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

Asbestos and benzo(a)pyrene diol epoxide (BPDE) are pulmonary carcinogens with synergistic interaction in causing lung cancer. We used Affymetrix microarrays to study gene modulation in vitro using normal human bronchial epithelial cells exposed to chrysotile asbestos and/or BPDE for 4 or 24 h. Linear models were used to compare treated cells to controls at each time point to identify statistically significant up- or downregulation of genes. Profiles of genes regulated by chrysotile were dominated by cytokines, growth factors, and DNA damage. Profiles of genes with BPDE and chrysotile regulation were correlated with proliferation, DNA damage recognition and nucleotide-excision repair, cytokines, and apoptosis. Chemokines, growth-regulated oncogene-alpha (Gro-alpha, CXCL-1), and IL-8, were significantly increased, and these had previously been observed in bronchoalveolar lavage from asbestos workers or in animal models. Interestingly, the Hermansky-Pudlak gene, which is mutated in an autosomal recessive form of pulmonary fibrosis, was downregulated threefold by BPDE at 4 h. This is an interesting example of gene (Hermansky-Pudlak syndrome) and environment (BPDE) interaction. Transcription factors, including activating transcription factor 3 and Cbp/p300-interacting transactivator, were upregulated by chrysotile. Real Time PCR for IL-8, ATF-3, GADD45B, CXC Ligand 1, and CTGF compared to GAPDH validated microarray findings at 24 h. These in vitro findings in NHBE cells model environment-gene interaction for asbestos and BPDE, highlighting effects of inflammation, fibrosis, proliferation, and DNA damage recognition and repair.
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PMID:Gene profiling of normal human bronchial epithelial cells in response to asbestos and benzo(a)pyrene diol epoxide (BPDE). 1819 26

Asbestos-exposure is associated with an increased risk of lung cancer, one of the leading causes of cancer deaths worldwide. Asbestos is known to induce DNA and chromosomal damage as well as aberrations in signalling pathways, such as the MAPK and NF-kappaB cascades, crucial for cellular homeostasis. The alterations result from both indirect effects through e.g. reactive oxygen/nitrogen species and direct mechanical disturbances of cellular constituents. This review describes the current knowledge on genomic and pathway aberrations characterizing asbestos-related lung cancer. Specific asbestos-associated molecular signatures can assist the development of early biomarkers, molecular diagnosis, and molecular targeted treatments for asbestos-exposed lung cancer patients.
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PMID:Molecular and genetic changes in asbestos-related lung cancer. 1836 47

Asbestos has been an indispensable insulating material for railway industries, especially steam locomotives (SLs). This review (1928-1987) consists of three parts. 1) Pleural plaques: Since the 1970s, pleural plaques have been regarded as evidence of past asbestos inhalation, and more recently recognized as a risk factor of asbestos-related malignancies. For diagnostic criteria on plain radiographs, the modified ILO 1980 International Classification of Radiographs of Pneumoconioses was used. Most cases had pleural plaques with normal lungs. Large plant workers showed a significantly higher rate of plaques than workers in smaller plants. Bilateral plaques were dominant followed by the left, then the right lung, and chest wall plaques were dominant over the diaphragm. The manifestation of pleural plaques was more correlated to years since the onset of the asbestos exposure than the sum of asbestos work years, although the result was not significant. The boilermen of railway ferry steamers had a significantly higher plaque rate than other seamen. CT studies on plaques started in 1978. 2) Asbestos-related malignancies: Five retrospective cohort studies 1960-1970 were made on primary lung cancer incidence and mortality among 350,000 active railway men with smoking information. The follow-up period was 20 yr at the longest. Almost all plant workers showed a tendency of higher incidence or mortality than the controls. Two cases of mesothelioma were reported in 1980. 3) Pneumoconioses: Most studies (1928-1975) had relatively low prevalence rates among SL-related workers.
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PMID:Railways and asbestos in Japan (1928-1987)--epidemiology of pleural plaques, malignancies and pneumoconioses-. 1849 13

