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

Lung cancer is associated with smoking and age, both of which are associated with comorbidity. We evaluated the impact of comorbidity on lung cancer survival. Data on 56 comorbidities were abstracted from the records of a cohort of 1,155 patients. Survival effects were evaluated with Cox regression (outcome crude death). The adjusted R(2) statistic was used to compare the survival variation explained by predictive variables. No comorbidity was observed in 11.7% of patients, while 54.3% had 3 or more (mean 2.97) comorbidities. In multivariate analysis, 19 comorbidities were associated with survival: HIV/AIDS, tuberculosis, previous metastatic cancer, thyroid/glandular diseases, electrolyte imbalance, anemia, other blood diseases, dementia, neurologic disease, congestive heart failure, COPD, asthma, pulmonary fibrosis, liver disease, gastrointestinal bleeding, renal disease, connective tissue disease, osteoporosis and peripheral vascular disease. Only the latter was protective. Some of the hazards of comorbidities were explained by more directly acting comorbidities and/or receipt of treatment. Stage explained 25.4% of the survival variation. In addition to stage, the 19 comorbidities explained 6.1%, treatments 9.2%, age 3.7% and histology 1.3%. Thirteen uncommon comorbidities (prevalence <6%) affected 21.2% of patients and explained 3.5% of the survival variation. Comorbidity count and the Charlson index were significant predictors but explained only 2.5% and 2.0% of the survival variation, respectively. Comorbidity has a major impact on survival in early- and late-stage disease, and even infrequent deleterious comorbidities are important collectively. Comorbidity count and the Charlson index failed to capture much information. Clinical practice and trials need to consider the effect of comorbidity in lung cancer patients.
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PMID:Impact of comorbidity on lung cancer survival. 1251 1

Although pulmonary fibrosis is a frequent and serious consequence of radiotherapy for thoracic malignant diseases such as lung cancer, the pathogenesis of this radiation-induced lung disorder remains unclear. To clarify the mechanisms underlying radiation pneumonitis and pulmonary fibrosis, we investigated the expression of platelet-derived growth factor receptor (PDGFR) on fibroblasts obtained from irradiated rat lungs and on control fibroblasts. Whole lungs of male Wistar rats were irradiated with a single dose of 15 Gy, and lung fibroblasts were isolated at 4 weeks after the irradiation. The chemotactic response of irradiated lung fibroblasts to PDGF-BB was significantly higher than that of control lung fibroblasts, whereas there was no significant difference between irradiated lung fibroblasts and control lung fibroblasts in the response to PDGF-AA. Receptor binding assay showed more specific binding sites for PDGF-BB on irradiated lung fibroblasts than on control lung fibroblasts, and the displacement of (125)I-labeled PDGF binding to fibroblasts by unlabeled PDGF showed that (125)I-labeled PDGF-BB was displaced by PDGF-BB but not by PDGF-AA. These results suggest that the increased binding sites for PDGF-BB on irradiated lung fibroblasts correspond mainly to PDGFRB. Scatchard analysis of the saturation data demonstrated an approximately twofold increase both in the number of PDGF-BB binding sites and in the binding affinity in irradiated lung fibroblasts compared to that in control lung fibroblasts. Those results suggest that the increased chemotactic response of irradiated lung fibroblasts to PDGF-BB is related to the overexpression of PDGFRB, which may have an important role in the pathogenesis of radiation-induced pneumonitis and pulmonary fibrosis.
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PMID:Increased binding and chemotactic capacities of PDGF-BB on fibroblasts in radiation pneumonitis. 1275 64

The occurrence of lung cancer in patients with diffuse interstitial pulmonary disease is well-known. The incidence, however, varies and ranges from 9.8 to 38%. The pathogenesis of lung cancer in pulmonary fibrosis is unclear, but genetic as well as environmental factors seem to be involved.
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PMID:Cancer in interstitial pulmonary fibrosis and sarcoidosis. 1290 10

