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

A semiautomated colorimetric assay (MTT assay), based on the ability of live cells to reduce a tetrazolium-based compound, 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide (MTT), to a purplish colored formazan product that can be measured spectrophotometrically, has recently been adapted for use in drug sensitivity analysis of cultured human tumor cell lines. We report the application of this assay for the evaluation of the growth factor requirements of human small cell lung cancer (SCLC) cell lines. Specifically, the growth stimulation of each constituent of a previously reported serum-free defined medium system for SCLC including various concentrations of hydrocortisone, insulin, transferrin, 17 beta-estradiol, and selenium (HITES) was evaluated. The optimal concentrations for insulin, transferrin, and selenium derived in the previously reported experiments with direct counting of viable cells were similar to optimal concentrations determined for the growth of three SCLC cell lines (NCI-H82, NCI-N417, NCI-H526) using the MTT assay. In contrast to the previous report, the growth-stimulating effects of hydrocortisone and 17 beta-estradiol were negligible. Using the MTT we have shown that a SCLC cell line, NCI-H345 (which has been previously reported to produce a transferrin-like molecule), was growth-inhibited by an anti-transferrin receptor antibody, when grown in transferrin-free media. The conditioned media from this cell line is stimulatory to other transferrin-sensitive cell lines, suggesting the possibility of an autocrine role for this transferrin-like molecule at least in that cell line. With carefully defined conditions for a given cell line in which cell density and other parameters are within a range of constant MTT metabolism, the assay is well suited for precise analysis of growth factor effects.
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PMID:Growth factor effects on small cell lung cancer cells using a colorimetric assay: can a transferrin-like factor mediate autocrine growth? 284 78

Three protocols were used to determine the effects of dietary selenium concentration on the development of gamma-glutamyl-transpeptidase (GGT)-positive foci and hepatocellular carcinoma induced by either diethylnitrosamine (DEN) or N-acetylaminofluorene in rats. In the first experiment, foci were induced by a carcinogenic dose of DEN (100 mg/kg body weight, p.o.) at 20-22 h after two-thirds partial hepatectomy. One wk after DEN administration, during which time 0.1 ppm (representing a control level), 3.0, or 6.0 ppm selenium as Na2SeO3 was fed for 8 or 16 wk, at which time focal analysis was conducted using quantitative stereology. The results demonstrated that 3.0 and 6.0 ppm dietary selenium, initiated 1 wk following carcinogen administration, decreased focal growth rate without affecting the number of GGT foci compared to 0.1 ppm selenium. Decreased focal growth was temporary and reversible with 6.0 ppm selenium which may be related to chronic selenosis observed after 16 wk of 6.0 ppm selenium feeding. A second experiment involved a noncarcinogenic dose of DEN (25 mg/kg body weight, p.o.), then 0.1 or 6.0 ppm selenium feeding for 8 wk, followed by 0.05% phenobarbital (PB), a liver tumor promoter in a diet containing 0.1 ppm selenium. Analysis of GGT foci at 5 or 8 wk of PB feeding indicated that 6.0 ppm selenium caused a trend towards an increase in the number of foci/cm3 of liver and mean focal volume and a significant increase in GGT focal volume as a percentage of liver volume by 8 wk of PB feeding. Thus, high dietary selenium concentrations prior to PB enhance the tumor-promoting ability of PB. In a third experiment, using male Fischer 344 rats (150 g), 0.1 or 6.0 ppm selenium was fed concurrently with 0.02% AAF which was fed in a cyclic regimen. After 4 cycles, where 1 cycle equalled 4 wk of AAF, followed by 1 wk of control diet (0.1 ppm selenium), 6.0 ppm selenium significantly decreased the mean focal volume and focal volume as a percentage of liver volume, while not affecting the number of foci/cm3 of liver, again indicating a selenium effect on focal growth while not affecting the number of "preneoplastic" lesions in the liver. Six ppm selenium feeding after AAF treatment had no effect on the percentage of incidence of hepatocellular carcinoma (100%) but did cause a significant decrease in the percentage of liver volume occupied by macroscopic subcapsular liver lesions compared to 0.1 ppm selenium.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Effects of dietary selenium concentration on the development of enzyme-altered liver foci and hepatocellular carcinoma induced by diethylnitrosamine or N-acetylaminofluorene in rats. 286 4

The phototoxicity of hematoporphyrin derivative (Hpd) to murine bladder tumor (MBT-2) cells was studied in vitro. It was observed that selenium in the form of sodium selenite enhanced Hpd-sensitized photodamage in MBT-2 cells under conditions where selenite alone was non-toxic. Sodium selenite enhanced the fluorescence emission of Hpd and augmented the Hpd-sensitized photooxidation of tryptophan. The data suggest that sodium selenite is able to disaggregate Hpd, thereby enhancing Hpd-sensitized phototoxicity.
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PMID:Selenium-induced enhancement of hematoporphyrin derivative phototoxicity in murine bladder tumor cells. 294 95

