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

Natural mineral fibers may produce pulmonary cancers and mesothelioma. In contrast with lung cancer, the incidence of fiber-induced mesothelioma is not enhanced in smokers compared to non smokers. It is therefore of special interest to use mesothelial cells to study the toxicity of natural or man made mineral fibers. Several years ago, we have developed a method to culture rat pleural mesothelial cells (RPMC). We have first studied the effects of asbestos fibers by the application of in vitro tests formerly developed to determine the genotoxicity and transforming potency of soluble xenobiotics. Moreover, we have determined whether RPMC expressed cytochromes P450 known to metabolize polycyclic aromatic hydrocarbons. This paper reviews the results obtained so far. It has been found that asbestos fibers produced a cell transformation and a genotoxicity characterized by the formation of aneuploid cells, abnormal anaphases, chromosomal aberrations and DNA repair (UDS). In addition, RPMC expressed different forms of cytochromes P450. It is nowadays suggested that the tumorigenic potency of asbestos fibers may be related to the fiber dimensions, to their surface properties and in vivo biopersistence; this term involves the fiber solubility in biological medium and the fiber epuration from the lung by clearance mechanisms. Experiments are now in progress to determine whether the in vitro effects are dependent on the fiber parameters suggested as playing a role in the carcinogenic potency.
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PMID:Use of mesothelial cell cultures to assess the carcinogenic potency of mineral or man made fibers. 144 51

Thirty nine phenotypes of human leucocyte antigens (HLA)-A-B-DR and DQ were obtained from 99 asbestos workers (one woman and 98 men). Presence or absence of antinuclear antibodies and rheumatoid factor was determined in 91 of them. Workers were divided into five groups: asbestos workers with no apparent disease (AW; n = 17), diffuse benign pleural disease (PD; n = 31), asbestosis (AS; n = 24), asbestosis with lung cancer (AS-CA; n = 14), and mesothelioma (M; n = 13). Compared with AW, several trends of differences of HLA antigen prevalence were found in patients with asbestos related disease, but these did not achieve statistical significance when p was corrected (pcorr) by number of analyses undertaken. Analysis of the results obtained in previous studies together with the results of this study showed that compared with AW, AS patients had decreased prevalence of HLA-DR5 (pcorr < 0.02). Reasons for the differences in results of previous studies and statistical methods commonly used to compare prevalences of HLA antigen are discussed.
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PMID:The histocompatibility antigen in asbestos related disease. 147 39

Asbestos-related diseases are dose-related. Among these, asbestosis has occurred only with the heavy exposures of the past, is a disappearing disease, and is of no concern with the very small exposures from building occupancy. A possibly increased incidence of lung cancer has been included in risk analysis, but probably is also related to high exposure in that both epidemiologic and experimental data suggest a link between the process of alveolar inflammation and fibrogenesis and carcinogenesis. The major concern has been mesothelioma in that it has occurred with much lower household and neighborhood exposure. Additionally, anxiety concerning buildings with ACM has been heightened by finding of friable asbestos in about 20% of public buildings, discovery of environmental asbestos fibers and asbestos bodies in autopsies, and demonstration of a linear relationship between exposure and lung cancer risk in occupational groups, inviting extrapolation to a much lower dose. Legislative and regulatory mandates, promotional activities of abatement companies, adverse court decisions placing the onus of repairs on asbestos manufacturers, and a "pandemic of mediagenic disease" all have contributed to panic among building owners, school boards, insurers, and others. In that there is neither clinical nor epidemiologic support for asbestos-related disease from building occupancy, risk estimates have been based on extrapolation from past experience with generally high-dose occupational exposure. However, only a few epidemiologic studies have contained quantitative estimates of exposure, and these have been measured in terms of all particles, with conversion to asbestos fibers uncertain and the fiber type and dimension largely unknown. To these uncertainties must be added the unproved assumption of a linear dose-response down to very low levels of exposure with no threshold. At the other end of the scale extrapolation has required measurements of present building exposure, and these have been revised downward as methods for collection and analysis have improved. Risk estimates in this country and abroad have assumed exposure to 0.001 f/mL, with indicated lifetime risks for cancer ranging from about 2 to 20 per 1 million students. However, these estimates have assumed mixed fiber exposure whereas most building exposure comes from chrysotile, which is much less toxic than the amphiboles.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Asbestos exposure in buildings. 151 51

