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)

Plasma membranes, isolated from Ehrlich ascites tumor cells, were dissolved in 2% cholate, 4 M urea and then reformed into liposomes upon dialysis at 4 degrees with exogenous phospholipids. Reconstituted vesicles regain the ability to transport amino acids. Na+ was shown to accelerate the uptake of alpha-aminoisobutyrate, phenylalanine, and methionine, but not leucine or epsilon-aminohexanoic acid. With the reconstituted vesicles, methionine, but not leucine, inhibited the uptake of alpha-aminoisobutyrate. An apparent Km value for alpha-aminoisobutyrate uptake of 3.0 mM was obtained. This value is close to that observed with the intact cells and the native membrane vesicles. A Na+ gradient (high Na+ outside) increased alpha-aminoisobutyrate uptake, whereas a reversed gradient (high Na+ inside) increased alpha-aminoisobutyrate efflux. The latter flux was increased by valinomycin, suggesting electrogenic transport. A modest extent of coupling between a Na+ gradient and uphill flow of alpha-aminoisobutyrate was observed.
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PMID:Sodium-dependent amino acid transport in reconstituted membrane vesicles from Ehrlich ascites cell plasma membranes. 56 50

The influence of chloramphenical (CAP) on toxic and therapeutic effect of N-nitrosomethyl urea (MNU) in mice of CBA line was studied. It is shown that in injection of lethal doses of MNU--0.08--0.1 mg/g in intact animals CAP reduced LD100 to LD50 and LD50 to LD0. Also CAP increased an average survival of animals with ascites Ehrlich tumor when injected the lethal dose of MNU--0.1 mg/g. Therapeutic effect of MNU in a dose of 0.05--0.075 mg/g in the presence of CAP was not changed and sometimes was even increased. Under discussion is the significance of the obtained results for chemotherapy of malignant tumors in man.
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PMID:[Effect of chloramphenicol on the toxic and therapeutic effect of N-nitrosomethylurea]. 60 81

Immunoreactive calcitonin released by a medullary thyroid carcinoma in tissue culture has been found to exhibit heterogeneity when analyzed by gel chromatography and radioimmunoassay, in a pattern analogous to that seen in the circulation of the patient from whom the neoplasm was removed. To examine the cause of the heterogeneity, the immunoreactive material released by the tumor into tissue culture medium was further analyzed by gel electrophoresis in the presence of the protein denaturant 8 M urea, by gel chromatography after reduction and alkylation, by affinity chromatography on concanavalin A-agarose, and by bioassay in a renal adenylyl cyclase system of enhanced sensitivity. The results suggest that the larger immunochemical forms of calcitonin described in the circulation of patients with medullary thyroid carcinoma may be released directly from the neoplasm and need not derive from peripheral metabolism of the monomer. It could be demonstrated that a major proportion of the immunochemical enlargement is dependent upon intermolecular disulfide bridge formation whereas aggregation or non-convalent protein binding account for a smaller component of the heterogeneity. In view of the absence of binding of the immunoreactive material to the lectin agarose, carbohydrate side chains, at least of the alpha-d glucosyl variety, do not seem to contribute significantly to calcitonin enlargement. Additionally, the studies indicate that, at least by in vitro assay, the larger immunochemical forms of calcitonin, representing the majority of the immunoreactivity released by a medullary thyroid carcinoma, are biologically inactive.
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PMID:Characterization of the immunochemical forms of calcitonin released by a medullary thyroid carcinoma in tissue culture. 62 Dec 83

Outbred Swiss mice of the Hebrew University strain were subtotally nephrectomized. The experimental and control animals were both divided into two subgroups, with one group kept on a regular animal house diet and one on a low-protein diet. All the animals were injected with Ehrlich's ascites tumor cells s.c. into the neck region. Two weeks later, the animals were killed and the tumor was excised and weighed to the nearest milligram. Tumor size in the uremic animals--the nephrectomized animals kept on a regular diet--was significantly smaller than in all other groups, which had blood urea nitrogen levels well within the normal range. It is suggested that urea may be a factor responsible for inhibiting tumor growth.
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PMID:Effect of uremia on tumor growth in mice. 72 26

