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

We treated twenty-three patients with secondary hypertrophic osteoarthropathy (SHO). Lung cancer was associated with SHO in 21 cases. The underlying conditions for the rest of the patients were pulmonary fibrosis, bronchiastasic, pneumonia and mediastinal cancer. The history, physical examination, radiography and bone-scan were performed. For bone-scan it was used intravenously instilled disfonate compound marked with 99 mTc-HMDP-"Osteocis" in the dosage of 740 MBq. Mild periostosis on the shaft bones was found in 5 patients with positive radio-labelling. In other patients bone-scan showed polytopic radiolabelling whilst radiography didn't show and periostosis. In conclusion we can say that the bone-scan is very sensitive method for the detection of the increase bone-tissue function.
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PMID:[Scintigraphy in the early diagnosis of the secondary hypertrophic osteoarthropathy syndrome]. 976 17

Lung cancer is a frequent complication in pulmonary fibrosis. Overexpression of p53 proteins has been demonstrated by immunostaining in bronchoepithelial cells in patients with idiopathic pulmonary fibrosis. However, it is still unclear whether this overexpressed p53 protein is wild-type or mutant. It was hypothesized that pulmonary fibrosis may be a precancerous lesion with deoxyribonucleic acid point mutations in bronchoepithelial cells. Mutations of the p53 gene were tested for by fluorescence-based single-strand conformation polymorphism (FSSCP), cloning-sequencing and immunostaining techniques. Out of 10 tissue samples that demonstrated overexpression of p53 protein by immunostaining, nine (90%) exhibited point mutations and eight (80%) exhibited heterogeneous point mutations of the p53 gene. The mutations found in pulmonary fibrosis were scattered throughout the central part of the p53 gene, and both guanine (G):cytosine (C) to adenine (A):thymine (T) and A:T to G:C transitions were frequently observed. In conclusion, frequent heterogeneous point mutations of the p53 gene were detected in pulmonary fibrosis. These mutations may have resulted from several types of deoxyribonucleic acid damage that occurred in bronchoepithelial cells and this may explain previous findings of a very high incidence of lung cancer complicating pulmonary fibrosis.
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PMID:Heterogeneous point mutations of the p53 gene in pulmonary fibrosis. 987 99

Several tools are available for the evaluation of the exposure to asbestos, particularly occupational questionnaire and mineralogical analysis of biological samples. These analysis allow quantification of the level of retention of asbestos fibres in the respiratory tract. Two groups of analysis may be used: quantification of asbestos bodies in sputum, bronchoalveolar lavage fluid or lung tissue samples using light microscopy; quantification and identification of asbestos fibres in bronchoalveolar lavage fluid or lung tissue using analytical electron microscopy. Profiles of lung retention of asbestos bodies or asbestos fibres have been described in various asbestos-related disorders, and reference values are available in control populations mainly for asbestos bodies using light microscopy. Mineralogical analysis of biological samples is not required for compensation of occupational asbestos-related diseases. However, this type of analysis may prove to be useful to the chest physician when looking for the etiology of some nonspecific respiratory diseases (interstitial pulmonary fibrosis, lung cancer), particularly when the occupational questionnaire is not contributive. As they are quite easier and less expensive, analysis using light microscopy will be performed first.
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PMID:[Mineralogical analysis and exploration of asbestos diseases]. 1002 48

Asbestos causes four diseases in humans: Lung fibrosis (asbestosis) follows heavy exposure and, in industrialized countries, is mainly a relic of past working conditions. The risk of pleural fibrosis and plaques is likely to be linearly dependent from time since first exposure and is present for all types of asbestos fibres. The diagnostic uncertainties regarding pleural plaques and the substantial degree of misclassification make it difficult to precisely estimate the shape of the dose-response relationship. The risk of lung cancer seems to be linearly related to cumulative asbestos exposure, with an estimated increase in risk of 1% for each fibre/ml-year of exposure. All fibre types seem to exert a similar effect on lung cancer risk; a multiplicative interaction with tobacco smoking has been suggested. Pleural mesothelioma is a malignant neoplasm which is specifically associated with asbestos exposure: the risk is linked with the cubic power of time since first exposure, after allowing for a latency period of 10 years, and depends on the fibre type, as the risk is about three times higher for amphiboles as compared to chrysotile. Environmental exposure to asbestos is also associated with mesothelioma risk.
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PMID:Health effects of asbestos exposure in humans: a quantitative assessment. 1021 36

The assessment of regional ventilation in human lungs is important for the diagnosis and evaluation of a variety of pulmonary disorders, including pulmonary emphysema, diffuse lung disease (e.g., sarcoidosis, and pulmonary fibrosis), lung cancer, and pulmonary embolism. This article introduces new MR imaging techniques of pulmonary ventilation and perfusion that will provide a framework for assessing regional pulmonary functions of the lung.
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PMID:Ventilation-perfusion MR imaging of the lung. 1038 68

