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

Colony formation of JB-1-E tumor cells was studied after hyperthermic treatment (42.5 degrees C) at a pH of 6.4 or 7.2 under hypoxic and euoxic conditions. At a pH of 7.2 and normal oxygen tension, there was a moderate decrease in colony formation with increasing duration of hyperthermic treatment (To = 65 min.). This effect was slightly enhanced under hypoxic conditions (To = 36 min.). The hyperthermic effect was enhanced to a considerably greater degree when treatment was performed at a pH of 6.4 (To = 19 min.), with no observable difference between hypoxia and euoxia. These findings indicate that environmental acidity is a determining factor in the hyperthermic effect. The hypoxic effect at a pH of 7.2 is probably due to a slight decrease in the intracellular pH caused by increased production of lactic acid.
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PMID:The influence of hypoxia and acidity on the hyperthermic response of malignant cells in vitro. 1

(1) The mitochondrial ATPase (EC 3.6.1.3) Ehrlich ascites cell mitochondria, was inhibited by D-glucose under physiological concentrations of ATP. The generation of ADP by the mitochondrial bound hexokinase, seems to be the reason for the D-glucose inhibitory effect. Reversal of the inhibitory effect of ADP on Ehrlich ascites cell mitochondria ATPase by an ATP-regenerating system was achieved. (2) Dissociation of mitochondrial bound hexokinase from the mitochondria eliminated the inhibitory effect of D-glucose. Rebinding of the hexokinase to the mitochondria regenerated the D-glucose inhibitory effect on Ehrlich ascites cell mitochondria ATPase. (3) Bioflavonoids such as quercetin inhibit the mitochondrial hexokinase activity, but do not change the mitochondrial ATPase activity of isolated Ehrlich ascites tumor cell mitochondria. (4) The inhibitory effect of bioflavonoids on mitochondrial bound hexokinase activity is shown to be dissociable from the ascites tumor cell mitochondria and seems to be associated with regulatory rather than catalitic sites of the enzyme.
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PMID:Bioflavonoid regulation of ATPase and hexokinase activity in Ehrlich ascites cell mitochondria. 1 95

Most (95%) of the poly-A-degrading activity of the mouse kidney was found in the cytoplasmic fraction and only 5% was found in the nuclear fraction; 43% of the poly-A-degrading activity of the cytoplasm was found in the mitochondria, 22% in the microsomes, and 30% in the soluble fraction. Differences in activity and specificity indicate that poly A is degraded in the nucleus by enzymes that are separate and distinct from the enzymes in the cytoplasm that degrade poly A. The nuclear poly-A-degrading activity can be separated into an endonuclease with a general specificity and exonuclease, similar to one found in Ehrlich ascites tumor cells, which shows some specificity for poly A.
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PMID:The subcellular distribution of poly-A-degrading activity in mouse kidney. 1 15

Prolactin binding in ovariectomy-responsive and ovariectomy-nonresponsive carcinoma in the Wistar/Furth rat is compared. The time course of binding of prolactin at 4, 24, ad 37 degrees for mammary tumor (MTW9) coimplanted with MtTW10, a mammosomatotropic pituitary tumor (MTW9-MtT) or with MTW9 maintained with daily perphenazine injections (MTW9-P) was measured. Maximum binding to membranes of both tumors occurred at 4 degrees after about 30 hours incubation. The binding was inhibited by polypeptide hormones that possess lactogenic activity. Mammary tumors from animals maintained on perphenazine had a 4-fold greater binding capacity than did tumors from MtT-supported animals. When perphenazine therapy was halted the binding capacity of MTW9-P membranes was unaffected. This result held when MTW9-P animals were ovariectomized. Resection of MtT resulted in tumor regression, a fall to normal of serum prolactin, and a nearly 3-fold increase in prolactin binding. Scatchard plots of prolactin binding data yield an apparent affinity constant, K(a) of 1.2 X 10(9) liters/mole for both tumors.
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PMID:Prolactin binding in ovariectomy-responsive and ovariectomy-nonresponsive rat mammary carcinoma. 1 19

In DA X Wistar F1 rats, growth of 10(4) Wistar-specific Sp 1 carcinoma cells s.c. was commonly prevented by a mild subclinical graft=versus-host reaction produced by injecting 50 X 10(6) Wistar spleen cells i.p. either concurrently with the tumor or 7 to 14 days previously, Spleen cells alone had no effect on established tumor, but their injection on Day 14 significantly reduced the recurrence rate after excision of tumor on Day 21. In vitro tests in tumor-bearing rats with graft-versus-host reactions showed increased spleen lymphocyte and serum cytotoxicity; these mechanisms may inhibit tumor growth in vivo. Because Wistar lymphocytes and Sp 1 cells are syngeneic, inhibition of tumor cannot be due to allograft rejection but is probably an effect of increased host immunoreactivity during the graft-versus-host reaction.
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PMID:Effects of graft-versus-host reaction on inhibition of tumor growth in vivo and on tumor cytotoxicity in vitro. 1 23

