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)

The antitumor activity of the cell-wall skeleton (CWS) of Propionibacterium acnes C7 was examined by using transplantable tumors in syngeneic mice and in guinea pigs, and autochthonous tumors in mice. P. acnes-CWS was shown to suppress the growth of fibrosarcomas, EL4 leukemia, and MH134 hepatoma in syngeneic mice, and to regress the established tumors of a fibrosarcoma (MC104) in C57BL/6J mice, and a hepatoma (line-10) in strain-2 guinea pigs. The oil-attached P. acnes-CWS mixed with fructose mycolate was effective for suppression of the autograft of fibrosarcoma in mice. The repeated intralesional injections of suspension of P. acnes-CWS in phosphate-buffered saline was effective for prolongation of survival period of mice bearing 3-methylcholanthrene-induced fibrosarcoma. The test results on the cell fractions of P. acnes indicated that the CWS, but not the cytoplasmic or glucan fraction, of P. acnes had anti-tumor activity. The activation of peritoneal macrophages of mice was observed when P. acnes-CWS, but not the cytoplasmic fraction, was injected intraperitoneally 4 days before. The relationship between the cytolytic activity of peritoneal macrophages and antitumor activities of P. acnes-CWS was also discussed.
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PMID:Antitumor activity of cell-wall skeleton of Propionibacterium acnes C7 in mice and guinea pigs. 39 8

The remodelling of bone grafts depends to a large extent upon the type of graft and the condition of the recipient site. We applied 99mTc-phosphate scintigraphy in a follow-up study on cases treated by bone grafting, and quantitative analysis of the scintigram by computer to make clear the difference of remodelling time or the process of acceptance between a cancellous and a cortical bone grafting or due to various graft and conditions. The result revealed that the grafted bones which were smoothly adapted for subsequent growths or functions could restore normal accumulation ratios by 36 months after the grafting. When the cancellous bone was grafted to grafting beds with good conditions such as osteotomy site in the cases with coxarthrosis deformans or congenital dislocation of the hip, it could attain the quickest recovery of the normal accumulation ratio. The next quickest recovery of accumulation ratio was attained by grafting the cancellous bone to the grafting beds with poor conditions such as osteomyelitis, pseudoarthrosis, and bone tumor. The third best accumulation ratio could be attained when the cortical bone was grafted to grafting beds with good conditions, while the slowest recovery to normal accumulation ratio was noted when the cortical bone was grafted to grafting beds with poor conditions.
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PMID:[Study on remodelling of bone grafts--an application of nuclear medicine (author's transl)]. 39 9

Treatment of NMRI mice i.p. with dehydrodipeptides [acetyldehydro-3-(2-thienyl)alanyltyrosine (SI); acetyldehydro-3-(2-furyl)alanyltyrosine (SII)] rendered macrophages cytolytic for several tumor cells in vitro. Normal peritoneal mouse macrophages from untreated mice not given injections of the peptides or from control mice given injections of phosphate-buffered saline were not cytotoxic. Moreover, supernatants from these in vivo-activated mouse peritoneal macrophages significantly increased the release of the cytoplasmic enzyme lactate dehydrogenase from freshly added target cells, showing that these cells had been killed. The macrophage activation to lyse tumor cells was sharply dose dependent and appeared about 48 hr after injection of the peptides. Although dehydrodipeptide SI was active in vivo at concentrations as low as 500 microgram/mouse, the same substance lacked activity in vitro at all concentrations tested up to 800 microgram/ml. Dehydrodipeptides activate macrophages through a T-cell-independent process to lyse tumor target cells. Macrophages from athymic nude (nu/nu) mice were less cytotoxic, but they still were stimulated; and the culture supernatants could kill about 50% of the tumor cells used. There are indications for a relative specific structure-activity relationship of dehydrodipeptides for inducing cytotoxic macrophages.
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PMID:Killing of tumor cells in vitro by macrophages from mice treated with synthetic dehydrodipeptides. 42 17