Cytokeratin 19 fragment (CK19) levels in serum have already been documented as a useful tumour marker for lung cancer. In the present study, it was hypothesized that CK19 may be increased in the serum and epithelial lining fluid of the respiratory tract from patients with pulmonary fibrosis. CK19 was measured in the serum and bronchoalveolar lavage fluid (BALF) of patients with pulmonary fibrosis and the correlation between CK19 levels and clinical parameters evaluated. Nineteen patients diagnosed with idiopathic pulmonary fibrosis (IPF), eight with pulmonary fibrosis associated with a collagen vascular disorder (PF-CVD), seven patients with acute interstitial pneumonia (AIP), and 10 normal smokers as a control group were studied. CK19 levels in sera of patients with IPF and patients with PF-CVD were significantly increased compared to those of normal smokers. CK19 levels in sera of patients with AIP were significantly increased compared to those of other groups. CK19 values in the BALF of patients with pulmonary fibrosis were significantly elevated compared to those of normal smokers. CK19 values in sera charged according to the progression or improvement of the acute lung injury. Immunohistochemical study using pulmonary tissues obtained from patients with AIP demonstrated that the hyaline membrane and proliferating type II pneumocytes were stained by anti-human cytokeratin 19 antibody. These data demonstrated that the measurement of cytokeratin 19 fragment is a useful parameter to evaluate the activity of lung epithelial cell damage and repair.
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PMID:Elevated serum and BAL cytokeratin 19 fragment in pulmonary fibrosis and acute interstitial pneumonia. 1054 77

It has been reported that lung cancer is frequently associated with idiopathic pulmonary fibrosis (IPF). The purpose of this study was to compare the intensity of lung infiltrates between the side associated with lung cancer and the side without lung cancer. Twenty-three patients (24 lung cancers) with primary lung cancer associated with pulmonary fibrosis were retrospectively evaluated. Chest CT findings were evaluated by three expert radiologists using the intensity scores. In 16 of the 23 patients, it was possible to compare the intensity of lung infiltrates between both sides of the lungs. As a result, increased intensity at the side in which lung cancer developed was demonstrated in 12 of 16 patients (75%). In the remaining four patients, intensity of lung infiltrates was the same in both lungs. In operated patients as well as autopsied patients, it was possible to evaluate the pathological findings of lung tissues around cancer cells. This study clearly demonstrates that the intensity of lung infiltrates increased at the side in which lung cancer developed.
Lung Cancer 1999 Dec
PMID:Increased intensity of lung infiltrates at the side of lung cancer in patients with lung cancer associated with pulmonary fibrosis. 1059 27

Mortality due to lung cancer was 25% (7/28) in this study of patients with diffuse interstitial pulmonary fibrosis. Opacities on the chest x-ray suggestive of lung cancer were observed in 5 of the 7 cases. All 7 had squamous cell carcinoma. The percentage of smokers was significantly higher in patients with pulmonary fibrosis who developed lung cancer than in those with fibrosis who did not develop lung cancer (p = 0.016). These 7 cases of lung cancer with pulmonary fibrosis were compared with 174 cases of lung cancer without associated fibrosis. Peripheral localizations and lower lobe involvement were higher in cases of lung cancer with pulmonary fibrosis.
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PMID:[Diffuse interstitial pulmonary fibrosis and bronchial cancer]. 1068 72

Psoriatic arthritis is an inflammatory arthritis associated with psoriasis. While an elevated incidence of lung cancer has been observed in patients with RA or psoriasis, there has been no report of psoriatic arthritis associated with lung cancer. We here report the first case of psoriatic arthritis which developed lung cancer. In this case, it was suspected that a combination of cigarette smoking, pulmonary fibrosis, and low-dose methotrexate therapy might have promoted the development of lung cancer.
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PMID:Psoriatic arthritis complicating lung cancer. 1073 43

Asbestos fibers have genotoxic effects and are a potential carcinogenic hazard to occupationally exposed workers. The ability of inhaled asbestos fibers to induce the formation of 8-hydroxy-2'-deoxyguanosine (8-OHdG) in the DNA of white blood cells (WBC) of workers highly exposed at the workplace has been studied. The 8-OHdG adduct level of asbestos-exposed workers was significantly increased (p<0.001) compared to that in the control group in all three years of the study. Asbestos-exposed individuals showed a mean value of 2.61+/-0.91 8-OHdG/10(5) dG (median 2.49, n=496) in 1994-1995, 2.96+/-1.10 8-OHdG/10(5) dG (median 2.76, n=437) in 1995-1996 and 2.55+/-0.56 8-OHdG/10(5) dG (median 2.53, n=447) in 1996-1997. For the control subjects, a mean of 1.52+/-0.39 (median 1.51, n=214) was determined. The results indicate that human DNA samples from exposed individuals contain between 1.7 times and twice the level of oxidative damage relative to that found in control samples in all 3 years of the study. The studies presented here show that asbestos exposure can result in oxidative DNA damage. Our data confirm that oxidative DNA damage occurs in the WBC of workers highly exposed to asbestos fibers, thus supporting the hypothesis that asbestos fibers damage cells through an oxidative mechanism. These in vivo findings underline the importance of oxidative damage in asbestos-induced carcinogenesis and highlight the need for exploring the molecular basis of asbestos-induced diseases, and for more effective diagnosis, prevention and therapy of mesothelioma, lung cancer and pulmonary fibrosis. In addition, preventive and therapeutic approaches using antioxidants may be relevant.
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PMID:Levels of 8-hydroxy-2'-deoxyguanosine in DNA of white blood cells from workers highly exposed to asbestos in Germany. 1088 96


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