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Query: UMLS:C0006826 (cancer)
 1,092,456 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The postulate that low intracellular pH acts as a preconditioner for the destructuve effects of hyperthermia (42 degrees C) was examined, using a heat-sensitive line of malignant cells derived from rat mammary gland (SDB). Intracellular pH (pHi) was measured indirectly, from the distribution of the weak, non-metabolizable organic acid 5,5-dimethyl-2,4-oxazolidinedione (DMO) between intra- and extra-cellular water. Respiration, aerobic and anaerobic and anaerobic glycolysis of the cells were studied at normal pHi (pH 7-0-7-4) or at low pHi (pH 6-2-6-6) and at 38 degrees C or 42 degrees C over 6 h in Warburg manometers; the ability of the cells to replicate in culture was examined after 3 h or 6 h incubation in the flasks. The relationship between pHi and extracellular pH (pHe) depended upon the buffer system used and the exact pH in question; no assumption regarding pHi based only on pHe measurement could be made. At 38 degrees C and low pHi, the Pasteur effect became negative due to a relatively greater inhibition of anaerobic than aerobic glycolysis. Respiration was unaffected and cell replicative ability unimpaired. At 42 degrees C and normal pHi, respiration was totally inhibited after 4 h and the Pasteur effect was decreased, in this case due to a compensatory increase in aerobic glycolysis without alteration in anaerobic CO2 production. Low pHi in the presence of hyperthermia enabled cell respiration to continue at a reduced level with no further change in glycolysis. There was delayed cell replication after 3 h at 42 degrees C and inability to multiply following 6 h hyperthermia: low pHi did not influence these results. It is concluded that with these cancer cells, pHi values maintained in the region of 1-0 pH unit below normal for 6 h had no deleterious effect on the cells. No sensitizing effect of the low pHi for the destructive effect of hyperthermia on the cells was observed.
Br J Cancer 1976 Sep
PMID:The sensitivity of a malignant cell line to hyperthermia (42 degrees C) at low intracellular pH. 0 69

Uridine 5'-diphosphoglucuronic acid-fortified hepatic microsomes from dogs, rats, or humans rapidly metabolized [3H]-N-hydroxy-2-naphthylamine (N-HO-2-NA) to a water-soluble product that yielded 98% of the parent N-hydroxy amine upon treatment with beta-glucuronidase. The metabolite was identified as N-(beta-1-glucosiduronyl)-N-hydroxy-2-naphthylamine from ultraviolet, infrared, and mass spectral analyses of the glucuronide and its nitrone derivative. Incubation of N-hydroxy-1-naphthylamine (N-HO-1-NA), N-hydroxy-4-aminobiphenyl (N-HO-ABP), or the N-hydroxy derivatives of 2-aminofluorene, 4-aminoazobenzene, or N-acetyl-2-aminofluorene with uridine 5'-diphosphoglucuronic acid-fortified hepatic microsomes also yielded water-soluble products. beta-Glucuronidase treatment released 80 to 90% of the [3H]-NHO-1-NA and [3H]-N-HO-ABP conjugates as tritiated ether-extractable derivatives. N-HO-1-NA, N-HO-2-NA, and N-HO-ABP and the glucuronides of these N-hydroxy arylamines were relatively stable and nonreactive near neutral pH. At pH 5, the N-glucuronide of N-HO-2-NA and the presumed N-glucuronides of N-HO-1-NA and N-HO-ABP were rapidly hydrolyzed to the N-hydroxy arylamines that were then converted to reactive derivatives capable of binding covalently to nucleic acids. These data support the concept that arylamine bladder carcinogens are N-oxidized and N-glucuronidated in the liver and that the N-glucuronides are transported to the urinary bladder. The hydrolysis of the glucuronides to N-hydroxy arylamines and the conversion of the latter derivatives to highly reactive electrophilic arylnitrenium ions in the normally acidic urine of dogs and humans may be critical reactions for tumor induction in the urinary bladder.
Cancer Res 1977 Mar
PMID:Hepatic microsomal N-glucuronidation and nucleic acid binding of N-hydroxy arylamines in relation to urinary bladder carcinogenesis. 1 29

At the present time, it is rarely necessary to operate after a digestive perforation complicating the ingestion of a caustic fluid. By contrast, cancer surgery progresses. Anaesthesia requires protection with a high degree of analgesia and curarisation. The use of a Carlens tube during oesophagectomy via a thoracic approach facilitates the surgeon's task. Compensation for blood and water losses should be generous. Insertion of a gastric tube through the plasty makes it possible to avoid gastrostomy. Finally, postoperative artificial ventilation is necessary in these individuals who often suffer from some form of respiratory pathology.
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PMID:[Anesthesia for esophageal surgery]. 2 77