The purpose of this study was to make a pathological evaluation of the tumor response and the lung injury of non-small cell lung cancer (NSCLC) patients after carbon ion therapy. We enrolled four NSCLC patients with chest wall invasion but without nodal and distant metastasis (T3N0M0). Only primary lesions were irradiated with carbon ions, followed by surgical resection. The patients consisted of three males and one female varying by age from 54 to 73 (average 66.3). Total treatment dose was 59.4 and 64.8 GyE, respectively, administered in 18 fractions over 6 weeks, or 72.0 GyE in 16 fractions over 4 weeks. Resection after radiation therapy was performed as a combination of lobectomy, lymph node dissection and chest wall surgery. After fixation, the lung was sliced into thin sections to match the CT image. Each slice was anatomically identified and the slices were compared with each other subjected to pathological analysis. No tumor cells were observed in two cases. The other two cases exhibited only a few tumor cells sparsely distributed in the lung tissue. There was evidence of dense pulmonary fibrosis in the limited space surrounding primary tumors, but its density was found to rapidly decrease in the narrow area toward the outside. The rate at which its density subsided mirrored the rapid decrease in the planning CT dose distribution. Microscopy showed no evidence of fibrosis in any of the fields irradiated with less than 15 GyE. Microscopy confirmed an outstanding tumor response with limited pulmonary fibrosis. This substantiates the superior dose localization and strong biological effect of carbon ion beams with a Bragg peak in the lung. The pathological findings have thus provided evidence of the safety and effectiveness of carbon beam therapy in the treatment of NSCLC.
Lung Cancer 2003 Oct
PMID:Preoperative carbon ion radiotherapy for non-small cell lung cancer with chest wall invasion--pathological findings concerning tumor response and radiation induced lung injury in the resected organs. 1451 92

Pulmonary gene therapy offers the hope of treatment for conditions such as cystic fibrosis, lung cancer, pulmonary fibrosis and acute respiratory distress syndrome for which current therapy is inadequate. Although initial clinical trials in cystic fibrosis and non-small cell lung cancer have shown promise the results have not been as good as might have been anticipated. However, clinical improvement has been demonstrated in conditions such as haemophilia [82], cardiovascular disease [83], head and neck cancer [84] and X-linked severe combined immunodeficiency disease [85]. The lack of success of pulmonary gene therapy is due, in part on the physical barriers to transfection perfected by the lung to prevent toxicity from inhaled particles, and partly due to the poor transfection efficiency of non-viral systems, and the immunogenicity of viral systems, of gene transfer. The LID vector goes some way to addressing the problems associated with current gene delivery strategies. With continued improvements in the properties of both viral and non-viral gene delivery systems leading to improved transfection efficiency with reduced toxicity, as well as the development of strategies aimed at reducing the physical barriers to pulmonary transfection, and targeting gene delivery systems to the site of injury, it is likely that pulmonary gene therapy will be used successfully to ameliorate a number of devastating pulmonary conditions.
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PMID:Pulmonary gene therapy. Realistic hope for the future, or false dawn in the promised land? 1453 78

Neurotrophins are growth factors that exert multiple actions on neuronal and nonneuronal cells. Neurotrophin receptors are expressed on central and peripheral neurons, lymphocytes, monocytes, mast cells, and fibroblasts. In accordance with the distribution of their receptors, neurotrophins control the development and function of neurons and regulate inflammatory processes. Production of neurotrophins is altered in asthma, lung cancer, and pulmonary fibrosis. Evidence from animal models has implicated nerve growth factor (NGF) as a mediator of pulmonary inflammation, bronchoconstriction, and airway hyperreactivity, all of which are hallmarks of asthma. NGF regulates the growth of lung tumor cells and cultured lung fibroblasts. Thus neurotrophins, particularly NGF, are candidate molecules for regulating disease processes in asthma, lung cancer, and pulmonary fibrosis.
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PMID:Neurotrophins and lung disease. 1456 56