Asbestos is a well-known cause of several neoplastic (malignant mesothelioma, lung cancer) and non-neoplastic (asbestosis, pleuropathies) occupational diseases. Lower-level exposure in the general environment may induce pleural plaques and thickenings, and is associated with an increased mesothelioma risk. We present two patients (a 68-year-old man and a 72-year-old woman) who developed asbestosis (in association with pleural plaques and calcifications), and a 78-year-old man who developed rounded atelectasis (with pleural plaques and benign effusion), after living for several decades in the proximity of large Italian asbestos-cement plant. None of them had been exposed to asbestos occupationally. Besides living in a contaminated area, the woman used to clean the work clothes of her brother, who was employed in the local asbestos factory. The three cases indicate that non-neoplastic, long-latency asbestos-related diseases which are usually observed as a consequence of occupational exposures, may rarely develop in subjects living in contaminated geographical sites and buildings. These unusual environmental diseases raise the diagnostic problem of differentiating them from other, more common respiratory illnesses, and impose the duties of patient notification, assessment and follow-up, to assess the possibility of progression of disease and increased neoplastic risk.
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PMID:Two cases of asbestosis and one case of rounded atelectasis due to non-occupational asbestos exposure. 1850 98

The asbestos industry has shifted from manufacture to stripping/removal work. The aim of this study was to investigate early indications of mortality among removal workers. The study population consisted of 31 302 stripping/removal workers in the Great Britain Asbestos Survey, followed up to December 2005. Relative risks (RR) for causes of death with elevated standardised mortality ratios (SMR) and sufficient deaths were obtained from Poisson regression. Risk factors considered included dust suppression technique, type of respirator used, hours spent stripping, smoking status and exposure length. Deaths were elevated for all causes (SMR 123, 95% CI 119-127, n=985), all cancers including lung cancer, mesothelioma, and circulatory disease. There were no significant differences between suppression techniques and respirator types. Spending more than 40 h per week stripping rather than less than 10, increased mortality risk from all causes (RR 1.4, 95% CI 1.2-1.7), circulatory disease and ischaemic heart disease. Elevated mesothelioma risks were observed for those first exposed at young ages or exposed for more than 30 years. This study is a first step in assessing long-term mortality of asbestos removal workers in relation to working practices and asbestos exposure. Further follow-up will allow the impact of recent regulations to be assessed.
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PMID:Occupational exposure to asbestos and mortality among asbestos removal workers: a Poisson regression analysis. 1872 72

Asbestos is a fibrous silicate which is recognized as causing a variety of lung disorders including malignant mesothelioma of the pleura, lung cancer and asbestosis. Asbestos use has been banned in most developed countries but exposure still occurs under strict regulation in occupational settings and also occasionally in domestic settings. Although the hazards of asbestos are well known in developed countries, awareness of its adverse health effects is less in other parts of the world, particularly when exposure occurs in non-occupational settings. Experience of asbestos use and its adverse heath effects in developed countries such as Australia have resulted in development of expertise in the diagnosis and treatment of asbestos-related diseases as well as in screening and this can be used to help developing countries facing the issue of asbestos exposure.
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PMID:Asbestos-related occupational lung diseases in NSW, Australia and potential exposure of the general population. 1908 5

Asbestos causes asbestosis (pulmonary fibrosis caused by asbestos inhalation) and malignancies (bronchogenic carcinoma and mesothelioma) by mechanisms that are not fully elucidated. Despite a dramatic reduction in asbestos use worldwide, asbestos-induced lung diseases remain a substantial health concern primarily because of the vast amounts of fibers that have been mined, processed, and used during the 20th century combined with the long latency period of up to 40 years between exposure and disease presentation. This review summarizes the important new epidemiologic and pathogenic information that has emerged over the past several years. Whereas the development of asbestosis is directly associated with the magnitude and duration of asbestos exposure, the development of a malignant clone of cells can occur in the setting of low-level asbestos exposure. Emphasis is placed on the recent epidemiologic investigations that explore the malignancy risk that occurs from nonoccupational, environmental asbestos exposure. Accumulating studies are shedding light on novel mechanistic pathways by which asbestos damages the lung. Attention is focused on the importance of alveolar epithelial cell (AEC) injury and repair, the role of iron-derived reactive oxygen species (ROS), and apoptosis by the p53- and mitochondria-regulated death pathways. Furthermore, recent evidence underscores crucial roles for specific cellular signaling pathways that regulate the production of cytokines and growth factors. An evolving role for epithelial-mesenchymal transition (EMT) is also reviewed. The translational significance of these studies is evident in providing the molecular basis for developing novel therapeutic strategies for asbestos-related lung diseases and, importantly, other pulmonary diseases, such as interstitial pulmonary fibrosis and lung cancer.
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PMID:Asbestos-induced lung diseases: an update. 1930 73

