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)

Injection of 5-fluorouracil (5-FUra) [12 mg/kg i.p. (0.1 ml) every other day] and chloroquine phosphate (CP) [10 mg/kg i.p. (0.1 ml) daily] after the 19th day postimplant brought about a 55% complete remission of mammary carcinoma (C3HBA) in 2 separate experiments. FUra used alone brought about 40% complete tumor remissions, whereas CP used alone resulted in 30% complete remissions. None of these tumors reappeared before 189 days postimplant in Experiment 1 and 120 days postimplant in Experiment 2. The 5-FUra + CP treatment showed statistically (P less than 0.05) smaller tumor sizes compared to control mice tumor sizes on each of 13 check days after treatment was begun. The CP-treated tumors were statistically smaller than the control tumors on 10 check days, whereas the 5-FUra-treated tumors were smaller than the control tumors on 9 check days. The 5-FUra-treated tumors were statistically smaller than the CP-treated tumors on 2 check days (23 and 33). The 5-FUra + CP-treated tumors were statistically smaller than the CP-treated tumors on 3 check days (36, 43, and 47), and the 5-FUra + CP-treated tumors were statistically smaller than the 5-FUra-treated tumors on the last 4 check days (54, 57, 61, and 64).
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PMID:Fifty-five percent complete remission of mammary carcinoma in mice with 5-fluorouracil and chloroquine. 67 73

Twenty-six patients (14 men and 12 women) with histologically proven advanced malignant melanoma, who previously had not responded to DTIC, methyl-CCNU, and procarbazine, received estramustine phosphate (estracyt) (15 mg/m2) in daily divided doses. All patients had measurable disease. One patient developed a complete remission and one patient had improvement in liver function without measurable regression in the tumor. In three other patients (11%), the disease remained static for a period of 3--5 months. The mean survival time from the beginning of therapy was 16.8 months for the patients with a response or static disease and 2.18 months for those who had no response. Gastrointestinal toxicity was minimal; no hematologic toxicity was observed. It appears that estramustine phosphate used as a single agent for treating advanced malignant melanoma after patients failed to respond to DTIC and to the combination of methyl-CCNU and procarbazine has a poor response rate.
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PMID:Estramustine phosphate in the treatment of advanced malignant melanoma. 68 76

Hypercalcemia causes lethargy and coma in patients with head and neck cancer. It is important to realize that coma may be due to hypercalcemia and need not be a terminal event in the progress of the tumor. Also, the development of hypercalcemia in a previously normocalcemic patient requires investigation as to the cause of the hypercalcemia. I report two cases of comatose patients, hypercalcemic from bony metastases from tongue cancer, in whom treatment by furosemide and intravenous fluid diuresis, prednisone, sodium phosphate, and mithramycin produced worthwhile remissions. Hypercalcemia may be due to (1) bony metastases, (2) pseudohyperparathyroidism, (3) unrelated associated parathyroid tumors, or (4) a second primary tumor. Even with treatment, hypercalcemia is a bad prognostic sign in patients with head and neck cancer.
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PMID:Hypercalcemia and head and neck cancer. Bony metastases from tongue cancer. 69 40

Radioiodinated membrane components of L-FM3ANo.2 cells, which were hybrid cells of C3H/He mouse mammary ascites tumor and mouse L cells, were solubilized with non-ionic detergent Nonidet P-40 and immunoprecipitated with anti-H-2k sera. The immune complexes were reduced and subjected to SDS-polyacrylamide gel electrophoresis. When the cells were lysed at a concentration of 2 X 10(7) cells/ml in 0.5% NP-40 buffer, only H-2 molecules including beta2-microglobulin were precipitated, but when the cells were lysed at a concentration of 8 X 10(7) cells/ml in 0.5% NP-40 buffer, two labeled components corresponding to molecules of 105,000 daltons and 85,000 daltons, respectively, were observed in addition to the characteristic radioactive peaks of the H-2 antigen. Dilution of the latter detergent lysate with phosphate buffered saline exhibited no effect on the detection of the two additional components, while further treatment of the lysate with NP-40 buffer abrogated them to be detected. The results indicate that the H-2 molecules were solubilized as physical complexes with certain membrane components of L-FM3ANo.2 cells when the cells were lysed at high cell concentrations in detergent, and suggest that the H-2 molecules and certain membrane components may be physically associated with each other on the cell surface of L-FM3ANo.2 cells.
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PMID:Solubilization of the H-2 antigen from hybrid cells of mouse mammary ascites tumor and mouse L cells at high cell concentrations in detergent. 71 35

