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Query: UMLS:C0242379 (lung cancer)
 71,905 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Epidemiological data and results of toxicity studies in experimental animals indicate the possible health risk of diesel exhaust exposure. Acute effects of this exposure include odor, eye irritations, lung function decrements, cardiovascular symptoms, and some non-specific effects. Most of these effects are reported among persons highly exposed to diesel exhaust. Lung function decrements are reported as chronic effects. Another chronic effect that has been studied extensively among occupationally exposed persons in lung cancer. In addition to lung cancer, but at a less frequent rate, an enhanced incidence of bladder cancer is reported. The carcinogenic action of diesel exhaust exposure is ascribed to effects of the soot particles, particle-associated organics, and/or gas phase compounds. Direct effects of the particle load may include retardation of lung clearance, inflammation, and increased cell proliferation. These effects were all demonstrated in rodents. The particles may also prolong the residence time of particulate organics or induce the generation of reactive oxygen species. These compounds are known to react with macromolecules, causing lipid peroxidation, DNA damage, and/or activation of other genotoxic substances such as polycyclic aromatic hydrocarbons (PAHs). However, these results have not yet been confirmed in mammals in vivo. A direct interaction of particles with lung tissue is also suggested as a cause of cancer but a mechanism for this interaction has not yet been proposed. Organics associated with the particles are known to contain genotoxic properties attributable to PAHs and their derivatives. A number of these compounds are also identified as carcinogens in animal studies. However, it is not clear whether parent PAHs, their nitro-, oxy-, alkylated, or heterocyclic derivatives, or possibly other compounds are principally responsible for inducing tumors in the lungs of animals after diesel exhaust exposure. Furthermore, the mechanism of the bioavailability of these organics is not completely understood. The effects of gas phase constituents on the carcinogenic properties of the particles and/or particle-associated organics either have not been investigated or the findings have been inconclusive.
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PMID:Combustion of diesel fuel from a toxicological perspective. II. Toxicity. 138 63

Epidemiologic studies have demonstrated an inverse relation between vitamin A intake and lung cancer rate. There is strong evidence that the provitamin A, beta-carotene, plays a more important role in the protective effect than vitamin A itself. The anticarcinogenic properties of beta-carotene have so far been attributed to its scavenger properties in deactivating or trapping reactive chemical species such as singlet oxygen and certain organic free radicals. Smoking results in increased excretion of detoxification products of electrophilic agents (mercapturic acids) in urine. Since reactive electrophilic intermediates are involved in carcinogenesis, we performed a double-blind, placebo-controlled intervention trial to investigate whether the intake of beta-carotene by smokers would affect urinary thioether excretion. Before the intervention the beta-carotene group (n = 62) and the placebo group (n = 61) had similar thioether excretion levels in urine (4.2 vs 4.3 mmolSH/mol creatinine). During the intervention (20 mg beta-carotene daily for 14 weeks) the placebo group showed a 12% increase, whereas the beta-carotene group showed a 5% decrease (P = 0.004). After the intervention the beta-carotene group had a 15% lower thioether excretion level than the placebo group (4.1 vs 4.7 mmolSH/mol creatinine; P = 0.0017). Our study shows that urinary thioether excretion varies considerably over time, and that smokers have a decreased excretion of thioethers in urine after the use of beta-carotene.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Decreased excretion of thioethers in urine of smokers after the use of beta-carotene. 139 32

Epidemiological data have revealed significant excesses of lung cancer among workers exposed to some types of man-made mineral fibers (MMMF), but inhalation experiments performed on rats have failed to reveal the origin of these excesses. Some of these materials, however, are able, in aqueous media, to exhibit surface oxidizing properties after reduction of oxygen by a radical pathway. Tests have been carried out with 12 MMMF samples collected from various sources without prior knowledge of their origin, to determine their oxidizing surface activity in relation to their divalent iron content. Some of these fibers were obtained from factories included in an epidemiological investigation. Only fibers coming from plants where excesses of lung cancer were observed are classified as active in an oxidative process and, consequently, probably toxic in biological media by an oxidative stress mechanism. We therefore propose an hypothesis of a causal relationship between these oxidizing properties and the ability of the materials to induce lung cancer.
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PMID:Man-made mineral fibers and lung cancer: an hypothesis. 154 87

