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

Carcinogenic metal levels in serum and tissue samples were measured in patients with bronchopulmonary or colorectal cancer. The cadmium and nickel tissue levels in the patients with lung cancer were significantly higher than in the controls. A statistical correlation was found between chromium and cadmium, as well as between cadmium and nickel in patients with colorectal cancer. In addition, prior to the operation, the tumor markers alpha-fetoprotein (AFP), carcinoembryonic antigen (CEA), carbohydrate antigen (Ca 19-9), polypeptide histidio antigen (TPA) and ferritin were analyzed. Their average concentrations were correlated with the existing concentrations of the metals. This was done for both types of cancer. Tumor marker detection showed an increase of CEA and TPA in patients with colorectal cancer. A statistical correlation was observed between AFP and zinc tumor tissue.
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PMID:Comparative analysis of certain metals and tumor markers in bronchopulmonary cancer and colorectal cancers. Metals and tumor markers in the neoplastic process. 210

The type of lung disease caused by metal compounds depends on the nature of the offending agent, its physicochemical form, the dose, exposure conditions and host factors. The fumes or gaseous forms of several metals, e.g. cadmium (Cd), manganese (Mn), mercury (Hg), nickel carbonyl (Nl(CO)4, zinc chloride (ZnCl2), vanadium pentoxide (V2O5), may lead to acute chemical pneumonitis and pulmonary oedema or to acute tracheobronchitis. Metal fume fever, which may follow the inhalation of metal fumes e.g. zinc (Zn), copper (Cu) and many others, is a poorly understood influenza-like reaction, accompanied by an acute self-limiting neutrophil alveolitis. Chronic obstructive lung disease may result from occupational exposure to mineral dusts, including probably some metallic dusts, or from jobs involving the working of metal compounds, such as welding. Exposure to cadmium may lead to emphysema. Bronchial asthma may be caused by complex platinum salts, nickel, chromium or cobalt, presumably on the basis of allergic sensitization. The cause of asthma in aluminium workers is unknown. It is remarkable that asthma induced by nickel (Ni) or chromium (Cr) is apparently infrequent, considering their potency and frequent involvement as dermal sensitizers. Metallic dusts deposited in the lung may give rise to pulmonary fibrosis and functional impairment, depending on the fibrogenic potential of the agent and on poorly understood host factors. Inhalation of iron compounds causes siderosis, a pneumoconiosis with little or no fibrosis. Hard metal lung disease is a fibrosis characterized by desquamative and giant cell interstitial pneumonitis and is probably caused by cobalt, since a similar disease has been observed in workers exposed to cobalt in the absence of tungsten carbide. Chronic beryllium disease is a fibrosis with sarcoid-like epitheloid granulomas and is presumably due to a cell-mediated immune response to beryllium. Such a mechanism may be responsible for the pulmonary fibrosis occasionally found in subjects exposed to other metals e.g. aluminium (Al), titanium (Ti), rare earths. The proportion of lung cancer attributable to occupation is around 15%, with exposure to metals being frequently incriminated. Underground mining of e.g. uranium or iron is associated with a high incidence of lung cancer, as a result of exposure to radon. At least some forms of arsenic, chromium and nickel are well established lung carcinogens in humans. There is also evidence for increased lung cancer mortality in cadmium workers and in iron or steel workers.
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PMID:Metal toxicity and the respiratory tract. 217 66

Cultural cells used were embryo cells collected from pregnant (12-14 days) golden hamster. 3,4B[a] P was used to induce transformation of the cells in vitro. 24 hours after the treatment, there appeared a random arrangement of the cells and loss of the contact inhibition and cell polarity. Some transformed foci were obtained on the 4th day with presence of atypical cells. Scanning electron microscopy showed presence of blebs, considerable ruffling particularly increase of small microvilli, and small projections on the surface of the transformed cells. Karyotypes of the cells showed decrease of diploid cells, but numbers of tetraploid, heteroploid as well as polyploid cells increased. Application of these criteria in identifying carcinogenesis of the industry dust from a zinc-product factory in the west area of Liaoning Province indicated that changes obtained in cells treated by this dust were similar to those obtained by using B[a]P alone. It is considered that carcinogenetic agents of lung cancer are present in the dust in the area.
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PMID:[Study of transformation of hamster embryo cells and its application to identification of environment carcinogen]. 227 11