Patients with poorly differentiated prostatic carcinoma and skeletal metastases were randomized to treatment with 2.6-cis-diphenylhexamethylcyclotetrasiloxane (2.6-cis) and estramustine-17-phosphate (estramustine). Parallel with the clinical study a group of non-randomized patients were treated with 2.6-cis. Cytological regression of the tumor could be registered in half of the estramustine group but not in the 2.6-cis group. There were no drug-related changes in blood chemistry, kidney function tests, hematology or liver enzymes. There was in increase in acid and alkaline phosphatase in both groups but more pronounced in the 2.6-cis group. In both groups follicle-stimulating and luteinizing hormone values were depressed. Testicular and penis atrophy was observed in the 2.6-cis group. Relief of pain and marked improvement of conditions occurred in the majority of the cases in both groups. In general, no tumor regression was observed during administration of 300 mg. 2.6-cis daily for at least 3 months. Some tumor regression was noted during 600 mg. estramustine therapy daily.
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PMID:Clinical experimental randomized study of 2.6-cis-diphenylhexamethylcyclotetrasiloxane and estramustine-17-phosphate in the treatment of prostatic carcinoma. 73 10

In a study of active site binding the inhibition of thymidylate synthetase derived from Escherichia coli, calf thymus, and Ehrlich ascites tumor was examined using eight inhibitors. 5-Substituted 2'-deoxyuridine 5'-phosphate analogues used in this study are the hydroxymethyl, methoxymethyl, benzyloxymethyl, formyl, acetyl, allyl, and two potential active site alkylating substituents: 2,3-oxypropyl and the azidomethyl analogues. All compounds were competitive with the substrate, 2'-deoxyuridine 5'-phosphate; the most potent inhibitor was 5-formyl-dUMP (Ki = 0.1, 0.09, and 0.08 muM for the respective enzyme). The 5-hydroxymethyl, 5-benzyloxymethyl, and 5-azidomethyl derivatives of dUMP showed some differential inhibition; these compounds were two to three times more active against the ascites tumor enzyme than against the thymus enzyme.
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PMID:Synthetic inhibitors of Escherichia coli, calf thymus, and Ehrlich ascites tumor thymidylate synthetase. 78 Dec 46

The total binding capacity of the cell receptors and not only the fraction required to elicit physiological response was detected and it is shown that specific receptors filled by endogenous estradiol were detected along with the unfilled sites. Changing the temperature of the incubation media altered intracellular distribution of bound estradiol. Late nucleolar retention of estradiol was shown after its release from nuclear protein. This unexpected finding may be a key event. Tumor tissues were obtained from 40 primary breast cancers, 2 endometrial carcinomas, and 1 lung and 1 gastric cancer; 2 normal human spleens, 2 mouse livers, and 1 breast from a 5-month pregnant women were processed. Tissue samples were transferred to a cold flask containing phosphate-buffered balanced salt solution. Further details of preparation are given to show typical estradiol-target cells containing variable amounts of specific estradiol-receptors. For immunofluorescence staining and indirect technique was used to show the in situ estradiol localization. The fluorescence staining showed 3 patterns. Cells incubated in the cold mostly displayed a bright, homogeneously diffuse fluorescence of the cytoplasm with the nuclear area unstained. There were some negative cells. The 2nd pattern of fluorescence was shown by those incubated at room temperature. Cytoplasmic staining was more marked and nuclear areas showed bright-fluorescent light stippling. A 3rd staining pattern was seen after slow postincubation warming up to 37 degrees C when increased nuclear staining occurred. Some cells did not show any nuclear labeling despite the clear cytoplasmic fluorescence. Preparations of human spleen, nontarget tumors, or mouse liver had no fluorescent cells. All fluorescent stainings were prevented by preincubation and washing in media containing Nafoxidine and N-ethylmaleimide. Control experiments confirmed the immune specificity of the detection of estradiol. Breast tissue cells from a pregnant women showed moderate cytoplasmic and faint nuclear fluorescence before incubation with estradiol, after which cytoplasmic staining was reinforced. Cells from the premenstrual beast cancers sometimes showed fluorescence without exposure to estradiol.
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PMID:Detection and dynamic localisation of estradiol-receptor complexes in intact target cells by immunofluorescence technique. 78 84