A high incidence of interstitial lung disease (ILD) has been reported in patients with non-small cell lung cancer (NSCLC) treated with gefitinib in Japan. We retrospectively analyzed 112 patients with advanced NSCLC who received gefitinib monotherapy. Univariate and multivariate analyses were used to identify risk factors for gefitinib-related ILD and predictive factors for tumor response to gefitinib. The incidence of ILD was 5.4%, and it was higher in the patients with pre-existing pulmonary fibrosis (33% versus 2%; P < 0.001). The results of a multivariate analysis showed that pulmonary fibrosis was a significant risk factor for ILD (odds ratio: 177, 95% confidence interval: 4.53-6927, P = 0.006). The response rate was 33% in the 98 evaluable patients and higher in women (53% versus 23%; P = 0.003), patients with adenocarcinoma (38% versus 6%; P = 0.010), never-smokers (63% versus 18%; P < 0.001), and the patients with no history of thoracic radiotherapy (39% versus 13%; P = 0.015). The results of a multivariate analysis showed that the predictors of tumor response were "no history of smoking" and "no history of thoracic radiotherapy". Never-smokers had a significantly longer survival time than smokers (P = 0.007). Although gefitinib therapy confers a clinical benefit on patients with advanced NSCLC, especially on women, patients with adenocarcinoma, never-smokers, and patients with no history of thoracic radiotherapy, it also poses a high risk of ILD, especially to patients with pulmonary fibrosis. The risk-benefit ratio must be carefully considered.
Lung Cancer 2004 Jul
PMID:Risk factors for interstitial lung disease and predictive factors for tumor response in patients with advanced non-small cell lung cancer treated with gefitinib. 1519 39

In developing countries, aggressive marketing of chrysotile asbestos continues as a result of restrictions on its use being imposed by the developed countries. In the Asian continent, China and India are emerging as the major users of asbestos. There is enough evidence to link chrysotile with pulmonary fibrosis and lung cancer in humans, even at low levels of exposure, hence the need to apply the Precautionary Principle for phasing out its use globally. Due to poor occupational health and safety systems in developing countries and difficulties in early detection of pulmonary malignancy related to asbestos, the statistics remain sketchy. This is hampering efforts to create pressure on policy makers and to counter the propaganda of the asbestos industry. The International Labour Office believes that more than 100,000 deaths a year occur from asbestos-related disease. In the view of studies published in Europe and Australia, the number of deaths due to such malignancies will peak around the year 2020 and could be anywhere between half a million to a million. That means more than a million deaths will occur in developing countries. At about the same time when asbestos-related deaths start to decrease in developed countries, their number will begin to rise in developing countries. This presents a major challenge to the international scientific community.
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PMID:Asbestos in developing countries: magnitude of risk and its practical implications. 1521 22

Histological examination was performed on 93 pulmonary nodules resected in 90 patients with known malignancy. The diameters of the coin lesions on CT scan were 3-10 mm in 42 cases and 11-30 mm in 51 cases. The most common sources of the previous malignancy were: large bowel (20), breast (14), uterus (12), kidney (11) and larynx (7). In 84 cases the nodules were radically resected through "wedge" resection and in 9 cases lobectomy was performed. Most frequently, coin lesion was caused by metastases of known malignancy (in 69.9%), pulmonary fibrosis (in 11.8%) and by primary lung cancer (in 7.5%). In general, pulmonary nodules were found malignant in 78.5% and benign in 21.5% of the cases. In the subgroup of coin lesions of diameter between 11 and 30 mm malignancy was noted in 94.1%--significantly more frequently than in subgroup of diameter between 3 and 10 mm (59.5%). No significant correlation was found between histological type of pulmonary nodules (malignant or benign) and the type of primary malignancy as well as the time from the treatment of primary malignancy to the detection of the coin lesion.
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PMID:[Coin lesion in the lung of patients with known malignancy]. 1530 57

Occupational exposure to crystalline silica has been linked to pulmonary fibrosis and lung cancer. Surface properties of crystalline silica are critical to the production of oxidant species, chemokines, inflammatory cytokines, and proliferative factors involved in the initiation and progression of silica-induced damage, inflammation, alveolar type II cell hyperplasia, fibroblast activation, and disease. The transcription factors nuclear factor kappaB (NF-kappaB) and activator protein 1 (AP-1) have been shown to play key roles in gene promotion for inflammatory mediators, oncogenes, and growth factors. This review summarizes evidence that in vitro and in vivo exposure to crystalline silica results in activation of NF-kappaB and AP-1. Signaling pathways for activation of these transcription factors are described. In addition, the role of silica-induced reactive oxygen species and nitric oxide in the activation of these signaling events is presented. Last, the generalizability of mechanisms regulating silica-induced pulmonary responses to pulmonary reactions to other occupational particles is discussed.
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PMID:Signaling pathways controlling the production of inflammatory mediators in response to crystalline silica exposure: role of reactive oxygen/nitrogen species. 1533 7


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