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)

Squamous cell carcinoma around the eyes of 3 horses was treated with liquid nitrogen, using cryotherapy probes as the method of application. In 2 cases, there was complete regression of the tumor; in the 3rd case, remission and relief of discomfort were temporary.
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PMID:Cryotherapy of periocular squamous cell carcinoma in the horse. 86 77

Using cells from our tissue culture of human melanoma cell line Na 11, we transplanted 1 X 10)6) tumor cells sc into athymic nude mice. Tumors appeared after a latent period of 4-10 days; when they reached a mean volume of 100 mm3 we irradiated them with various doses of X-rays. Some tumors were irradiated while the mice were still alive; others were treated 10 minutes after the animals had been asphyxiated with nitrogen. All irradiation was done in the presence of oxygen. These tumors were excised, and cell suspensions were prepared; the cells formed colonies with a mean plating efficiency of 29%. In another series of experiments, we irradiated tumor cells in vitro 2 hours after excision, when most cells were fixed and presumably oxygenated. We then calculated survival curves for the tumor cells irradiated under these three conditions and found an average anoxic cell fraction of 85%, which was much higher than that reported in many other tumor systems. We explored several possible explanations for this phenomenon.
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PMID:Survival curve of a human melanoma in nude mice. 86 46

Finely minced explants from 54 TCC2 of the human urinary tract were cultured in vitro in an attempt to establish cell lines. Cells with epithelial morphology grew out from 48 tumor explants, and long-term cell cultures were established from 10. Six of the cell cultures have been maintained for over 18 months with 50 to 70 transfers and, therefore, are considered permanent cell lines. The epithelial cells in the established cultures are small, exhibit rapid doubling time, and show multilayering. The cells were examined both microscopically and by cultivation techniques, and they were found to be free from contaminating microorganisms, including Mycoplasma. The established cultures grow rapidly in roller bottles and, therefore, can be produced in large quantities. These cells also remain viable after being stored for 3 years in liquid nitrogen.
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PMID:In vitro cultivation of epithelial cells derived from tumors of the human urinary tract. 94 89

Acute renal failure developed in nine of 78 patients who were subjected to hepatic artery ligation for nonresectable and extensive malignant tumor of the liver. Of those nine, six had hepatomas, one cholangiocarcinoma, one metastatic islet-cell carcinoma and one metastatic melanoma. Preoperative renal function as reflected in blood-urea-nitrogen and serum creatinine values was within normal limits. There were marked elevations of serum glutamic-oxalacetic transaminase and lactic dehydrogenase levels after hepatic artery ligation, an indication of massive ischemic injury of the tumor and the liver. A diagnosis of acute renal failure was established within 14 to 70 hours after hepatic artery ligation. In five patients, oliguric renal failure developed, and in four, high urinary output renal failure. In only three patients did systemic hypotension and hypovolemia precede acute renal failure. Seven of the nine patients died. Postmortem examination was done in five patients, and in only two was there evidence of renal tubular necrosis. The factors contributing to acute renal failure appear to be extensive involvement of the liver by tumor, presence of ascites and jaundice, occlusion of the portal vein and hyperuricemia. The presence of any one of the foregoing contraindicates the procedure.
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PMID:Acute renal failure after ligation of the hepatic artery. 95 59

In vivo treatment of sensitive tumor cells with nitrogen mustard (HN2) results in marked inhibitions of protein and nucleic acid synthesis by mitochondria subsequently isolated from these cells. This inhibition occurs at doses of drug which produce no apparent inhibition of total RNA synthesis. The inhibition gradually reverses itself in sensitive cells and is less severe and more rapidly reversed in resistant cells. The in vivo sensitivity of the mitochondria is in striking contrast to their in vitro behavior; isolated mitochondria resist 50 times the in vivo ID50 level of the drug. The sensitivity of protein and RNA synthesis in mitochondria is presumed to be related to the differences in organization between the nucleocytoplasmic processes and the mitochondrial. But the data also suggest that the in vivo effects on mitochondria are indirect, either acting via the cytoplasm or nucleus or via a carrier mechanism having mitochondrial affinity.
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PMID:Comparison of the effects of nitrogen mustard on the functional properties of mitochondria from sensitive and resistant strains of Ehrlich ascites tumors. 97 18

Incubation of Chinese hamster ovary cells and KHT murine fibrosarcoma tumor cells in the absence of oxygen with 1-[2-14C]nitro-1-imidazolyl)-3-methoxy-2-propanol, one of the most effective radiation sensitizers of hypoxic cells, results in the preferential reduction of 1-[2-14C]nitro-1-imidazolyl)-3-methoxy-2-propanol. The radioactivity associated with the acid-insoluble precipitate from cells incubated in nitrogen is about four times higher than that of cells incubated in air. When aqueous extracts of tissues of a C3H mouse bearing the KHT tumor, after i.p. injection with 1-[2-14C]nitro-1-imidazolyl)-3-methoxy-2-propanol, are analyzed, a reduction product is found in relatively higher yields in the tumor than in normal tissues. The relative radioactivity in the pellet from the tumor homogenate is also high in comparison with those of most normal tissues. These results provide suggestive evidence for a higher degree of hypoxic in the tumor than in most normal tissues. The formation of reduction products and their subsequent binding to macromolecules may explain the preferential toxicity of nitro compounds to mammalian cells under hypoxia conditions. These results suggest that some nitro compounds may be useful for the treatment of tumors having a high fraction of hypoxic cells even in the absence of radiation.
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PMID:Hypoxia-dependent reduction of 1-(2-nitro-1-imidazolyl)-3-methoxy-2-propanol by Chinese hamster ovary cells and KHT tumor cells in vitro and in vivo. 98 41