Several anticancer chemicals containing a quinone group were found to stimulate the aerobic oxidation of NADPH by liver microsomes. The enzyme responsible for the above reaction was identified as NADPH-cytochrome c reductase (EC 1.6.2.4), one of the microsomal flavoproteins. The fact that a catalytic amount (20 micronM) of these anticancer chemicals was sufficient to oxidize all the NADPH (100 micronM) indicates that they function as electron carries from the flavoprotein to molecular oxygen. As a corollary, Mitomycin-C and Carbazilquinone stimulated oxygen uptake by Ehrlich ascites tumor cells in the presence of glucose that Daunomycin and Adriamycin failed to do so, although the reason for it remains to be elucidated. Carbazilquinone, in contrast to others, also stimulated the microsomal NADH oxidation.
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PMID:Stimulation of microsomal NADPH oxidation by quinone group-containing anticancer chemicals. 1 20

The effects of different cell dose inoculation of plasmocitoma MOPC-315 and ADK-1t in Balb/c syngeneic mice are discussed in this work. Inoculated cell dose and neoplasia percent incidence have been noticed to be closely related, but unexpectedly two doses exist for each tumour, a comparatively small one and a definitely larger one, which cause nearly the same percent incidence. This paradox phenomenon is discussed also with reference to other researchers remarkers.
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PMID:[Effect of the cell dose on the development of 2 transplantable tumors in a syngeneic host]. 1 19

1. Due to their common origin from the neural crest the hormonogenic cells of the intestinal tract show similar cyto-chemical and ultra-structural characteristics. 2. Hyperplasiae and tumors of these cells lead to excessive hormone production with its consequences on the reacting organs. 3. Hormone producing tumors can be confined to one organ only, but as multiple endocrine adenomatosis they can afflict several organs. 4. Diagnosis of most hormone producing tumors is possible with the adequate radio-immunologic tests. Radiologic and endoscopic examinations can contribute to the localization of the tumor. 5. Surgical resection of the tumor or of the reacting organs impaired by the overproduction of hormones from the tumor is the indicated therapy. Medicamentous therapy is rarely successful. 6. The growth of most hormonogenic tumors is relatively slow. Rates of survival of up to 30 years have been known, even after formation of metastases of the tumor. Effects of hormone overproduction on other organs can reduce the prognosis.
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PMID:[Hormone producing gastrointestinal neoplasms]. 1 37

Indolyl-3-alkane alpha-hydroxylase, a novel tryptophan-metabolizing enzyme, was prepared in crystalline form from soil isolate organism Pseudomonas XA. Emission spectroscopy and atomic absorption analyses of purified enzyme revealed the presence of iron (0.8 mol/mol of protein), and a number of observations supported the presence of heme prosthetic group (1.1 mol/mol of protein). The S20,w value of indolyl-3-alkane alpha-hydroxylase is 10.2 S, and the molecular weight by sedimentation equilibrium ultracentrifugation is 250,000. The E1%280 of the enzyme is 21, and the isoelectric point by isoelectric focusing on ampholine polyacrylamide gel plates is 4.8. The enzyme catalyzes hydroxylation on the side chain of a variety of 3-substituted indole compounds, including certain tryptophan-containing oligopeptides. The reaction product from tryptamine was identified by proton nuclear magnetic resonance and gas chromatography/mass spectroscopy analyses. While the indole ring remained intact, hydroxylation occurred at the side chain carbon adjacent to the ring. Nuclear magnetic resonance studies indicated that hydroxylation always took place at the same position when the substrate was tryptophan methyl ester, tryptophol, indole-3-propionate, or indole-3-butyrate. No other chemical change occurred when these substrates were incubated with the enzyme. The Km value of indolyl-3-alkane alpha-hydroxylase for L-tryptophan is 2.4 X 10(-6) M, at pH 7.2. The enzyme is inhibited by potassium cyanide (0.1 mM) or hydroxylamine (1mM), but not by NaBH4 (25 mM), aminooxyacetic acid (7mM), quinacrine (1 mM), chlortetracycline (1 mM), p-mercuribenzoate (0.1 mM), or ethylenediaminetetraacetate (1 mM). The plasma half-life (t1/2) of indolyl-3-alkane alpha-hydroxylase in tumor-bearing mice is approximately 25 h.
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PMID:Isolation, crystallization, and properties of indolyl-3-alkane alpha-hydroxylase. A novel tryptophan-metabolizing enzyme. 1 94

Tyrosine hydroxylase, dopa oxidase, and peroxidase activities were studied in soluble fractions of B16 melanoma tumor homogenates by polyacrylamide gel disc electrophoresis. Stained gels were scanned photometrically and gel slices were assayed radiometrically. In these preparations, the two bands of tyrosine hydroxylating activity were completely separated from the peroxidase activity but coincided with two major bands of dopa oxidase activity. The third dopa oxidase band coincided with the single band of peroxidase activity. The soluble fraction of cultured cell homogenates had no peroxidase activity, but the two tyrosine hydroxylase bands coincided exactly with the two dopa oxidase bands. Therefore, in the soluble fraction of the murine melanoma bifunctional tyrosinase does exist as two electrophoretically separable forms which are independent of peroxidase.
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PMID:Characteristics of tyrosinase in B16 melanoma. 1 62


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