Neuroendocrine lung cancers can be induced in hamsters within 8-12 weeks by combined exposure to N-nitrosodiethylamine (DEN) and hyperoxia. The expression of the c-Ki-ras gene in this lung cancer model was studied using polymerase chain reaction analysis of mRNA (RNA/PCR). We used four different groups of hamsters, exposed for 6 weeks to DEN with hyperoxia (60% oxygen), DEN, hyperoxia, or ambient air, respectively. Total RNA was isolated from lung tissues and cDNA made prior to PCR amplification. A 234-bp product was amplified from c-Ki-ras cDNA and quantitated using scanning laser densitometry. The data obtained were normalized to the expression of the house keeping gene B-actin. The c-Ki-ras products were present after amplification of all hamster lung RNA samples. The hamster lungs exposed to DEN with hyperoxia displayed higher c-Ki-ras protooncogene expression than hamsters exposed to DEN, hyperoxia, or ambient air alone. Since the animals studied were sacrificed at 6 weeks, prior to the appearance of tumors, we conclude that this increased expression may indicate a role for c-Ki-ras in the initial steps in malignant transformation of neuroendocrine cells.
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PMID:Increased c-Ki-ras expression in hamster lung exposed to N-nitrosodiethylamine and hyperoxia as detected by the polymerase chain reaction. 171 35

Syrian Golden hamsters received 8 weekly intratracheal instillations of 0.2 microCi of the alpha-emitting isotope Po210 while being exposed to an atmosphere of 65% oxygen in the inspired air. Three months later, 42% of the animals had poorly differentiated lung carcinomas. On the other hand, no lung tumors were found in hamsters that received intratracheal instillations of Po210 and were kept in air. It is concluded that diffuse cell hyperplasia in the lung, caused by an inhalant, may constitute an additional risk factor in the pathogenesis of alpha-radiation induced lung cancer.
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PMID:Diffuse and continuous cell proliferation enhances radiation-induced tumorigenesis in hamster lung. 175 8

Parameters of functional status of the hemostatic system were studied in 76 breast and lung cancer patients in the course of radiotherapy using TTC-10 hypoxic gas mixture (oxygen--10% and nitrogen--90%) as radioprotector. The thrombophilic status of the blood in breast and lung cancer patients established prior to treatment was accounted for by increased functional activity of platelets, increased capillary blood coagulability, formation of dense clot and inhibition of fibrinolysis. In the course of hypoxyradiotherapy, blood thrombogeneity becomes lower due to a decrease in platelet adhesion.
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PMID:[The hemostatic state of patients with breast and lung cancer undergoing hypoxic radiotherapy]. 184 52

We describe eight patients who had terminal lung cancer causing severe dyspnea unrelieved by oxygen, nonnarcotic drugs, or intermittent bolus narcotics. We treated these patients with continuous intravenous infusion of morphine, beginning with bolus IV injections of 1 or 2 mg of morphine every 5 to 10 minutes until the patient reported relief. A continuous morphine infusion was then started, with the hourly dose equal to 50% of the cumulative bolus dose. Vital signs, degree of sedation, and blood gases were serially followed. Six patients achieved good dyspnea relief, one had moderate relief, and one had a poor response. Variable changes were noted in the PaO2, whereas PaCO2 steadily increased in five of seven patients, and pH decreased in six. There was little change in systolic blood pressure or pulse, and only one individual had less than 10 respirations per minute. The major side effect of treatment was sedation, treated by temporarily discontinuing morphine until the patients' mental status improved and then restarting the infusion at a 50% lower hourly morphine dose. Mean time of study was 30 hours (range 16 to 87 hours). Seven of the eight study patients died during treatment. Whether morphine therapy shortened survival is uncertain. We conclude that continuous morphine infusion is effective therapy for severe dyspnea. The treatment is ethically justified. Relief of suffering is the primary goal of therapy, and less risky treatments are unavailable.
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PMID:Continuous intravenous infusion of morphine for severe dyspnea. 189 95

