrease in wet weights of adipose tissues like epididymal fat, inguinal fat, and intermuscular fat with tumor growth in the CBA strain which was not observed in the Swiss-Webster strain at the corresponding stage of tumor growth. Study of these strain diffeences may lead to an understanding of factors that regulate hyperlipidemia.
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PMID:Hypertriglyceridemia in Ehrlich ascites carcinomatous mice: tumor and mouse strain differences. 84 97

BCG vaccine inhibits the growth of intramuscular transplants of Krebs-2 carcinoma, when given in mixture with the tumor cells, and stimulates it in contralateral administration. When BCG and the tumor cells are injected separately in the region, drained by one and the same lymph node, no antitumor effect of the vaccine is observed. It is suggested that BCG effect on experimental tumor growth is mainly based not on the immunological mechanisms, but is the result of redistribution of cells participating in nonspecific antitumor resistance.
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PMID:[Effect of BCG on the growth of Krebs-2 carcinoma]. 90 9

The use of serum transfusion to remedy radiation-induced damage to established antitumor resistance was investigated in female C3H mice. The mice, which had been actively immunized against a syngeneic mammary carcinoma, were injected i.v. and s.c. with suspensions of cells from the same tumor and were then given 300 R extensive-field irradiation to the abdomen two times. Tumor cells implanted outside the irradiated area grew better in irradiated mice than in unirradiated controls. Under these experimental conditions, protection could be transferred to radiation-impaired hosts with several injections of cell-free immune serum. Transfers of normal serum provided a detectable but low degree of protection. The corrective effect of serum transfers to radiation-impaired hosts was clearly expressed against pulmonary tumor growth (i.v. challenge), provided the transfusions were started no later than the first day after the injection of the tumor cells. Serum transfusions were ineffective against the growth of tumors implanted s.c. Transfers of serum from hosts carrying large (15 mm) s.c. tumor implants had a negative effect on the resistance of irradiated recipients. The results indicate that humoral resistance factors, both normal and immune, may act against metastatic spread of solid tumors.
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PMID:Serum therapy for radiation-induced impairment of immune resistance to metastasis. 90 7

Experimental studies on the mechanims of transductal dissemination of the pancreas carcinoma was made in rabbit by injection of VX2 carcinoma suspension into the pancreatic duct. Ductal occlusion was conductive to nidation and growth in the pancreas of intraductal floating cancer cells, but tumor growth also occured in 40% of animals in which the duct was not occluded. The mechanisms of nidation in the pancreas of intraductal floating cancer cells were direct embedding into the ductal wall, and leakage of cancer cells from the duct in the process of pancreatic fibrosis due to ductal obstruction. Expansive tumor growth in the pancreas was more vigorous the smaller the degree of fibrosis of the pancreas, and was most active where associated acute pancreatitis was seen or where the pancreas was X-irradiated one week before injection of carcinoma suspension.
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PMID:Experimental study of transductal dissemination of cancer of the pancreas. 92 87

The effect of massive doses of vitamin A was studied as applied to the tumor growth in rats with Guerin's carcinoma, protein biosynthesis in them and enzymic activity. It is established that intraperitoneal administration of vitamin A massive doses (the total quantity being 4000 000 and 2000 000 I.U.) in equal doses for 6 days decreases tumor sizes and weight, intensity of protein biosynthesis by the cell-free protein-synthetizing system of the small intestine mucosa, intensifies activity of retinylpalmitate hydrolase, decreases that of retinylpalmitate synthetase, increases the activity of alanine aminotransferase. The authors assume that under the effect of vitamin A massive doses the capacity of retinol-binding protein transporting vitamin A is exhausted, the latter being transported in a cell by lipoproteids, which causes the cell membrane lysis.
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PMID:[On the potential protective properties of vitamin A in carcinogenesis]. 92 12