Previous studies from this laboratory on the mechanism of O-alkyl bond formation using a microsomal system from Tetrahymena pyriformis have shown that O-alkyl lipid synthesized from dihydroxyacetone phosphate has exchanged one hydrogen stereospecifically from the 1-sn position of the glycerol moiety. Indirect evidence suggested that acyldihydroxyacetone phosphate, an intermediate in )-alkyl lipid synthesis, is probably not the locus of the exchange. In the present study in was shown that stable acyldihydroxyacetone phosphate incubated in the presence of tritiated water and Tetrahymena microsomes does not become tritiated. When hexadecanol is added to the system O-alkyl lipid is produced which has incorporated one atom of hydrogen for each mole of hexadecanol at all time periods examined. Experiments in Ehrlich ascites tumor cells have shown that the hydrogen exchange also occurs in a mammalian system. The results indicate that the mechanism of O-alkyl lipid ether bond formation involves a hydrogen exchange and that this exchange occurs after the formation of acyldihydroxyacetone phosphate.
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PMID:The formation of tritiated O-alkyl lipid from acyldihydroxyacetone phosphate in the presence of tritiated water. 80 79

The effects of fixation with glutaraldehyde (GA), formaldehyde (FA), glutaraldehyde-formaldehyde (GA-FA), flutaraldehyde-osmium tetroxide (GA-Os04) and osmium tetroxide (OsO4) on cel volume were studied in control, p-chloromercuribenzene sulfonic acid (PCMBS)-treated and hypotonically-treated Ehrlich ascites tumor cells. Among the variables investigated were concentration of the tixative agent, osmolity of the buffer, total osmolaity of the fixation solution, osmolaltity of the postfixation buffer and the time of fixation and postfixation treatment; in addition, the effects of adding calcium and high molecular weight compounds to the fixative solution were studied. When the effects of standard fixatives on control, PCMBS- and hypotonically-treated cells were compared, marked differences were apparent in the behavior of control and injured cells. Control cells retained near prefixation volume in 3% GA and 3% GA-1% OsO4, swelled in 4% FA or 1% OsO4 and phosphate buffer (tkrp), whereas tpcmbs (310 mosM KRP)- and hypotonically-treated cells (103 mos M KRP) shrank in all aldehyde fixatives but swelled in 1% OsO4. Reducing the buffer osmolality had similar effects on control and injured cells although, there were variations in degree...
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PMID:Effects of fixation and postfixation treatments on volume of injured cells;. 80 69

Gastric juice was neutralized (nGJ) in vivo by 80 ml of a phosphate buffer containing radiolabelled vitamin B12 as dilution indicator. Unprocessed nGJ was analyzed in the double gel diffusion technique for the presence of serum proteins using monospecific antisera. Alpha1-Acid glycoprotein (AGP) was found in a high incidence (36 out of 38 subjects) in nGJ of gastric cancer patients. AGP was also observed less frequently in nGJ of patients with Billroth II resections (6/15), metaplasia (11/52), gastric ulcer (3/24), chronic atrophic gastritis (2/26) and chronic gastritis (3/63). AGP was absent in the control group (0/21), in patients with surface gastritis (0/38) and in subjects with normal acid secretion (0/45). Immunochemical studies demonstrated no identity of AGP with human "gastrointestinal tumor associated antigens." In 7 out of 17 AGP positive samples immunochemical differences between gastric and serum AGP were observed.
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PMID:Alpha 1-acid glycoprotein in gastric cancer juice. 80 43


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