Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0242379 (lung cancer)
 71,905 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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

Idiopathic pulmonary fibrosis (IPF) is a disease of unknown etiology associated with DNA damage and malignancy. Bronchogenic carcinoma is the cause of death in 10% to 13% of IPF patients. Microsatellite instability (MSI) and loss of heterozygosity (LOH) are frequently detected in cancers. If these genetic alterations could be observed in IPF, they might explain the higher relative risk of lung cancer in this disease. We investigated the incidence of MSI and LOH in sputum cytologic specimens from 26 IPF patients and 26 healthy, matched subjects, using 10 highly polymorphic microsatellite markers. The electrophoretic pattern of each specimen was compared with that of corresponding peripheral blood. Thirteen (50%) patients showed genetic alterations, consisting either of MSI or LOH. Five (19%) patients exhibited MSI and 10 (39%) exhibited LOH in at least one microsatellite marker. Three (12%) patients showed LOH in more than one marker. None of the healthy subjects exhibited genetic alterations in the studied markers. No correlation was found between the detected genetic alterations and age, disease duration, blood gases, or spirometric parameters of the patients. Our findings suggest that the genetic alterations that we studied are frequent in IPF, are apparently unrelated to the severity of the disease, and may be related to tumorigenesis.
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PMID:Frequent genetic alterations at the microsatellite level in cytologic sputum samples of patients with idiopathic pulmonary fibrosis. 1098 39

CYFRA 21-1 and ProGRP have recently been established as new tumor markers for lung cancer. However, there are few reports evaluating concentrations in their bronchoalveolar lavage (BAL) fluid. In this study, we examined 81 patients with benign lung disease. The mean values of CYFRA 21-1 in the BAL fluid of each lung disease were as follows: bronchiolitis obliterans organizing pneumonia (BOOP), 3.9 +/- 2.1 ng/ml (positive rate 50%); collagen vascular disease associated interstitial pneumonia (CVD-IP), 10.7 +/- 15.7 ng/ml (positive rate 50%); diffuse panbronchiolitis (DPB), 4.2 +/- 6.4 ng/ml (positive rate 29%); idiopathic pulmonary fibrosis (IPF), 1.5 +/- 2.1 ng/ml (positive rate 17%); pulmonary infiltration with eosinophilia, 6.3 +/- 7.1 ng/ml (positive rate 44%); sarcoidosis, 4.6 +/- 6.2 ng/ml (positive rate 27%); and healthy volunteer (HV), 0.6 +/- 0.6 ng/ml; and total, 4.4 +/- 5.6 ng/ml (positive rate 32%). The mean values of ProGRP in the BAL fluid were as follows: DPB, 5.0 +/- 7.6 pg/ml (positive rate 0%); IPF, 6.4 +/- 10.6 pg/ml (positive rate 0%); HV, 12.4 +/- 8.3 pg/ml; and total, 5.6 +/- 8.7 pg/ml (positive rate 0%). These results indicate that the two tumor markers have no disease specificity in benign lung disease.
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PMID:[Evaluation of CYFRA 21-1 and ProGRP in serum and bronchoalveolar lavage fluid of patients with benign lung disease]. 1110 1

Mutations of the tumour suppressor gene p53 lead to accumulation of the mutated p53 protein and subsequent production of antoantibodies against p53 proteins, which are also detected in lung cancer. Lung cancer is frequently associated with idiopathic pulmonary fibrosis (IPF). Therefore, we hypothesized that there might be a relationship between the p53 mutation and high prevalence of lung cancer in IPF. To test this hypothesis, we measured serum p53 antibody levels by an ELISA in various lung diseases including lung cancer (n=98), IPF (n=46; with lung cancer, n=14 and without lung cancer, n=32), pulmonary emphysema (PE, n=23) and healthy controls (HC, n=93). The median values of the serum anti-p53 antibody in each group were 8.78, 9.18, 8.08 and 4.95 for patients with lung cancer, IPF with lung cancer, IPF without lung cancer and PE, respectively, and 2.2 for the healthy control group. The groups of IPF (with and without lung cancer) showed a similar level of median values to the lung cancer group and a tendency for a higher level than the PE group. When the cut-off value was set at 7.7 according to the 95% specificity level for normal control, the incidence of positive anti-p53 antibody was significantly higher in lung cancer (61.2%), IPF with lung cancer (57.1%) and IPF without lung cancer (53.1%) than PE (21.7%). These results suggest that p53 mutations occur frequently and substantially in IPF, resulting in a high prevalence of lung cancer.
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PMID:Serum anti-p53 autoantibodies from patients with idiopathic pulmonary fibrosis associated with lung cancer. 1112 96