A study was made of the effect of combined adriamycin and hyperthermic treatment in a solid mouse mammary carcinoma in vivo. This study demonstrated: (a) that, when given separately, adriamycin and hyperthermia enhance the destruction of a solid mouse mammary carcinoma in vivo; hyperthermia (40.5-42.5 degreesy greatly increases tumor destruction and, in a number of cases, caused initial and long-time regression; (c) that whole-body hyperthermia in combination with adriamycin gives a significant delay in tumor growth as compared with the controls, but not to the same degree as the local combined therapy; and (d) that treatment with local hyperthermia and adriamycin gives a pronounced decrease in the lethal toxicitity of adriamycin. The effect of adriamycin and heat treatment may be due to hyperthermic cell destruction in the central area of the solid tumor, together with a synergistic effect of heat and adriamycin on the proliferating peripheral tumor cells. Furthermore, local heat application may increase the adriamycin concentration in the heated tumor area, which causes a high destructive effect and a less toxic influence on the nonheated normal tissue.
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PMID:Combined adriamycin and hyperthermia treatment of a murine mammary carcinoma in vivo. 97 75

A similiarity is found in the regression and regrowth curves of normal and malignant tissues after radiation treatments. The similarity implies that even in malignant tissues there is the practical, at least, limitation of tumor growth as in a normal organ, which is due to growth rate retardation. The retardation is considered to be the result from homologous inhibition of tumor cells. A tumor has its own growth rate which varies according to its total cell number and its environment. Approximately six months old skin metastases from breast carcinoma are still growing but are very close to the asymptote size which appears to be about 1000 cubic millimeters.
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PMID:Growth retardation in normal and malignant tissues. 100 16

Histopathological characteristics of the tumor growth were studied in 59 small carcinomas detected in thyroids at autopsy and in 33 from surgically removed thyroids. Tumor size was less than 5 mm in 56 of the 59 carcinomas (95 per cent) detected in autopsy materials. Histological findings of the small carcinomas were papillary adenocarcinoma in 45 of 59 (76 per cent), and sclerosing carcinoma in 32 (54 per cent). Among these 59 small carcinomas, intrathyroid metastases were found in six (10.2 per cent). In small carcinomas measuring less than 5 mm, carcinomas in females had an average diameter of 2.19 mm and were significantly larger than those found in male, having an average diameter of 1.14 mm (p less than 0.05). In small carcinomas from the surgical specimen, incidence lymph node metastasis was high when associated with numerous intrathyroid metastases and when the distance was great between the edge of the primary tumor and the farthest satellite metastatic focus.
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PMID:Histological appearance of small thyroid carcinoma. 101 95

For the purpose of predicting the effect of carcinostatic agents on tumor-bearing host in vitro, a sensitivity test of a drug in tumor bearers was developed. This test is based on the change in the specific activity of acid phosphatase of individual tumor and liver tissue, and the difference in them was used as an indicator of effectiveness. The value was called the "effective value." The present papar is concerned with the relationship between the effective value and effectiveness of the agents in rodents and man. The results showed that the effective value became higher with increasing concentration of Mitomycin-C incubated with tumor and liver tissues. The survival time of Ehrlich carcinoma-bearing mice, which were given Mitomycin-C intraperitoneally, was longer and increase in the dose of Mitomycin-C. In ascitic or subcutaneous form of Ehrlich carcinoma, AH-130, and Yoshida sarcoma, the effective value was parallel with the survival time of or the inhibition of tumor growth in tumor-bearing animals treated with Mitomycin-C. In 25 patients with gastric carcinoma treated with Mitomycin-C, the postoperative survival time was more closely correlated with the effective value calculated by the titers of both tumor and liver than the value of tumor alone.
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PMID:Predication of the effect of carcinostatic agents on tumor-bearing host by the sensitivity test using acid phosphatase activity in vitro. 101 80

The effect of antitumor agents (lentinan, PS-K, Mitomycin-C, 6-mercaptopurine, etc.) on the antitumor delayed hypersensitivity reaction (DHR) measured by the foot-pad test was compared with their effect on tumor growth in ddY mice with Ehrlich tumor. These agents all inhibited growth of Ehrlich carcinoma. Lentianan and PS-K enhanced the antitumor DHR, but Mitomycin-C and 6-mercaptopurine did not. By plotting the effect of agents on the anti-tumor DHR against these effects on tumor weight, host-mediated antitumor agents could be differentiated from mitotic poisons. Attempts to distinguish these two types of agents by the same method using a syngeneic tumor system were unsuccessful.
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PMID:Differentiation of host-mediated antitumor agents from mitotic posons by the antitumor foot-pad reaction in Ehrlich carcinoma-ddY mouse system. 101 84


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