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

Several radiopharmaceuticals have recently been shown to have a considerable affinity for malignant tissue. All the tumor-seeking radiopharmaceuticals in current use are nonspecific and may also be picked up by benign tumors and infectious processes, including abscess and granuloma. The sensitivity of the tumor-imaging procedure depends on the radiopharmaceutical employed, the type of tumor, its size and location, and previous or current treatment. Gallium-67 citrate (67Ga), the most widely used tumor-seeking radiopharmaceutical, seems to have its greatest value in detecting bronchogenic carcinomas irrespective of cell type. The sensitivity for lung cancer in 489 studies was 93 per cent. Gallium-67 is also of great value in the staging of Hodgkin's disease, in which its sensitivity is 87 per cent. Non-Hdgkin's lymphomas are detected with only slightly lower sensitivity. There is, in fact, evidence that 67Ga is at least complemenatry, if not more sensitive than lymphangiography, in the staging of lymphoma. However, adenocarcinomas originating in the gastrointestinal tract are detected by 67Ga with a sensitivity of only about 40 per cent, whereas various chelates of bleomycin (including 111In-Bleo, 99mTc-Bleo and 57Co-Bleo) detect adenocarcinoma of the gastrointestinal tract with considerably higher sensitivity. In the few studies available comparing bleomycin chelates, 57Co-Bleo and 99mTc-Bleo appear to be more sensitive in detecting tumor than 111In-Bleo. Other tumor-seeking radiopharmaceuticasl which have been employed with somewhat less success include selenium compounds, labeled pyrimidines, several inorganic cations, lanthanide chelates and labeled proteins. Yet to be evaulated clinically is the efficacy of radiolabeled antibodies which are specific for tumor antigens, such as 131I-anti-CEA (carcinoembryonic antigen).
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PMID:Cancer diagnosis. The role of tumor-imaging radiopharmaceuticals. 5 31

On 25 rats with DMBA induced mammary gland adenocarcinoma, there was shown the capacity of a tumoritropic labelled preparation sodium selenium-75-selenite be be absorbed by tumors in the amounts exceeding those in the adjacent muscle days after the administration. A coefficient of the differential accumulation characterizing the level of the isotope uptake by a tumor during the whole period of observation was 3--4. First, there was shown the possibility to use the model of mammary gland tumors induced by DMBA to test labelled tumoritropic compounds.
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PMID:[Study of the tropism of sodium Selenium-75-selenite to experimental cancer of the mammary gland]. 11 38

Groups of male Sprague--Dawley rats were maintained on three regimens: I. basal diet plus 0.05% 3'-methyl-4-dimethylaminoazobenzene (3'-MeDAB), II. same as I plus 6 ppm selenium (Na2SeO3) in the drinking water, and III. same as I plus 6 ppm selenium added to the diet in the form of a high selenium yeast. The 3'-MeDAB was incorporated in the diet for 8 weeks and then removed. The selenium supplements in Groups II and III were continued for an additional 4 weeks. At sacrifice the liver tumor incidence from was ascertained as the ratio of animals with tumors/total number of surviving animals per group. Selenium reduced the incidence from 92% (11/12) in the Group I control, to 46% (7/15) in Group II and to 64% (9/14) in Group III.
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PMID:Effects of selenium on azo dye hepatocarcinogenesis. 19 14

Xeroradiography, a method of X-ray imaging based upon selenium photoconductivity, was used for the study of experimental osteosarcoma induced by MSV-M virus in rats. Due to the peculiar features of xeroradiographic image (enhancement of details and lowering of the overall contrast) good pictures of osseous structures together with soft tissues were obtained even in very young animals. Serially perfomred xeroradiographies gave a permanent representation of tumor evolution with time. Advantages and drawbacks of this method are discussed, particularly with respect to radiation dosage. Xeroradiography is proposed for the study of the response to antiblastic chemotherapy of experimental bone tumors.
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PMID:Xeroradiographic evaluation of murine osteosarcoma. 27 Aug 62

Selenium (Se) inhibition of either the activation of test compounds and/or mutagenic events elicited by activated compounds is suggested by experimental rat assays, mutagenesis assays, and assays with human lymphocytes in culture. The colon tumor incidence in 1,2-dimethylhydrazine (DMH)-treated rats was reduced from 87% to 40% by 4 ppm Se supplements in the drinking water. Supplemental Se decreased the total number of colon tumors induced by DMH more than three-fold and by methylazoxymethanol (MAM) almost two-fold. Coexposure of Salmonella typhimurium TA 1538 to an effective molar ratio of Se/2-acetylaminofluorene=10, Se/N-OH-acetylaminofluorene=10 and SE/N-OH-aminofluorene=300 reduced the mutagenicity to 65, 68, and 61% of their respective controls with mutagen alone. With a molar ratio of Se/N-OH-AAF=100, Se reduced the activity to 28% of the mutagenicity of N-OH-AAF alone. Preliminary data indicating MAM is mutagenic in S. typhimurium TA 1535 and His G 46(6837) are presented. In toxicity studies exposure of human lymphocyte cultures to 1.3 X 10(-9) to 1.6 X 10(-5) M Se yielded sister chromatid exchange (SCE) rates equivalent to background levels of 6--7 SCE per cell. The SCE frequencies of lymphocytes cultured with Se and selected carcinogens are discussed.
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PMID:Inhibitory effects of selenium on 1,2-dimethylhydrazine and methylazoxymethanol colon carcinogenesis: correlative studies on selenium effects on the mutagenicity and sister chromatid exchange rates of selected carcinogens. 33 88