The most common pathologic form of idiopathic pulmonary fibrosis is usual interstitial pneumonia, which is characterized by patchy fibrotic areas, marked increase in the number of fibroblasts and type II pneumocytes, and excessive deposition of extracellular matrix proteins, especially collagen. Heat shock protein 47 is a collagen-binding stress protein and has a specific role in intracellular processing of procollagen molecules as a collagen-specific molecular chaperone. However, its role in the causation of fibrosis in usual interstitial pneumonia is unknown. In this study, we examined the expression of heat shock protein 47 and type I procollagen in 12 patients with usual interstitial pneumonia by immunohistochemistry on sequential sections. Heat shock protein 47 was localized predominantly in alpha-smooth muscle actin-positive myofibroblasts and surfactant protein-A-positive type II pneumocytes in active fibrotic areas of usual interstitial pneumonia. Type I procollagen was also expressed in those cells. In contrast, heat shock protein 47 and type I procollagen were weakly or not at all expressed in myofibroblasts and type II pneumocytes in bronchiolitis obliterans organizing pneumonia and normal lung tissue samples obtained from excised lung cancer tissues. The numbers of heat shock protein 47- and type I procollagen-positive cells to type II pneumocytes or myofibroblasts were significantly higher in usual interstitial pneumonia than in bronchiolitis obliterans organizing pneumonia and normal lung tissue specimens. Our results suggest that myofibroblasts and type II pneumocytes play an important role in the progression of fibrosis through the induction of heat shock protein 47, which regulates the synthesis/assembly of type I procollagen in usual interstitial pneumonia. HUM PATHOL 31:1498-1505.
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PMID:Involvement of collagen-binding heat shock protein 47 and procollagen type I synthesis in idiopathic pulmonary fibrosis: contribution of type II pneumocytes to fibrosis. 1115 Mar 75

Idiopathic pulmonary fibrosis (IPF) was reported to be associated with increased risk of lung cancer as a result of the occurrence of atypical or dysplastic epithelial changes in fibrosis which progressed to invasive malignancy. In that situation, the cancer will develop in the area of major fibrosis. To investigate the direct relationship between fibrosis and cancer development, the real concordance rate of the two lesions in the chest computed tomography (CT) was analysed and compared to the histological types of lung cancer. The subjects included 63 patients with combined lung cancer and IPF (IPF-CA), 218 patients with lone IPF, and 2,660 patients with primary lung cancer. All patients were diagnosed at Asan Medical Center during the same period. The age, percentage of smokers, and the male sex were significantly higher in IPF-CA compared with lone IPF. The odds ratio of smoking was 2.71 compared to nonsmoking IPF controls. In IPF-CA, 56% of the cancer was located in the periphery of the lung and 52% in the upper lobe. The majority of the cancers (64%) were found in the nonfibrotic area at chest CT. The most frequent cell type was squamous cell carcinoma (35%), and there was no significant difference in the cancer cell type between IPF-CA and total lung cancer population. These findings suggest that in combined lung cancer and idiopathic pulmonary fibrosis patients, the features of the lung cancer are similar to the total lung cancer population.
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PMID:Lung cancer in patients with idiopathic pulmonary fibrosis. 1149 Nov 67

The reported frequency of lung cancer in the setting of diffuse pulmonary fibrosis varies greatly, depending on the country of origin and the type of study. Most recent reports regarding diffuse pulmonary fibrosis in general and idiopathic pulmonary fibrosis in particular and lung cancers come from Japan; only a few clinical studies of this issue are available from other countries of the world, including the United States. The reported frequency ranges from 4.8% in the United States to 48.2% in Japan. The most frequent type of cancer is adenocarcinoma. Risk factors may include cigarette smoking, exposure to metal dusts, onset of idiopathic pulmonary fibrosis at an older age, and male predominance. Possible pathologic mechanisms are summarized. Given the very poor prognosis of idiopathic pulmonary fibrosis itself, with a mean survival of only 2.8 years, and that different diagnostic criteria were used in each study, it is likely that many of these studies are flawed because they evaluate lesions other than idiopathic pulmonary fibrosis. Thus, the frequency of lung cancer in idiopathic pulmonary fibrosis is still uncertain, and clearly requires follow-up of cohorts of clinically well-characterized patients, using standard diagnostic criteria for idiopathic pulmonary fibrosis. Finally, if the association between idiopathic pulmonary fibrosis and lung cancer is reconfirmed in these studies, the molecular and genetic mechanisms governing the development of lung cancer in this setting require additional study.
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PMID:Idiopathic pulmonary fibrosis and malignancy. 1158 76

