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

Bone metastases are a major cause of cancer morbidity. Bone metastases are associated with pain, fractures, spinal cord compression, ineffective haematopoiesis, and hypocalcaemia of malignancy. The goals of treatment for bone metastases are to prevent disease-related skeletal complications, palliate pain, and maintain quality of life. Bisphosphonates are a standard part of supportive care for patients with bone metastases. Zoledronic acid, a nitrogen containing third generation bisphosphonate, is the most active and is the most thoroughly investigated bisphosphonate for metastatic bone disease. The efficacy and safety of zoledronic acid has been established in three pivotal prospective, randomized controlled trials involving more than 3000 subjects. The evidence is reviewed here with a focus on clinical relevance. Across a broad array of tumour types, zoledronic acid (4 mg intravenously over 15 min every 3-4 weeks) decreased the frequency of skeletal-related events, delayed the time to a first skeletal-related event, and reduced pain. Zoledronic acid is more effective than pamidronate in breast cancer and the only bisphosphonate proven effective for metastatic prostate cancer, lung cancer, renal cell carcinoma and other solid tumours.
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PMID:Zoledronic acid to prevent skeletal complications in cancer: corroborating the evidence. 1622 55

Recent studies suggest that reactive oxygen (ROS) and nitrogen species (RNS) are highly associated with the pathogenesis of cigarette smoke related lung diseases but their role in the malignant conversion of bronchial epithelium is unclear. The immunohistochemical expression of inducible, endothelial and neuronal nitric oxide synthases (iNOS, eNOS and nNOS) and nitrotyrosine as a biomarker of oxidative/nitrosative stress was evaluated in 79 cases including 13 non-smokers, 20 smokers without chronic obstructive pulmonary disease (COPD), 22 with COPD and 24 with metaplasia-dysplasia-sequence of the bronchial epithelium. Normal lung of non-smokers was mainly negative for nitrotyrosine, while it was higher in the alveolar macrophages of cigarette smokers and COPD than in non-smokers (p=0.025, p<0.001), and in the alveolar epithelium of smokers and COPD than in non-smokers (p=0.049). There were no major differences in the nitrotyrosine immunoreactivity between the metaplastic/dysplastic lesions and bronchial epithelium of cigarette smokers. Inducible NOS and nNOS were mainly non-detectable or weak in the normal looking bronchial epithelium of smokers and COPD, whereas metaplasia and dysplasia showed positivity for iNOS (22/24) and nNOS (14/24) in the majority of cases. Strong immunoreactivity for iNOS and nNOS was also found more often in dysplastic than metaplastic (p=0.011 and p=0.049, respectively) specimens. Thus, smoking can cause protein nitration also in normal lung. Prominent iNOS and nNOS immunoreactivity in the metaplasia-dysplasia-lesions suggests a divergent role of NOSs in lung carcinogenesis.
Lung Cancer 2006 Mar
PMID:Nitric oxide synthases are associated with bronchial dysplasia. 1642 Sep 64

Epidemiological evidence has concurred with clinical and experimental evidence to correlate current levels of ambient air pollution, both indoors and outdoors, with respiratory effects. In this respect, the use of specific epidemiological methods has been crucial. Common outdoor pollutants are particulate matter, nitrogen dioxide, carbon monoxide, volatile organic compounds and ozone. Short-term effects of outdoor air pollution include changes in lung function, respiratory symptoms and mortality due to respiratory causes. Increase in the use of health care resources has also been associated with short-term effects of air pollution. Long-term effects of cumulated exposure to urban air pollution include lung growth impairment, chronic obstructive pulmonary disease (COPD), lung cancer, and probably the development of asthma and allergies. Lung cancer and COPD have been related to a shorter life expectancy. Common indoor pollutants are environmental tobacco smoke, particulate matter, nitrogen dioxide, carbon monoxide, volatile organic compounds and biological allergens. Concentrations of these pollutants can be many times higher indoors than outdoors. Indoor air pollution may increase the risk of irritation phenomena, allergic sensitisation, acute and chronic respiratory disorders and lung function impairment. Recent conservative estimates have shown that 1.5-2 million deaths per year worldwide could be attributed to indoor air pollution. Further epidemiological research is necessary to better evaluate the respiratory health effects of air pollution and to implement protective programmes for public health.
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PMID:[Air pollution and the lung: epidemiological approach]. 1682 33