An investigation was conducted to determine the effect of the dietary level of selenium on the induction of tracheal cancer by 1-methyl-1-nitrosourea (MNU). Male Syrian golden hamsters received intratracheal instilations of a 0.5% MNU solution once weekly for 12 weeks. Two weeks prior to the initiation of carcinogen treatment, animals were placed on a semisynthetic, 30% torula yeast diet to which either no selenium or 1 or 5 mg selenium/kg of diet as sodium selenite was added. Animals were maintained on their respective diets for the duration of the study which was terminated 195 days after the first MNU treatment. No significant differences among groups in the incidence of either benign lesions or carcinomas was observed and the distribution of tumor type was similar irrespective of selenium treatment. The results of this study indicate that selenium exerts no chemopreventive effect against MNU-induced tracheal carcinogenesis.
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PMID:Effect of graded dietary levels of selenium on tracheal carcinomas induced by 1-methyl-1-nitrosourea. 50 5

The effect of Ehrlich ascites tumor growth on selenium-turnover rates and selenium-75 distribution in liver, kidney, and immunological tissues (spleen, thymus, and lymph nodes) was investigated in Swiss Webster mice that had been prelabeled with selenium-75. Ehrlich ascites tumor caused a decrease in the selenium-75 content of liver, kidney, and thymus; it also decreased the rate of the total-body selenium-turnover. In liver, depletion of selenium-75 was almost as great as that produced by a selenium and vitamin E-deficient diet. When mice had been fed an antioxidant-deficient diet, considerable quantities of selenium-75 were accumulated by the tumor; the specific activity of the tumor increased 9-fold over that in antioxidant-supplemented mice. The same diet produced a premature, and in some cases drastic, contraction in tumor volume. The possible significance of tumor-induced antioxidant deficiencies to the etiology of certain paraneoplastic syndromes is discussed.
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PMID:Antioxidant effects in the development of Ehrlich ascites carcinoma. 62 17

Inbred female C3H/St mice exhibit the normal incidence of spontaneous mammary adenocarcinoma of 80--100% if they are maintained on a standard commercial laboratory diet containing 0.15 ppm of selenium with meat and dried skimmed milk as major sources of protein. The tumor incidence drops to 42% if animals of the same strain are kept on a diet containing 0.45 ppm of selenium, with fishmeal as the main source of protein. The tumor incidence declines further to 25, 19 and 10% if the animals in addition receive 0.1, 0.5, and 1.0 ppm of selenium in the drinking water. Selenium supplementation at these levels has no noticable adverse effects on weight-grains and survival of the mice. Selenium supplmented groups of animals also remained tumor-free for longer periods than the unsupplemented controls. The results of this study indicate that a diet rich in seafoods and cereals provides more selenium and may in turn lower the probability of cancer development. Reference is made to the average human diet in the U.S.A., which only contains 0.07--0.15 ppm of selenium due to the comparatively low consumption of cereals and seafoods. An equivalent mouse diet would not have any cancer-protecting effect in the C3H/St mice of our study. Australian workers have reported significantly lower tumor incidence in a different strain of C3H mice if it was kept in Australia rather than in the U.S.A. We have found that the Australian feed contained three times more selenium than that employed in the U.S.A. and propose that this difference in selenium content was primarily responsible for these previous observations.
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PMID:Selenium and cancer: effects of selenium and of the diet on the genesis of spontaneous mammary tumors in virgin inbred female C3H/St mice. 68 69

The essential trace element selenium retards the growth of certain chemically induced tumors in animals. The addition of subtoxic amounts of this element in form of selenite to the supply water lowers the incidence of spontaneous mammary tumors in female C3H mice significantly without affecting the health and life-span of the animals. Arsenic, a selenium antagonist, administered in form of arsenite in the supply water, also lowers the tumor incidence at dosage levels of 10 ppm, but those animals which develop spontaneous mammary tumors under these conditions demonstrate dramatically enhanced tumor growth rates. The results of initial epidemiological studies suggest that the human cancer mortality is lower in areas providing an adequate dietary intake of selenium as estimated from the selenium content in grains and forage crops in various regions of the United States, or the dietary selenium intakes as calculated from food consumption data in various countries.
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PMID:Selenium and cancer: a review. 76 40

Age-corrected mortalities from cancer at 17 major body sites were correlated with the apparent dietary selenium intakes estimated from food-consumption data in 27 countries. Significant inverse correlations were observed for cancers of large intestine, rectum, prostate, breast, ovary, lung and with leukemia; weak inverse associations were found for cancers of pancreas, skin and bladder. Similar inverse corelations were found between cancer mortalities at the above sites and the selenium concentrations in whole blood collected from healthy human donors in the U.S. and different countries. The results support the hypothesis that selenium has cancer-protecting effects in man. Other studies are cited which demonstrate that selenium prevents or retards tumor development in animals. A change of diet aimed at increasing the dietary selenium supply is suggested as a possible means of lowering the human cancer risk. It is postulated that the cancer mortalities in the U.S. and other Western industrialized nations would decline significantly if the dietary selenium intakes were increased to approximately twice the current average amount supplied by the U.S. diet.
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PMID:Cancer mortality correlation studies--III: statistical associations with dietary selenium intakes. 85 91


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