A case-control study was conducted of the risk of lung cancer and mesothelioma from environmental and occupational exposures associated with sugarcane production. A slight, not statistically significant, excess risk of lung cancer was observed among participants who reported working in the sugarcane industry (odds ratio 1.8, 95% confidence interval 0.5-7.5). No increased risk was observed among our population, associated with living near sugarcane growing areas. Little difference was observed between cases and controls in years employed in the industry or jobs performed. Only one mesothelioma case and no controls reported working in the sugarcane industry.
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PMID:Sugarcane exposure and the risk of lung cancer and mesothelioma. 151 73

A prospective cohort study of 3,893 shipyard workers, mainly exposed to chrysotile, indicated no increased risk of lung cancer 7-15 yrs after exposure to asbestos had ceased. The shipyard workers, however, had an increased risk of pleural mesotheliomas with 11 observed cases versus 1.5 expected. An explanation for these observations may be that asbestos may have different carcinogenic mechanisms in causing lung cancer and mesothelioma. A non-increased risk of lung cancer some years after exposure to asbestos has stopped is in accordance with asbestos acting as a promotor. The high risk of mesothelioma, on the other hand, may indicate that asbestos acts as a complete carcinogen in developing this disease.
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PMID:The risk of lung cancer and mesothelioma after cessation of asbestos exposure: a prospective cohort study of shipyard workers. 142 29

We performed an investigation focusing on the distribution of tumor types responsible for positive pleural effusions in 143 patients who died of malignancy and underwent autopsy. The principal malignant tumors were lung carcinoma (41 cases, 51.2%) and pleural mesothelioma (23 cases, 28.7%) in males and breast carcinoma (24 cases, 38.2%) and lung carcinoma (13 cases, 20.6%) in females. Histologically, most of the cases belonged to the adenocarcinoma category. The first morphologic diagnosis was a cytologic one in 86 cases (60.1%), especially regarding lung cancer. In breast cancer a positive pleural effusion always preceded recurrent disease with a rapidly progressive course, even a long time after the initial surgery. The results of this study, based on both cytomorphologic features and postmortem data on the tumor sites, may be a useful working framework for the cytologist dealing with a positive pleural effusion.
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PMID:The positive pleural effusion. A retrospective study of cytopathologic diagnoses with autopsy confirmation. 158 Jan 16

Asbestos is a versatile fibrous mineral that can cause lung disease and death. Asbestosis, benign pleural disease, lung cancer, and mesothelioma can all result from inhaling asbestos. The history of disease and exposure risks are discussed. The difficult assessment of risk and the long latency period for development of disease demand evaluation and regular surveillance of asbestos-exposed workers.
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PMID:Asbestos-related lung disease. 160 90

A total of 2,208 male subjects, enrolled as merchant marine seamen at the Civitavecchia (Italy) harbor from 1936 to 1975 were followed up through 1989 in order to evaluate their mortality experience. Available information about the number of sailings made it possible to divide subjects into two subgroups: 948 workers with at least one sailing (cohort A) and 1,260 with no reported sailing (cohort B). Fewer than expected overall deaths were observed in both cohorts (cohort A: SMR = 0.83; cohort B: SMR = 0.81), mainly due to a lower mortality from circulatory, respiratory, and digestive diseases. Lung cancer deaths were significantly increased in cohort A (O = 30, SMR = 1.71, 95% CI = 1.15-2.44), whereas no excess was observed in cohort B (O = 6, SMR = 0.57, 95% CI = 0.21-1.26). Among subjects employed aboard ship, a trend in SMRs for lung cancer increasing with duration of employment was observed. Furthermore, three neoplasms of other parts of the respiratory system (including one mesothelioma) were detected in cohort A (SMR = 5.87), and one in cohort B. The study substantiates an increased risk of respiratory cancer among subjects with an occupational history of sailing; past exposure to asbestos and to other environmental carcinogens aboard could be implicated.
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PMID:A mortality cohort study of seamen in Italy. 162 94