This study investigated the concentration-response relation between air pollution (nitrogen dioxide and particulate matter pollutants PM(10) and PM(2.5)) and cause-specific mortality. The population included all inhabitants of Oslo, Norway, aged 51-90 years on January 1, 1992 (n = 143,842) with follow-up of deaths from 1992 to 1998. An air dispersion model (AirQUIS; Norwegian Institute for Air Research (NILU), Oslo, Norway) was used to estimate levels of exposure in 1992-1995 in all 470 administrative neighborhoods. These data were linked to census, education, and death registries. A consistent effect on all causes of death was found for both sexes and age groups by all indicators of air pollution. The effects appeared to increase at nitrogen dioxide levels higher than 40 micro g/m(3) in the youngest age group and with a linear effect in the interval 20-60 micro g/m(3) for the oldest. An effect of all indicators on cardiovascular causes, lung cancer, and chronic obstructive pulmonary disease was also found in both age groups and sexes. The effects were particularly strong for chronic obstructive pulmonary disease, which appeared to have linear effects, whereas cardiovascular causes and lung cancer seemed to have threshold effects. Results show that vulnerable persons with chronic obstructive pulmonary disease and the elderly seem to be susceptible to air pollution at lower levels than the general population.
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PMID:Relation between concentration of air pollution and cause-specific mortality: four-year exposures to nitrogen dioxide and particulate matter pollutants in 470 neighborhoods in Oslo, Norway. 1713 27

High levels of ethylene oxide (EO) and acetaldehyde (AE) were detected, using gas chromatography and a portable gas detector, among volatile organic compounds (VOC) emitted during simulated frying of herbs and spices in soybean oil at temperatures between 120 degrees C and 200 degrees C. Both EO and AE were distributed between the gas phase and oil phase after cooking each vegetable at 150 degrees C for 5min under either nitrogen or air at 1atm. EO concentrations in the gas phase (25-75ppm) exceeded the threshold limit value of 1ppm, the TLV TWA value established by the American Conference of Government Industrial Hygienists and permitted by the Occupational Safety and Health Administration. EO has been identified as a significant carcinogen. Thus, while no causal relationship can be concluded from this study, the results suggest a possible relationship between the high levels of EO emitted during frying and the high incidence of lung cancer among Taiwanese women engaged in traditional cooking.
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PMID:Emission of ethylene oxide during frying of foods in soybean oil. 1714 88

Hazardous chemicals escape to the environment by a number of natural and/or anthropogenic activities and may cause adverse effects on human health and the environment. Increased combustion of fossil fuels in the last century is responsible for the progressive change in the atmospheric composition. Air pollutants, such as carbon monoxide (CO), sulfur dioxide (SO(2)), nitrogen oxides (NOx), volatile organic compounds (VOCs), ozone (O(3)), heavy metals, and respirable particulate matter (PM2.5 and PM10), differ in their chemical composition, reaction properties, emission, time of disintegration and ability to diffuse in long or short distances. Air pollution has both acute and chronic effects on human health, affecting a number of different systems and organs. It ranges from minor upper respiratory irritation to chronic respiratory and heart disease, lung cancer, acute respiratory infections in children and chronic bronchitis in adults, aggravating pre-existing heart and lung disease, or asthmatic attacks. In addition, short- and long-term exposures have also been linked with premature mortality and reduced life expectancy. These effects of air pollutants on human health and their mechanism of action are briefly discussed.
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PMID:Human health effects of air pollution. 1764 40

There is growing evidence of a distinct set of freshly-emitted air pollutants downwind from major highways, motorways, and freeways that include elevated levels of ultrafine particulates (UFP), black carbon (BC), oxides of nitrogen (NOx), and carbon monoxide (CO). People living or otherwise spending substantial time within about 200 m of highways are exposed to these pollutants more so than persons living at a greater distance, even compared to living on busy urban streets. Evidence of the health hazards of these pollutants arises from studies that assess proximity to highways, actual exposure to the pollutants, or both. Taken as a whole, the health studies show elevated risk for development of asthma and reduced lung function in children who live near major highways. Studies of particulate matter (PM) that show associations with cardiac and pulmonary mortality also appear to indicate increasing risk as smaller geographic areas are studied, suggesting localized sources that likely include major highways. Although less work has tested the association between lung cancer and highways, the existing studies suggest an association as well. While the evidence is substantial for a link between near-highway exposures and adverse health outcomes, considerable work remains to understand the exact nature and magnitude of the risks.
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PMID:Near-highway pollutants in motor vehicle exhaust: a review of epidemiologic evidence of cardiac and pulmonary health risks. 1768 99