Using a chemically defined medium containing hydrocortisone, insulin, transferrin, 17 beta-estradiol and selenium, with or without serum supplementation (2.5% v/v), continuous cell lines can be established from 72% of all fresh biopsy specimens of small cell lung cancer (SCLC) containing tumor cells. No differences were observed in the rate of establishing cell lines from newly diagnosed untreated patients, or from patients who have relapsed from prior therapy, or from a variety of different organ sites. Biochemical characterization of 50 SCLC cell lines for the expression of L-dopa decarboxylase; bombesin-like immunoreactivity; neuron-specific enolase, and the brain isozyme of creatine kinase, revealed that SCLC cell lines can be subdivided into two distinct classes: classic SCLC cell lines (35 lines), which express elevated levels of all four biomarkers; and variant SCLC cell lines (15 lines) which have undetectable levels of L-dopa-decarboxylase and bombesin-like immunoreactivity, but continue to express neuron-specific enolase and the brain isozyme of creatine kinase. The presence of the latter two markers distinguishes variant lines fron non-SCLC cell lines. In addition, four distinct classes were identified morphologically. The biomedical differences among established SCLC cell lines may account for the differences in response rates to cytotoxic therapy observed in newly diagnosed SCLC patients. A prospective study of biomarker characterization of SCLC tumors will determine if clinical differences exist between classic and variant SCLC tumors.
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PMID:Establishment and identification of small cell lung cancer cell lines having classic and variant features. 298 57

Glutathione peroxidase (GSH-Px), glutathione S-transferase (GSH-Tr) and glutathione reductase (GSSG-Rx) activities have been determined in normal and neoplastic human breast tissues. Large interindividual variations in the activities of all enzymes tested were found in both tumor and non-tumor specimens. In general a significant increase in the activities of the 3 enzymes was found in tumors, whereas in fibroadenoma they were as high as in healthy tissues. When a comparison was made between normal and neoplastic tissues of the same individual, GSH-Tr and GSSG-Rx activities were found to be higher in 15 and 11 cases, respectively, out of 17. GSG-Px activity was higher in all cases. From measurement of GSG-Px activity with both H202 and cumene hydroperoxide, it was deduced that human breast contains only the selenium-dependent form.
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PMID:Glutathione peroxidase, glutathione S-transferase and glutathione reductase activities in normal and neoplastic human breast tissue. 299 88

Research in varied populations, in appropriate animal models, and through other laboratory techniques, in great part fostered through the National Large Bowel Cancer Program of the National Cancer Institute, has provided a reasonable basis for assessing environmental elements as to risk for large bowel cancer. It was noted that the term large bowel cancer needs to be specifically related to subsections of the large bowel that appear to have different risk factors. For the major type of neoplastic disease in the large bowel, that in the descending and sigmoid colon, there is a good association with nutrition and specific nutritional elements. The risk of this type of colon cancer is proportional to the customary dietary fat intake--high in the western world and low in the Orient. It is inversely proportional to stool bulk, itself related to cereal fiber intake. These two major elements are sufficiently secure as to underlying scientific data and understanding of mechanisms to permit utilizing them for personal modification of risk. Thus, a dietary regimen low in total fat, 20% of calories, and higher in cereal fiber, of the order of 30 g per day, are indicated and would serve to reduce risk not only in the general population, but most likely also in patients who have been successfully treated through conventional modalities. There are also suggestions that regular intake of yellow and green vegetables, of foods with calcium salts, selenium, and other micronutrients, lower risk even more. Further research is needed to provide the data base necessary for deliberate interventions with these agents.
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PMID:Potential for personal modification of risk for developing colon cancer. 299 20

The influences of vitamin C and vitamin E on cancer reported in the literature are reviewed. Several correlational studies and case-control studies suggest that the consumption of vitamin C-containing foods is associated with lower risk for certain cancers, particularly gastric and esophageal cancer. No definite links between dietary vitamin E and human cancer have been demonstrated. Animal and in vitro studies have shown that vitamins C and E can effectively inhibit the formation of carcinogenic nitrosamines. However, animal studies examining the effects of these two vitamins on other chemically-induced cancers are not conclusive. Vitamin C supplementation has been reported to inhibit skin, nerve, lung and kidney carcinogenesis. Vitamin E has been shown to inhibit skin, liver, oral, ear duct, and forestomach carcinogenesis; and to enhance, to have no effect on, or to inhibit mammary gland or colon carcinogenesis, depending upon the method of administration, the level of dietary selenium or fat, and the species and strain of animals used. Both vitamin C and vitamin E can inhibit mutagenesis and carcinogenesis in vitro. Each of the vitamins has been shown to inhibit tumor cell growth and carcinogen-induced DNA damage. The mechanism of action of the two vitamins against carcinogens is not clearly understood. Several suggested mechanisms of action include modification of the metabolism of polycyclic hydrocarbons, reduction of mutagenic activity and reaction with genotoxic free radicals. It is concluded that the potential usefulness of vitamin C and vitamin E in the prevention and treatment of cancer should not be ignored because under certain experimental conditions these two vitamins exert inhibitory effects on chemical carcinogenesis. More carefully standardized and controlled experiments are required to adequately evaluate this potential.
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PMID:Vitamin C, vitamin E and cancer (review). 305 51