Male and female Wistar rats were administered sodium saccharin for life (2 yr) either in the drinking water or diet. The maximum palatable dose of saccharin in the drinking water was found to be 2 g/kg/day and, even then, there was some voluntary restriction of fluid intake in the males. By contrast, double this dose--namely 4 g/kg/day, was palatable in the diet. A control group of rats of both sexes received saccharin-free diet and drinking water. Mild urothelial hyperplasias developed from 85 weeks in rats of both sexes receiving saccharin either in the drinking water or diet; the incidence was statistically significant in both the bladders and kidneys of rats receiving the higher dose of saccharin in the diet, but in the kidneys only of rats receiving the lower dose of saccharin in the drinking water. Telangiectasia of the vasa recta was significant in saccharin-treated rats of both sexes at both doses. A very low incidence of bladder tumours, exclusively in males receiving the higher saccharin dose in the diet was seen from 95 weeks. No consistent relationship between bladder epithelial hyperplasias and crystalluria could be demonstrated, although all 3 bladder tumours were associated with some form of mineralisation. Results suggest a particular susceptibility of males to saccharin treatment. The possibility that saccharin may promote, or enhance, the development of latent tumour cells already present in the experimental population, rather than initiate carcinogenesis per se is considered.
Br J Cancer 1979 Apr
PMID:Response of the rat to saccharin with particular reference to the urinary bladder. 3 23

A procedure is described for maintaining primary cultures of adult rat hepatocytes on a layer of irradiated C3H/10T1/2 cells. These hepatocytes were capable of metabolizing the liver carcinogen N-2-acetylaminofluorene to water-soluble products and after 14 days in culture could still metabolize approximately 70% of the Day 1 level. Hepatocytes maintained on the C3H/10T1/2 cells were inducible for the liver-specific enzyme tyrosine aminotransferase, and exhibited approximately a 4-fold induction by hydrocortisone during a 10-day culture period. Morphologically, these hepatocytes retained many characteristics of hepatocytes in vivo. By contrast, hepatocytes maintained on plastic lost both N-2-acetylaminofluorene-metabolizing ability and tyrosine aminotransferase activity by Day 5. This was presumably due to degeneration of the hepatocytes and an overgrowth by fibroblasts. The maintenance of morphologically and biochemically functional hepatocytes in culture on feeder cells may provide a valuable approach for studying drug metabolism and liver cell transformation in vitro.
Cancer Res 1979 Sep
PMID:Maintenance of adult rat hepatocytes on C3H/10T1/2 cells. 3 5

A high pH therapy for cancer arrived at theoretically was tested in mice by feeding them rubidium carbonate. Tumours were transplanted in the abdomen of mice and allowed to grow for 8 days. The mice were then divided into two groups. The control group was continued on conventional mouse chow. The test group, in addition to the mouse chow, was force-fed 1.11 mg of rubidium carbonate dissolved in distilled water. At the end of 13 more days the tumours in the controls had grown to a large size so all the mice were sacrificed. The tumours were then removed and weighed. The tumours in the test animals weighed essentially one eleventh of those in the controls. In addition the test animals were showing no adverse effects from the cancers. The probability that this marked difference in tumour size could have come about by chance is exceedingly small.
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PMID:The effects of rubidium on mammary tumour growth in C57 blk/6J mice. 4

A radioimmunoassay for the antigens of the mouse mammary tumour virus has been developed. -125Iodine-labelling of intact virus [derived from mammary tumours of (C3H TIMES 020)F1 mice] followed by ether extraction and separation of the ether and water layers resulted in a separation of the labelled material into two main groups of antigenic components. The intact labelled material from each group was separated from viral debris and other possible contaminants by affinity chromatography. The antigens of the ether phase were proved to belong mainly to the viral nucleoid whereas the water phase contained mainly envelope antigens. No type-specific antigens could be demonstrated in either of the phases. Radioimmunological assessment of plasma revealed that in the plasma of MTV-S- and MTV-P-positive animals viral antigens were only measurable when palpable mammary tumours were present, whereas in MTV-L-positive tumour-bearing animals some negative samples were found. In milk of individual nontumour-bearing mice a close correlation was found between the expression of viral antigens and the generally accepted presence of virus in the strain of mice. In milk, viral antigen levels tend to increase with parity with a possible decrease after a finite number of pregnancies. In a pilot study the presence of MTV antigens could also be demonstrated in epididymis extracts of male GRS/A mice. Genetical analysis of the low-virulent MTV-L by radioimmunoassay of milk is in progress.
Int J Cancer 1975 Feb 15
PMID:Quantitative estimation of mouse mammary tumor virus (MTV) antigens by radioimmunoassay;. 4 46