Nitrosamines are know as the most potent group of carcinogens. Approximately 300 of these compounds have been tested, and about 90% of them have been found to be carcinogenic in laboratory animals. N-nitrosodimethylamine causes liver cancer, whereas some of tobacco specific nitrosamines causes lung cancer. Volatile N-nitrosamines induce tumors in a variety of human organs, including the tongue, esophagus, lung, pancreas, liver, kidney and bladder. They are formed during reaction of secondary or tertiary amino compounds and nitrite or nitrogen oxides. Nitrosamines occurs as contaminants in many foodstuff including food and beverages: beers, cheeses, sausages, smoked and pickled foods. They are formed during frying, smoking and food preserved with pickling salt. These compounds can also be produced in man and other mammals under the acidic conditions in the stomach. The present study was carried out to determine level of N-nitrosodimethylamine in selected 13 meat products. The extraction procedure was based on Raoul's method, ie. on two consecutive extraction-concentration step using extrelut and florisil columns. The level of N-nitrosodimethylamine was varied from 0.049 mg/kg to 16.47 mg/kg. The highest level of NDMA was found in smoked sausage.
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PMID:[A comparison of N-nitrosodimethylamine contents in selected meat products]. 1771 96

A common approach to construct a bioartificial renal tubule system is to utilize renal tubular cells seeded in porous polymer membrane hollow fibers. We have reported that overgrowth of renal tubular cells was not beneficial for the transport and reabsorption functions of bioartificial tubules. Therefore, long-term maintenance of a confluent monolayer of cells in hollow fibers is essential and technically challenging. In this study, we examined whether MEK inhibitor, U0126, could maintain the monolayer of Lewis-lung cancer porcine kidney 1 (LLC-PK(1)) cells on polystyrene plates and in a dialysis module housing hollow fibers made of ethylene vinyl alcohol (EVAL). We also evaluated the leakage of urea nitrogen (UN) and creatinine (Cr) through the cell-lined hollow fibers, and reabsorption of glucose and sodium by the cells, comparing the U0126-treated cells with nontreated cells in the module. Treatment with 50micromol l(-1) U0126 prevented the overgrowth of cells cultured on polystyrene plates. Moreover, U0126-treatment reduced the leakage of UN, and increased the reabsorption of electrolytes in 65cm(2) modules. Scanning electron microscopy revealed that it also prevented the overconfluence of cells in modules. Therefore, application of U0126 is a potentially effective method to improve the performance of the device.
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PMID:Prevention of LLC-PK(1) cell overgrowth in a bioartificial renal tubule device using a MEK inhibitor, U0126. 1788 23

The lung is a highly specialized organ that facilitates uptake of oxygen and release of carbon dioxide. Due to its unique structure providing enormous surface area to outside ambient air, it is vulnerable to numerous pathogens, pollutants, oxidants, gases, and toxicants that are inhaled continuously from air, which makes the lung susceptible to varying degrees of oxidative injury. To combat these unrelenting physical, chemical, and biological insults, the respiratory epithelium is covered with a thin layer of lining fluid containing several antioxidants and surfactants. Inhaled toxic agents stimulate the generation of reactive oxygen/nitrogen species (ROS/RNS), which in turn provoke inflammatory responses resulting in the release of proinflammatory cytokines and chemokines. These subsequently stimulate the influx of polymorphonuclear leukocytes (PMNs) and monocytes into the lung so as to combat the invading pathogens or toxic agents. In addition to the beneficial effects, persistent inhalation of the invading pathogens or toxic agents may result in overwhelming production of ROS/RNS, producing chronic inflammation and lung injury. During inflammation, enhanced ROS/RNS production may induce recurring DNA damage, inhibition of apoptosis, and activation of proto-oncogenes by initiating signal transduction pathways. Therefore, it is conceivable that chronic inflammation-induced production of ROS/RNS in the lung may predispose individuals to lung cancer. This review describes the complex relationship between lung inflammation and carcinogenesis, and highlights the role of ROS/RNS in cancer development.
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PMID:Inflammation and lung cancer: roles of reactive oxygen/nitrogen species. 1817 84


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