Idiopathic pulmonary fibrosis (IPF) is well known to be associated with lung cancer. Several atypical epithelial lesions are frequently observed in the fibrotic area in IPF patients, and they have been suspected to be related to lung carcinogenesis. Several studies have suggested that p53 protein accumulation and mutation occur in the early pathogenesis of squamous cell carcinoma of the lung, suggesting some abnormality of the p53 tumor-suppressor gene in interstitial lung diseases. To examine the cause of the high frequency of lung cancer in IPF, we examined the p53 changes in atypical epithelial lesions and carcinoma in patients with IPF by immunohistochemistry and mutational analysis. We examined 19 lung cancer patients with IPF who underwent surgical resection for lung cancer in our institute. Paraffin-embedded tissues were treated by microwave and stained with an anti-p53 antibody (RSP53) by the avidin-biotin-peroxidase complex method. Mutations in exons 5 through 8 of the p53 gene were also examined by polymerase chain reaction mediated single-strand conformation polymorphism (polymerase chain reaction-single-strand conformation polymorphism) analysis and DNA sequencing. p53 protein was immunohistochemically detected in 13 (62%) of 21 squamous cell carcinomas, 3 (60%) of 5 squamous metaplasia with atypia, 16 (54%) of 30 squamous metaplasia, and 1 (4%) of 26 other hyperplastic lesions. p53 mutation was detected in 12 (57%) of 21 squamous cell carcinomas, 2 (40%) of 5 squamous metaplasia with atypia, 7 (23%) of 30 squamous metaplasia, and 0 (0%) of 26 other hyperplastic lesions. In conclusion, there are frequent p53 gene alterations in squamous metaplasia, which is distributed in the peripheral zone of the fibrotic area in patients with IPF. The present findings might provide a clue to the molecular mechanisms underlying the high incidence of lung cancer, especially peripheral-type squamous cell carcinoma in IPF patients, and suggest that p53 gene alterations play an important role in the early stages of lung carcinogenesis in patients with IPF.
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PMID:p53 gene alteration in atypical epithelial lesions and carcinoma in patients with idiopathic pulmonary fibrosis. 1167 37

Important recent changes have occurred in our understanding of the IIPs. IPF (characterized histologically as UIP) is recognized as a progressive disease with a relatively poor prognosis, and with a characteristic CT appearance. The radiologist must be able to distinguish between UIP and the other IIPs. Complications of IPF include accelerated progression, lung cancer, and secondary infection. NSIP has a better prognosis than IPF, and has ground-glass attenuation as its salient CT feature. COP (formerly known as BOOP) is included as an IIP because its clinical, physiologic, and imaging features overlap with those of the other IIPs. It is characterized on CT by consolidation and ground-glass attenuation. AIP is the idiopathic form of ARDS. LIP and DIP are less common IIPs, both characterized by ground-glass attenuation.
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PMID:High-resolution CT of idiopathic interstitial pneumonias. 1169 66

In the normal human life span, there occur lifestyle-related diseases that may be preventable with nontoxic agents. This paper deals with the preventive activity of green tea in some lifestyle-related diseases. Green tea is one of the most practical cancer preventives, as we have shown in various in vitro and in vivo experiments, along with epidemiological studies. Among various biological effects of green tea, we have focused on its inhibitory effect on TNF-alpha gene expression mediated through inhibition of NF-kappaB and AP-1 activation. Based on our recent results with TNF-alpha-deficient mice, TNF-alpha is an endogenous tumor promoter. TNF-alpha is also known to be a central mediator in chronic inflammatory diseases such as rheumatoid arthritis and multiple sclerosis. We therefore hypothesized that green tea might be a preventive agent for chronic inflammatory diseases. To test this hypothesis, TNF-alpha transgenic mice, which overexpress TNF-alpha only in the lungs, were examined. The TNF-alpha transgenic mouse is an animal model of human idiopathic pulmonary fibrosis which also frequently develops lung cancer. Expressions of TNF-alpha and IL-6 were inhibited in the lungs of these mice after treatment with green tea in drinking water for 4 months. In addition, judging from the results of a prospective cohort study in Saitama Prefecture, Japan, green tea helps to prevent cardiovascular disease. In this study, a decreased relative risk of death from cardiovascular disease was found for people consuming over 10 cups of green tea a day, and green tea also had life-prolonging effects on cumulative survival. These data suggest that green tea has preventive effects on both chronic inflammatory diseases and lifestyle-related diseases (including cardiovascular disease and cancer), resulting in prolongation of life span.
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PMID:A new function of green tea: prevention of lifestyle-related diseases. 1179 18


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