Of 63 99mTc-phosphate bone images in 49 patients with neuroblastoma, 41 were abnormal, 17 showed tracer uptake within the primary tumor, 29 showed evidence of skeletal metastatic disease, and 17 demonstrated renal/urinary tract involvement. The metastases were asymmetric in 24 patients and symmetrical in 9, in whom they involved the metaphyses and epiphyses of the long bones. Except for one patient with multiple "cold" areas, all metastases were seen as focal hyperactive regions. Eleven of 42 skeletal radiographic surveys were abnormal. The radionuclide study appears to be more accurate than skeletal radiography in estimating bone involvement in neuroblastoma. Primary tumor concentration of the tracer is almost pathognomonic of neural crest neoplasms in childhood.
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PMID:Radionuclide skeletal survey in neuroblastoma. 44 41

The activities of glucose-6-phosphate dehydrogenase, 6-phosphogluconate dehydrogenase and transketolase were studied in the cytoplasmic fractions of transplanted mouse hepatomas differing in their growth rates, and in the liver, spleen and cortical layer of kidneys of tumour carriers and normal mice. It was shown that transplantation of hepatomas changes the activity of the pentose phosphate pathway enzymes in tumour carrier tissues unaffected by neoplasm. Deviations from normalcy were mainly similar to those observed in the hepatomas. The changes in the enzymatic activities were especially well-pronounced in the mice having rapidly growing hepatomas. This may be due to a generalized effect of the tumour on the organism, which is concurrent with malignancy.
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PMID:[Activities of dehydrogenases of the pentose phosphate pathway and transketolase in transplanted mouse hepatomas with different growth rates and in organs of tumor carriers]. 45 18

The effect of uracil on the metabolism of 5-fluorouracil (5-FU) in vitro was studied. 5-FU was mainly phosphorylated in intact Yoshida sarcoma cells, whereas it was mainly degraded in liver slices. Uracil inhibited degradation of 5-FU much more than its phosphorylation; incubation of 2,500 microM of uracil with 2.5 microM of 5-FU (molar ratio, 1,000:1) inhibited the degradation of 5-FU by 70%, but did not affect its phosphorylation. With homogenates of Yoshida sarcoma or liver uracil inhibited degradation of 5-FU greatly, phosphorylation of 5-FU by alpha-D-ribose 1-phosphate (RiblP) and ATP to some extent, and phosphorylation by 5-phospho-alpha-D-ribosyl diphosphate (PPRibP) very little. The activities of the enzymes involved in the metabolism of 5-FU in various tissues were also determined. Degradation of 5-FU was much faster in liver than in other tissues and was very slow in tumor tissue. Phosphorylation of 5-FU with RiblP and ATP was rapid in Yoshida sarcoma and bone marrow. Phosphoribosyltransferase activity was high in Yoshida sarcoma and thymus, but low in bone marrow.
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PMID:Effect of uracil on metabolism of 5-fluorouracil in vitro. 46 97

The aldolase activity was measured using two substrates fructose-I-phosphate (FIP) and fructose-1,6-diphosphate (FDP) in the supernatant fraction of homogenates of different mice organs (liver, muscle, brain) and hepatoma tissues during growth of hepatoma 22a. Kinetic parameters Km and Vmax were calsulated. The most essential changes in the activity of aldolase were found during the latent and terminal stares of the hepatoma development. The changes in the aldolase activity observed during development of hepatoma 22a were characterized by altered substrate specificity VFDP /VFIP activity gatio). This ratio was not changed distinctly in liver tissue; in muscles the value decreased from 50 (tumor-free control) to 15 during terminal stages; in brain, to the contrary, it was increased from 20 to 50. The values of Km, Vmax and VFDP /VFIP were similar both in the hepatoma at the eleventh day and in normal brain tissue. The specific inhibition of FDP aldolase activity by ATP was found. Substitution of aldolase B by aldolase AC apparantly ossurred in hepatoma 22a. The data obtained suggest that alteration in the parameters studied may be due to variation in the ration of isozymes.
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PMID:[Change in aldolase activity in the organs of mice in the process of hepatoma 22a development]. 49 46