Selected immunotherapies (tumor necrosis factor, interleukin-1, interleukin-2, and gamma interferon), chemotherapeutic agents (mitomycin, platinum, doxorubicin [Adriamycin], and bleomycin), and radiation therapy have been described to exert cytotoxicity through the generation of reactive oxygen species, including superoxide and hydrogen peroxide. Tumor necrosis factor, however, has been shown to impart increased resistance in vitro and in vivo against reactive oxygen species stress, including radiation therapy and oxygen toxicity, possibly because of the induction of increased cellular buffering capacities. It is unknown whether the sensitivity of a lung cancer cell to reactive oxygen species therapy is altered by tumor necrosis factor through the induction of free radical scavenging enzymes such as manganese superoxide dismutase. This question was investigated as follows: A549 lung adenocarcinoma cells, exposed for 24 hours to 0, 0.1, 1.0, or 10 micrograms/ml concentrations of tumor necrosis factor, were exposed to hypoxanthine plus xanthine oxidase, a superoxide generating system, for varying intervals. The number of cells surviving 5 days after the stress was determined, and cells exposed to tumor necrosis factor were examined by Northern Blot analysis for induction of the manganese superoxide dismutase gene. The hypoxanthine-xanthine oxidase stress alone caused a time-dependent decrease in survival; however, pretreatment with tumor necrosis factor increased cell survival significantly. Moreover, the cells exposed to tumor necrosis factor had a fivefold increase in the number of manganese superoxide dismutase transcripts. These findings suggest that tumor necrosis factor may confer resistance of lung cancer cells to subsequent reactive oxygen species-based therapies, and the resistance of these cells may be due to increased expression of manganese superoxide dismutase. Clinical treatment failures may result, especially if tumor necrosis factor is given concurrently with other therapies.
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PMID:Tumor necrosis factor-alpha alters response of lung cancer cells to oxidative stress. 196 Sep 95

The evidence that ETS increases risk of death from heart disease is similar to that which existed in 1986 when the US Surgeon General concluded that ETS caused lung cancer in healthy nonsmokers. There are 10 epidemiological studies, conducted in a variety of locations, that reflect about a 30% increase in risk of death from ischemic heart disease or myocardial infarction among nonsmokers living with smokers. The larger studies also demonstrate a significant dose-response effect, with greater exposure to ETS associated with greater risk of death from heart disease. These epidemiological studies are complemented by a variety of physiological and biochemical data that show that ETS adversely affects platelet function and damages arterial endothelium in a way that increases the risk of heart disease. Moreover, ETS, in realistic exposures, also exerts significant adverse effects on exercise capability of both healthy people and those with heart disease by reducing the body's ability to deliver and utilize oxygen. In animal experiments, ETS also depresses cellular respiration at the level of mitochondria. The polycyclic aromatic hydrocarbons in ETS also accelerate, and may initiate, the development of atherosclerotic plaque. Of note, the cardiovascular effects of ETS appear to be different in nonsmokers and smokers. Nonsmokers appear to be more sensitive to ETS than do smokers, perhaps because some of the affected physiological systems are sensitive to low doses of the compounds in ETS, then saturate, and also perhaps because of physiological adaptions smokers undergo as a result of long-term exposure to the toxins in cigarette smoke. In any event, these findings indicate that, for cardiovascular disease, it is incorrect to compute "cigarette equivalents" for passive exposure to ETS and then to extrapolate the effects of this exposure on nonsmokers from the effects of direct smoking on smokers. These results suggest that heart disease is an important consequence of exposure to ETS. The combination of epidemiological studies with demonstration of physiological changes with exposure to ETS, together with biochemical evidence that elements of ETS have significant adverse effects on the cardiovascular system, leads to the conclusion that ETS causes heart disease. This increase in risk translates into about 10 times as many deaths from ETS-induced heart disease as lung cancer; these deaths contribute greatly to the estimated 53,000 deaths annually from passive smoking. This toll makes passive smoking the third leading preventable cause of death in the United States today, behind active smoking and alcohol.
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PMID:Passive smoking and heart disease. Epidemiology, physiology, and biochemistry. 191 25

Antioxidant micronutrients are one of the body's primary defenses against free radicals and reactive oxygen molecules. Carotenoids, vitamin C, and vitamin E trap these molecules, and selenium is an essential component of an antioxidant enzyme. There is considerable support from animal studies for a protective effect of antioxidant micronutrients on cancer. However, the role of these micronutrients in cancer prevention in humans is less clear. Diet studies suggest protective effects of fruits and vegetables on risk of cancer at several sites. Inverse associations between dietary carotenoids and serum beta-carotene and lung cancer have been observed repeatedly. Vitamin C has also been consistently inversely associated with risk of oral and esophageal cancer in diet studies and with stomach cancer in both diet and plasma studies. It remains unknown, however, whether carotenoids and vitamin C or some other component of fruits and vegetables, the primary sources of these micronutrients, prevent cancer in humans. Selenium has been inversely correlated with cancers at numerous sites in ecologic studies, but observational studies do not provide strong support for a protective effect of selenium on cancer at any site. There also is not strong support for a protective effect of vitamin E on cancer in humans. Results of studies on the association of antioxidant micronutrients with cancer at many sites are inconsistent. This could be due to lack of a true protective effect or could be related to methodologic problems in assessing dietary intake in epidemiologic studies.
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PMID:Antioxidant micronutrients in cancer prevention. 202 68


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