The effect of the AC33 tumor on protein synthesis in Lewis-Wistar rats was investigated under four different dietary regimens. The four diets used were: (a) 1.25 g amino acids plus 12.5 g glucose per day, (b) 1.25 g amino acids, (c) 1.25 g glucose per day, and (d) 12.5 g glucose per day. The rats were maintained on these four diets for 4 days. On the 5th day, 65 to 75 mg 99.2% [15N] glycine were added to the infusate and infused at a constant rate for the next 18 hr. The rats were then sacrificed and the liver, lung, heart, kidney, anterior tibialis muscle, and tumor were rapidly removed and frozen in liquid nitrogen. The rate of protein synthesis for these tissues was calculated from the ratio of 15N in the tissue protein to that in the tissue intracellular fluid. The protein synthesis rates were compared with the values found for a series of nontumor control rats fed the same diets. Relative to the control rats, muscle protein synthesis decreased on Diet 1, and liver protein synthesis increased with the three deficient diets.
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PMID:Tumor-caused changes in host protein synthesis under different dietary situations. 108 30

Infusion of cycloheximide i.v., an antibiotic known to inhibit synthesis of protein, at a rate of 0.2 mg/kg/hr, reliably caused lysis of fever in 15 chronically febrile patients with Hodgkin's disease who did not have detectable bacterial, fungal, or viral infection. Antipyretic effects were also seen in some patients with reticulum cell sarcoma, lymphosarcoma, acute leukemia, histiocytic medullary reticulosis, plasma cell myeloma, carcinoma of the lung, and carcinoma of the cervix. The drug failed to produce defervescence in four patients with normal granulocyte reserves, who were febrile due to bacterial infection. When infused at a rate of 0.2 mg/kg/hr, the drug apparently caused an acute alteration of protein metabolism in man in that plasma amino acid nitrogen rose acutely while plasma levels of muramidase and ribonuclease fell during the period of the infusion. The data suggest that continuing synthesis of protein may be involved in nonbacterial fever of neoplastic disease. Mammalian granulocytes and monocytes are known to elaborate a pyrogenic protein following appropriate stimulation; it is suggested that in some types of neoplastic disease, particularly Hodgkin's disease, tumor cells may produce and release a pyrogenic protein and that drug-induced inhibition of its synthesis is responsible for the observed lysis of fever.
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PMID:Antipyretic effect of cycloheximide, and inhibitor of protein synthesis, in patients with Hodgkin's disease or other malignant neoplasms. 109 49

Aflatoxin B1-2,3-dichloride (AFB1-Cl2) was synthesized as a model for the probable ultimate carcinogen, aflatoxin B1-2,3-oxide. As expected for aflatoxin B1-2,3-oxide, AFB1-Cl2 has an electrophilic carbon 2; it decomposed in water (half-life of 0.5 min in 10% dimethyl sulfoxide, pH 7.4) with the formation of 3-chloro-2,3-dihydro-2-hydroxyaflatoxin B1 and 2,3-dihydro-2,3-dihydroxyaflatoxin B1. AFB1-Cl2 formed covalent adducts with DNA and RNA with retention of one-half of the chlorine; the major products apparently contained glycosidic bonds between carbon 2 of the aflatoxin residues and nitrogen or oxygen atoms in the nucleic acids. Polyguanylic acid was the most reactive homopolymer toward AFB1-Cl2. AFB1-Cl2 was less reactive toward mononucleotides than toward polynucleotides. The major adducts formed on incubation of AFB1-Cl2 with protein contained little chlorine and could have resulted from alkylation of primary amino groups or from reactions with the hydrolysis products. Similarly, incubation of AFB1-Cl2 with amino acids apparently resulted in Schiff base formation between primary amino groups and the dialdehyde rearrangement forms of the hydrolysis products of AFB1-Cl2. AFB1-Cl2 was much more active than aflatoxin B1 in inducing sarcomas at the s.c. injection site in rats, in the initiation of papillomas on the skin of mice, and in the induction of lung tumors in mice. AFB1-Cl2 was also highly mutagenic for Salmonella typhimurium TA 98 and TA 100. Aflatoxin B1 and its 2,3,-dihydro- (aflatoxin B2), 2,3-dihydro-2-hydroxy- (aflatoxin B2a), 2,3-dihydro-2,3-dihydroxy-, and 3-chloro-2,3-dihydro-2-hydroxy- derivatives were inactive in the mutagenicity tests; and the latter four compounds were also inactive as initiators of papillomas of the skin in mice. The structures of the macromolecular adducts of AFB1-Cl2 formed in vitro, the carcinogenicity of this electrophile, and the lack of carcinogenicity of its hydrolysis products indicate that alkylation of nucleic acids is a critical reaction in tumor induction with this carcinogen and aflatoxin B1.
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PMID:The reactivity and carcinogenicity of aflatoxin B1-2,3-dichloride, a model for the putative 2,3-oxide metabolite of aflatoxin B1. 110 59

When 14C-labeled cyclophosphamide and nitrogen mustard were incubated separately with normal lymphocytes and lymphocytes from patients with chronic lymphocytic leukemia, the amount of radioactivity associated with the normal cells far exceeded that detected on the leukemic lymphocytes. This comparative diminution may be analogous to the impaired PHA response and excess surface immunoglobulin which serve as identifying markers of the malignant B cell. Cytotoxicity and neuraminidase experiments indicated that drug uptake by lymphocytes is not capricious and may occur in an optimum, predetermined fashion. Although surface uptake and therapeutic response are not necessarily directly interrelated, initial peripheral contact with an antineoplastic agent may be an essential step which modifies tumor sensitivity or resistance.
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PMID:Differential uptake of alkylating agents by normal and leukemic lymphocytes. 110 34


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