An antigen was detected in pooled human nephroblastomas using antiserum prepared in rabbits against an ethylemediaminetetra acetic acid (EDTA) extract of the tumors. This antigen was not found in normal human plasma or kidney extracts, and was not related to the ABO or Forssman blood groups. The antigen was detected in extracts of cultured nephroblastoma cells, but was not present in extracts of normal human fetal kidney cell cultures. The antigen is believed to be present at the cell surface, as cell viability was not significantly lowered during the extraction procedure. A reaction of complete identity was demonstrated by Ouchterlony double diffusion experiments with this antigen and purified bovine fetuin. The antigen was not found in extracts of human fetal spleen, thymus or kidney, nor in human fetal serum. Furthermore, the antigen does not possess determinants in common with the human alpha-fetoprotein of hepatomas, nor was it detected in human renal clear cell carcinoma. Initial characterization of the antigen showed it to be nondialysable, not sedimentable at 100,000 times g for 2 h, stable to repeated freeze-thawing and to incubation at 56 degrees C for 1 h, and water soluble over a wide pH range. The antigen was susceptible to digestion with pronase and trypsin and possibly hyaluronidase, but not to ribonuclease or neuraminidase. The protein portion is therefore of major importance to the structural integrity of this antigen. The relationship between this antigen and other abnormal materials reported previously in nephroblastoma patients is being studied.
Int J Cancer 1975 Aug 15
PMID:A fetuin-like antigen from human nephroblastoma. 5 Feb 93

Twenty-three patients with stage III germinal neoplasia of the testis were treated with a variation of our original vinblastine-bleomycin program. This modification consisted of 0.4 mg/kg of vinblastine given in two fractions on Days 1 and 2 followed by continuous intravenous administration of 30 units of bleomycin in 1000 cc of 5% glucose and distilled water over a 24-hour period for 5 successive days beginning on Day 2. Therapy was repeated every 28-35 days as toxicity permitted. There were 17 responses, nine of which were complete (39%). Eight of the complete responses were in patients with massive disease in whom a low complete response rate was expected. Toxic effects consisted of severe leukopenia in 90% thrombopenia in 50%, and unexplained transient hyperbilirubinemia in about 30% of the patients. Bleomycin pneumonitis occurred in one patient and resulted in death. Hypertension was a new and unexpected side reaction experienced by four patients. Further trials are indicated since the complete response rate in patients with advanced massive disease appears to be improved.
Cancer Chemother Rep
PMID:Continuous intravenous bleomycin (NSC-125066) therapy with vinblastine (NSC-49842) in stage III testicular neoplasia. 5 12

Chick embryo cells transformed by the Bryan "high titer" strain of Rous sarcoma virus (RSV-BH) are heavily vacuolated. A variety of microscopic techniques have been used demonstrating that the vacuoles are cytoplasmic, bounded by membrane, and are composed largely of water. Proteins, lipids, glycoproteins, glycolipids, glycosaminoglycans, glycogen, and nucleic acids were undetectable in the vacuoles. Physiological requirements for development of the vacuoles, and reversal of vacuolization, were examined in cells infected with a virus mutant, RSV-BH-Ta, which induces reversible temperature-dependent transformation. Na+ was the only component of the cell culture medium found essential for both the development and reversal of vacuoles. Glucose depletion or dinitrophenol treatment inhibited vacuolization, suggesting a possible energy requirement in the vacuolization process. Ouabain, an inhibitor of Na+-K+ ATPase, enhanced vacuolization, but a variety of other substances affecting cell surface components were in active. Two sugars, glucosamine and mannosamine, prevented the disappearance of vacuoles. The observations suggest that cellular vacuolization may be a normal physiological response to an increase in water and Na+, and, in the specific case of transformation by RSV-BH, may be relevant to the physiological basis for malignancy.
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PMID:Transformation of cells by rous sarcoma virus: cytoplasmic vacuolization. 5 59


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