Asbestos is a carcinogen that causes diseases such as mesothelioma and lung cancer in humans. There was a sharp increase in the use of asbestos in Korea in the 1970s as Korea's economy developed rapidly, and asbestos was only recently banned from use. Despite the ban of its use, previously applied asbestos still causes many problems. A series of asbestos-related events that recently occurred in Korea have caused the general public to become concerned about asbestos. Therefore, it is necessary to take proper action to deal with asbestos-related events, such as mass outbreaks of mesothelioma among residents who lived near asbestos textile factories or asbestos mines. Although there have been no rapid increases in asbestos-related illnesses in Korea to date, such illnesses are expected to increase greatly due to the amount of asbestos used and long latency period. Decreasing the asbestos exposure level to levels as low as possible is the most important step in preventing asbestos-related illnesses in the next few decades. However, there is a lack of specialized facilities for the analysis of asbestos and experts to diagnose and treat asbestos-related illnesses in Korea; therefore, national-level concern and support are required.
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PMID:Overview of asbestos issues in Korea. 1954 18

Asbestos minerals are thin fiber type of minerals and honorably said as "the minerals of the miracle" because of their valuable natures even in the strategic field. On the other hand, the relation between asbestos exposure and diseases such as lung cancer and malignant mesothelioma was proved around 1970 by epidemiology and an animal experiment in relation to their microstructures. Here, microstructures of chrysotile asbestos, a mainstream of asbestos substances, are shown. It is also shown that in what kinds of environment people are exposed to asbestos and what kinds of biological or epidemical things happen after asbestos exposure. Many kinds of fibrous materials as the substitutes of asbestos are described in relation to their carcinogenicity.
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PMID:Microstructures and biological influence of environmental exposure of asbestos. 1958 18

Asbestos is a recognised carcinogen, one of the most dangerous pollutants in the human environment. This is associated with a huge accumulation of asbestos-containing materials that, as a result of their degradation, release fibres that are practically indestructible. It is estimated that in recent years, asbestos was responsible for ca. 100 thousand death cases p.a. The pathogenic effects of asbestos on the respiratory system (the target organ) result from the inhalation of the respirable asbestos fibres suspended in the ambient air. The fibres accumulate in the lung tissue during the whole human lifetime, and the pathogenic effects become evident after a long period of latency, ranging from 20 to 40 years. A specific feature of asbestos activity is that the pathologies appear even after cessation of the exposure; another feature is the development of mesotheliomas associated with the environmental exposure. In Poland, the Act of 1997 banning the use of asbestos products has solved the problems associated with the occupational exposure in the asbestos processing industry, and prevented further accumulation of asbestos products. However, problems of the environmental exposures to asbestos remain unsolved. In spite that no worker has been occupationally exposed to asbestos during the recent 10 years, new cases of asbestosis, lung cancer pleural mesothelioma, non-malignant pleural diseases continue to be detected each year among the former workers of asbestos processing industry ("Amiantus" project). This paper reports on the current status of asbestos-related diseases in Poland and worldwide, risk of the development of lung cancers and asbestos-specific mesotheliomas and gives recent recommendations for diagnosing and certification of asbestos-related diseases.
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PMID:[Asbestos as a risk factor for pulmonary diseases]. 1962 51


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