This review concerns primarily the health effects that result from indoor air exposure to radon gas and its progeny. Radon enters homes mainly from the soil through cracks in the foundation and other holes to the geologic deposits beneath these structures. Once inside the home the gas decays (half-life 3.8 d) and the ionized atoms adsorb to dust particles and are inhaled. These particles lodge in the lung and can cause lung cancer. The introduction to this review gives some background properties of radon and its progeny that are important to understanding this public health problem as well as a discussion of the units used to describe its concentrations. The data describing the health effects of inhaled radon and its progeny come both from epidemiological and animal studies. The estimates of risk from these two data bases are consistent within a factor of two. The epidemiological studies are primarily for hard rock miners, although some data exist for environmental exposures. The most complete studies are those of the US, Canadian, and Czechoslovakian uranium miners. Although all studies have some deficiencies, those of major importance include uranium miners in Saskatchewan, Canada, Swedish iron miners, and Newfoundland fluorspar miners. These six studies provide varying degrees of detail in the form of dose-response curves. Other epidemiological studies that do not provide quantitative dose-response information, but are useful in describing the health effects, include coal, iron ore and tin miners in the UK, iron ore miners in the Grangesburg and Kiruna, Sweden, metal miners in the US, Navajo uranium miners in the US, Norwegian niobian and magnitite miners, South African gold and uranium miners, French uranium miners, zinc-lead miners in Sweden and a variety of small studies of environmental exposure. An analysis of the epidemiological studies reveals a variety of interpretation problem areas. The major and almost universal problem is in estimating exposure levels. In many cases there were no direct measurements of radon or radon progeny and the exposure levels are estimates based on irregular measurements and known levels in nearby mines. Perhaps the most important variable or complicating factor in the determination of the risk due to radon exposure is the confounding factor of exposure to cigarette smoke. The general scientific concensus is that, although the interaction could be somewhere between linear and supramultiplicative, it is likely a combination, and closer to multiplicative. A number of other complexities contribute to the uncertainty in the risk estimates, likely to a lesser degree than those of exposure measurements and cigarette smoke confounding.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Indoor air radon. 240 87

The role of nutrients in cancer causation has been a subject of considerable interest, research, and public discussion in recent years. Results from epidemiologic, clinical, and animal studies have suggested that: 1) a reduction in total calories decreases risk for a number of tumor types; 2) dietary protein is directly correlated with liver, prostate, and colon cancer, among others, with increasing dietary protein increasing the risk; 3) increased dietary fat is correlated with increased risk for breast cancer; the evidence for an effect of fat on colon cancer is equivocal in human and animal studies; 4) a deficiency of vitamin A may enhance lung and colon tumors in animal experiments but in human this is equivocal. Increasing vitamin A above normal levels, as an anticarcinogenic effect, has not been satisfactorily demonstrated in animal models. The synthetic retinoid, 13-cis retinoic acid, inhibits both colon and lung cancer in animal models; 5) zinc deficiency is associated with enhanced esophageal cancer in humans and markedly enhances animal tumors; selenium inhibits this form of neoplasia in animals, 6) diets low in lipotropes enhance liver cancer induced by a variety of hepatocarcinogens. Our data from studies in animal models agree in some cases with epidemiological observations, but disagree with others, particularly fat and colon cancer. Overall, some forms of cancer are enhanced by excessive calories, increased dietary protein and fat, and by deficiencies of vitamin A, selenium, zinc, and lipotropes. Decreasing total intake of calories, protein, and fat, and ensuring adequate dietary levels of vitamin A, selenium, zinc, and lipotropes decreases risk for some forms of cancer.
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PMID:The role of nutrients in cancer causation. 243 54