Results of a study of estrogen Rc receptors in 32 primary human breast cancer cytosol preparations are presented. Tritiated sulfate activation to tritiated adenosine 3'-phosphate 5'-phosphosulfate and subsequent formation of tritiated estrogen sulfotranferase levels was assessed in these preparations. 2 groups of tumors were identified: a low estrogen sulfurylation which was predominantly Rc negative, and a high estrogen sulfurylation with almost exclusive Rc -positivity. In the 1st type of tumor, in which estrogen sulfotranferase levels were low (40 pmol of 17beta-estradiol 3-sulfate formed/mg of protein/2 hours) and were independent of tritiated adenosine 3'-phosphate 5'-phosphosulfate production from tritiated sulfate and adenosine triphosphate, and in the 2nd type of tumor, in which estrogen sulfotransferase levels ranged from 50-200 pmol of 17 beta-estradiol 3-sulfate/mg of protein/2 hours, there was a correlation between the 2 in terms of tritiated adenosine 3'-phosphate 5'-phosphosulfate formation (P.005). 11 of 16 of the 1st type of tumor were estrogen receptor negative, whereas 2 of 16 of the 2nd tumor type were receptor negative. In receptor-negative tumors, the estrogen sulfotransferasse levels were significantly lower than those in receptor-positive tumors (rho=.025).
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PMID:A correlation between estrogen sulfotransferase levels and estrogen receptor status in human primary breast carcinoma. 49 39

Mild, acidic hydrolysis of 3-O-benzoyl-1,2,:5,6-di-O-isopropylidene-alpha-D-allofuranose gave a diol that was selectively benzoylated at O-6 in high yield by intermediate conversion to the stannylene derivative. The 3,6-dibenzoate was converted to the 5-O-tosyl derivative and thence to a mixture of iodides, which were reduced with tributylstannane to 3,6-di-O-benzoyl-1,2-O-isopropylidene-alpha-D-ribo-hexofuranose (6). Acetolysis gave an anomeric mixture of diacetates, which, when treated with N-acetylbis(trimethylsilyl)cytosine gave the protected nucleoside, which was deprotected to free "homocytidine", 1-(5-deoxy-beta-D-ribo-hexofuranosyl)cytosine (11), by alklaine methanolysis. This was N-acetylated and then treated with acetone to give a protected nucleoside, which was labelled by oxidation to the aldehyde, reduction with sodium borotritide, and deprotection. Acidic methanolysis of 6 gave a mixture of methyl 2,6- and 3,6-di-O-benzoylfuranosides, the hydroxyl groups of which were treated by the tetrachloromethane-triphenylphosphine reagent to give the 2-chloro-2-deoxy (21) and 3-chloro-3-deoxy derivatives. Reduction of 21 gave methyl 3,6-di-O-benzoyl-2,5-dideoxy-D-erythro-furanoside, further transformed in 1-(2,5-dideoxy-beta-D-erythro-hexofuranosyl)cytosine mixed with the alpha anomer. Phosphates and diphosphates of the nucleosides were prepared by extensions of known methods. The phosphate and the diphosphate of 11 act neither as substrates nor as inhibitors of a ribonucleotide-reductase from rat asicites tumor.
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PMID:[Synthese of 1-(5-deoxy-beta-D-ribo-hexofuranosyl)cytosine and 1-(2,5-dideoxy-beta-D-erythro-hexofuranosyl)cytosine, and their phosphates. Specificity of an mammalian (rat) ribonucleotide-reductase]. 51 57

Recognition of the presence of a malignant pericardial effusion is important because of the insidious onset and life-threatening potential. This report presents data on three patients with metastasizing carcinoma of the breast, all admitted with a presumptive clinical diagnosis of malignant pericardial effusion. Two of the three revealed a diffuse concentration of Tc-99m PPi within the myocardium. In these cases the diagnosis was confirmed by identification of malignant cells in the pericardial fluid. We suggest that the use of labeled phosphate agents may allow early recognition of myocardial involvement in patients with disseminated neoplasm that results in malignant pericardial effusion.
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PMID:Myocardial accumulation of labeled phosphate in malignant pericardial effusion. 54 95


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