Sera from Fischer rats 3 to 13 days after i.p. injection of syngeneic 13762A mammary adenocarcinoma contain three factors specifically blocking cell-mediated cytotoxicity (CMC). The major blocking factor is a 160,000-dalton IgG that combines specifically to cytolytic lymphocytes but not to tumor cells or tumor antigen, and that is not dissociated after treatment with 8 M urea. The other factors have been putatively identified as tumor antigen (less than 70,000 daltons) and as soluble antigen-antibody complexes (greater than 200,000 daltons). Injecting the tumor antigen into tumor-free rats induced spleen cells specifically cytotoxic to the 13762A tumor and provided partial protection to challenge with live tumor cells. Treating soluble antigen-antibody complexes with 8 M urea decreased the size of the blocking activity from greater than 200,000 to less than 70,000 daltons. Although the IgG fraction dissociated from the complex did not block CMC, it did recombine with the tumor antigen fraction to transfer activity to the greater than 200,000-dalton fraction. In contrast, mixing tumor antigen with the IgG fraction that did block CMC did not alter the size of the blocking activities.
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PMID:Immune response to a mammary adenocarcinoma. V. Sera from tumor-bearing rats contain multiple factors blocking cell-mediated cytotoxicity. 72 81

Six female beagle dogs were given, by capsule, a daily dose of 100 mg 4,4'-methylene-bis(2-methylaniline) (MeMDA), 3 times per week for 6 weeks, then 5 times per week for 5 weeks, at which time the dose was reduced to 50 mg 5 times per week, continuously for periods up to 7.0 years. Six female beagle dogs were kept as untreated controls for several studies and were sacrificed after 8.3 to 9 years test. MeMDA dogs developed renal atrophy with an elevated blood urea nitrogen during an approximate six-month period prior to death or being sacrificed in extremis. As three of three MeMDA dogs that survived for 5.2 years to 7.0 years developed hepatocellular carcinomas and two of the three dogs also developed primary lung tumors, with no liver or lung tumor in six control dogs, MeMDA was considered to be carcinogenic for the dog (liver tumors: p less than .05; lung tumors: p less than 10; Fisher's Exact Test, one tail).
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PMID:Liver and lung tumors in dogs from 4,4'-methylene-bis(2-methylaniline). 72 95

A factor responsible for stimulating an increase in ornithine decarboxylase activity in the liver of mice was found in tumor cell-free ascites fluid of mice 3 days after inoculation of tumor cells. The factor was purified about 70-fold in 25% yield from tumor cell-free ascites fluid. As little as 1 microgram of protein of purified fraction, injected intraperitoneally into normal mice, significantly increased the activity of ornithine decarboxylase in the liver. The most active preparation of the factor formed two major protein bands on analytical polyacrylamide gel electrophoresis and both these bands stained with periodic acid-Schiff's reagent. The factor was a heat-labile, alkaline-stable, acidic protein with a molecular weight of more than 300 000. It was inactivated by treatment with 10 mM dithiothreitol, 5 M urea, pronase or mixed glycosidase, but was stable on treatment with DNAase, RNAase or neuraminidase.
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PMID:Partial purificationand characterizationof a factor which stimulates an increase in ornithine decarboxylase activity in the liver from tumor cell-free ascites fluid. 76 Aug 23

Peracetic acid was a potent tumor promoter and a weak complete carcinogen on the skin of female ICR Swiss mice. "Decomposed peracetic acid" was inactive as a tumor promoter, as were 3% [hydrogen peroxide and 5%] urea peroxide; 1% perbenzoic acid and m-chloroperbenzoic acid were active tumor prototers.
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PMID:Cocarcinogenic activity of peroxy compounds. 81 10

Charts were reviewed of 519 patients with stage II (League of Nations) carcinoma of the cervix to determine those factors in the history, work-up, and treatment which affected survival. Those factors which correlated with a significant decrease in five-year survival were abnormal admission blood urea nitrogen level or excretory urogram, a history of pelvic pain or weight loss over 10 kg (20 lbs.), or tumor extension to the endocervix or uterus. These factors, as well as the results of lymphangiography, should be included in the staging of carcinoma of the cervix.
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PMID:Factors affecting survival in over 500 patients with stage II carcinoma of the cervix. 84 48

Abnormalities in taste sensation have been studied in 15 patients consisting of five normal controls, five patients with diffuse neoplasm and five patients post hypophysectomy. Threshold recognition for salt and HC1 in the three groups studied was the same. Sucrose and urea recognition was higher in patients with neoplasm as compared to normal controls. Patients post hypophysectomy had a lower threshold recognition for sucrose than both normal individuals and patients with neoplasm. The threshold recognition has markedly shifted for both sucrose (decreased) and urea (increased) post hypophysectomy. These observations are in support of previous findings and suggest that the pituitary plays at least a necessary permissible factor in the development of abnormalities in taste as observed in patients with disseminated cancer.
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PMID:Posthypophysectomy taste abnormalities: their relationship to remote effects of cancer. 85 48


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