Projections have been made of the number of mesotheliomas, lung cancers, and cases of asbestosis that might occur over the period 1987 to 2020 in former workers at the Wittenoom crocidolite asbestos mine in Western Australia. Predictions were based on the observed mortality to the end of 1986 and modelling of the mesothelioma rate. Elimination of crocidolite from the lungs was included in the model. Between the years 1987 and 2020 it is predicted that between 250 and 680 deaths will occur due to mesothelioma. This wide range is due to uncertainty on the functional form of the relation between mesothelioma rate and time, and insufficient data to estimate the elimination rate of crocidolite from the lungs. The most likely range is the lower half of this total range--that is, between 250 and 500. It is predicted that between 340 and 465 deaths will occur due to lung cancer. About 45% of these deaths would be attributable to exposure to asbestos. It is estimated that currently there are up to 200 cases of undiagnosed asbestosis. Of these about 50 will die of lung cancer or mesothelioma and are therefore also included in the figures above. Up to 60 former workers may develop the first signs of asbestosis in the future but any such cases are likely to progress to more serious disease at a much slower rate than the cases that have already been identified.
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PMID:Prediction of mesothelioma, lung cancer, and asbestosis in former Wittenoom asbestos workers. 160 35

Altered and deregulated cellular oncogenes were found in many human solid tumors. Except for a few types of tumors that consistently exhibited specific altered proto-oncogenes, the majority of tumors are associated with a number of transcriptionally activated cellular oncogenes. In the heterologous group of non-small-cell lung cancer (NSCLC), nothing about a specific pattern of proto-oncogene expression is known. Therefore, we investigated the expression of a panel of cellular oncogenes in NSCLC cell lines. DNA and RNA from 11 established NSCLC cell lines (4 adenocarcinoma cell lines, 3 squamous cell carcinoma cell lines, 3 large-cell carcinoma cell lines and 1 mesothelioma cell line) were isolated and analysed using the Southern, dot blot and Northern hybridization technique. c-myc RNA expression was found in all NSCLC cell line, L-myc expression only in 1 adenocarcinoma cell line, N-myc and c-myb expression in none of the 11 cell lines examined. No c-myc amplification could be detected in the DNAs. v-sis-related mRNA was observed in 5/11 cell lines without association to a specific NSCLC subtype. v-src-related mRNA, found in all tested cells, exhibited increased levels in 1 adenocarcinoma cell line (A-549) compared to the other cell lines. Binding sites for epidermal growth factor (EGF) had been described previously in NSCL, therefore we found erbB homologue transcripts coding for the EGF receptor in all NSCLC cell lines. Also, c-raf1-, N-ras-, Ki-ras-, and H-ras-related RNA expression was observed in all lines. We conclude that L-myc, N-myc, and c-myb expression does occur less frequently in NSCLC than in SCLC. Also amplification does not appear to be an important mechanism by which the c-myc proto-oncogene is activated in NSCLC. A specific pattern of oncogene expression could not be detected in NSCLC cells; each cell line examined showed its own pattern. However, transcriptional activation of a proto-oncogene like erbB, ras, raf, src, and c-myc, which are all involved in the progression pathway of EGF, may be a common feature of NSCLC.
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PMID:Different pattern of expression of cellular oncogenes in human non-small-cell lung cancer cell lines. 169 Feb 10


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