The goal of this study has been to identify and characterize metalloproteinases from a highly metastatic human small cell lung cancer cell line. The cytosol isolated from NCI-H82 lung cancer cells propagated as solid tumors in nude mice contained a gelatinolytic enzyme that was subjected to ammonium sulfate precipitation, zinc chelate Sepharose column chromatography, anion exchange chromatography and gel permeation chromatography. This purification scheme resulted in a 280-fold enrichment of an active gelatin and type IV collagen-degrading enzyme. On gelatin zymography two bands of gelatinolytic activity were detected, corresponding to Mr of 75,000 and 63,000. Gelatinolytic activity was inhibited by metal chelators, tetracyclines, and serum. On immunoblotting using an affinity-purified polyclonal rabbit antibody to a peptide region of type IV collagenase, the tumor enzyme was identified as type IV collagenase. A second tumor metalloproteinase of Mr = 29,000, which degraded proteoglycan substrates, was also isolated.
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PMID:Gelatin-degrading type IV collagenase isolated from human small cell lung cancer. 254 76

Angiotensin-converting enzyme activity and its kinetic parameters were determined in both serum and lung tissue samples obtained from 17 patients with lung cancer and 21 control subjects, regardless of ethical base. The specific activities for cancerous and normal lung tissues were 67.2 +/- 27.3 (mean +/- SD) U/g protein and 28.5 +/- 5.4 U/g protein, respectively (P less than 0.001). Serum enzyme activity, on the other hand, was found to be higher in controls (198 +/- 42 U/L) than in patients (237 +/- 68 U/L) (P less than 0.01). The effects of chloride and zinc ions, pH and temperature on the enzyme activity were investigated as kinetic parameters in both serum and tissue samples.
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PMID:Kinetic parameters of serum and lung tissue angiotensin-converting enzyme in patients with lung cancer. 255 46

Taste recognition thresholds for four basic tastes, sweet, salty, and bitter, have been examined in 36 advanced lung cancer patients to identify the presence or absence of taste abnormalities in such patients. Twenty-six untreated lung cancer patients, or 65.3%, demonstrated an abnormal taste threshold for at least one of the 4 taste, a result varying significantly from suitable controls (p less than 0.05). Among the total 36 lung cancer patients, the number of those showing a threshold abnormality was no different between the smoker and non-smoker groups, though abnormalities were higher in the low serum zinc level group than in the normal serum zinc level group (p less than 0.05). We also observed transient threshold elevations after chemotherapy including Cisplatin. Thus, it is thought that taste abnormalities are more prevalent in advanced lung cancer patients.
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PMID:[Clinical study of taste abnormalities in advanced lung cancer cases]. 259 29

The mortality experience of 1392 lead-zinc-silver miners (Gorno, Northern Italy) employed in the period 1/1/1950-31/12/1980 and followed-up to 31/12/1986 was examined. Two separate estimates of the radon exposure level are available: 0.60 and 0.36 working levels respectively. The silica exposure level was not assessed. Vital status was ascertained for 95.6% of the cohort members and their mortality was compared with expected deaths based on national rates. Significant excess mortality from esophageal cancer, stomach cancer, lung cancer, respiratory tuberculosis, respiratory diseases and deaths from external causes was found among underground miners. Surface workers show significantly increased mortality from liver and bile ducts cancer, hepatic cirrhosis, respiratory tuberculosis and respiratory diseases. Based on the 16.4 excess lung cancer cases among underground miners and their cumulative radon exposure, an attributable risk estimate ranging from 9.78 and 16.31 cases per million person-years and WLM (Working Level Month) was calculated.
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PMID:[Mortality among lead-zinc miners in Val Seriana]. 263 Aug 93

Pathological changes of lung cancer in miners of Yunnan Tin Mine were studied, and additionally, mineral dust in the miners' lung were also investigated by using scanning electronic microscope, energy disperse X-ray spectrometer and electronic probe. The results showed: 1. mineral dust caused active hyperplasia, atypical hyperplasia, metaplasia and atypical metaplasia of the epithelial of alveoli and bronchi, which was able to induce cancer. 2. Pneumoconiosis-like changes in the miner's lung are correlated with the high incidence of lung cancer. 3. Correlated also with copper, lead, zinc and iron may be the high incidence of lung cancer. 4. Transition form from hyperplasia and atypical hyperplasia of alveolar epithelia to malignancy was observed. It suggests that lung squamous cell carcinoma probably originates from the alveolar epithelia of the lung.
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PMID:[Pathological survey of lung cancer induced by tin mine dust in Yunnan]. 263 64


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