The objectives of this study were a) to compare the efficacy of inorganic and organic selenium compounds in protecting against mammary tumorigenesis induced by 7,12-dimethylbenz[a]anthracene [(DMBA); CAS: 57-97-6] in rats and b) to study the interaction of vitamin C with either selenite (inorganic) or seleno-DL-methionine (organic) in chemoprevention. Control Sprague-Dawley rats were fed a purified 5% corn oil diet containing 0.1 ppm selenium. Selenite or seleno-DL-methionine was added to the basal diet in concentrations of 2, 3, or 4 ppm starting 1 week after DMBA administration. The inhibitory response in mammary tumorigenesis with selenium supplementation was dose dependent. Both selenium compounds were found to be equally efficacious in prophylaxis, although at the 4-ppm level a slight reduction in growth was observed. In the second experiment, different concentrations of vitamin C (0.2, 0.5, and 1%) were tested. In general, there was no change with the two lower levels; but a slight, although insignificant, increase in tumor yield was detected in rats supplemented with 1% vitamin C in the diet. The interaction of 0.5% vitamin C with either selenite or seleno-DL-methionine (3 ppm) was studied in the third experiment. Results showed that the protective effect of selenite in tumorigenesis was nullified by vitamin C, whereas the chemopreventive action of seleno-DL-methionine was not affected. It is possible that selenite is reduced by vitamin C to elemental selenium and is therefore not available for uptake by tissues. This hypothesis was indirectly supported by tissue selenium measurements showing that 0.5 or 0.25% of vitamin C in the diet completely negated in blood, liver, and mammary gland the accumulation of selenium induced by 3 ppm of selenite supplementation. Lower levels of vitamin C (less than or equal to 0.1%) were found to have no effect on tissue selenium concentrations. Furthermore, the presence of 0.1% vitamin C in the diet no longer abolished the anticarcinogenic effect of selenite. This study suggests that high levels of vitamin C can interfere with the accumulation of tissue selenium and that an increased titer of this trace element in cells is essential for retarding tumor development.
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PMID:Interaction of vitamin C and selenium supplementation in the modification of mammary carcinogenesis in rats. 308 12

Selenium is effective in inhibiting the incidence and total number of tumors resulting from treatment with various chemical carcinogens. This inhibition occurs both at the initiation and promotion phases of chemical carcinogenesis. At least part of the inhibition of the initiation stage is associated with changes in the metabolism of the parent carcinogen. Studies with 7,12-dimethylbenz(a)anthracene suggest that selenium specifically blocks the enzyme(s) responsible for the formation of anti-dihydrodiol epoxide adducts to DNA. Selenium is also effective in reducing the in vitro and in vivo growth of numerous neoplastic cells. However, differences in the sensitivity to selenium are evident in the various tumor cell lines that have been examined. Continuous selenium intake appears to be necessary to maximal inhibition in both models of carcinogenesis. Evidence suggests that selenodiglutathione or some other intermediate in selenium metabolism is responsible for the anticarcinogenic and antitumorigenic properties of this trace element. The mechanism by which selenium produces these effects is unknown, but it may relate to alterations in either RNA transcription or translation. These and other data strongly suggest that selenium is a naturally occurring anticarcinogenic and antitumorigenic agent.
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PMID:Inhibition of chemical carcinogenesis and tumorigenesis by selenium. 310 18

The role of nutritional factors in the management of acquired immunodeficiency syndrome-related, or epidemic, Kaposi's sarcoma (EKS) is complex, since there are known interactions between malnutrition, immunodeficiency, and cancer. Malnutrition is a well-established cause of immune aberrations, which are seen in deficiencies of both protein and energy, as well as specific nutrients, particularly trace metals. Conversely, malnutrition is a common result of both cancer and immunodeficiency. Cancer patients without an obviously immunological pathogenesis frequently have malnutrition and cachexia, mainly as a result of a decreased dietary intake and poorly defined host-tumor interactions (commonly labeled "hypermetabolic"). Patients with primary immunodeficiency syndromes similarly experience a triad of diarrhea, malabsorption, and weight loss, which are responsible for the development of malnutrition. This triad is common in patients with AIDS, with or without the presence of Kaposi's sarcoma. The specific mechanisms of these interactions in EKS patients are largely unexplored; although some can be explained by the enteropathic effects of opportunistic infections, others can not. Some investigators have advocated careful nutritional evaluation of all AIDS patients, with vigorous nutritional support to be provided where assessment reveals suboptimal nutritional status. Specific nutrient deficiencies have been reported, of which selenium may be the most interesting; preliminary data indicate that it may be responsible for a malnutrition-related immunodepression seen with AIDS. Such supportive measures may significantly improve symptomatic relief, but there is as yet no evidence that they alter the course of the disease.
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PMID:Nutritional factors in epidemic Kaposi's sarcoma. 311 Sep 57


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