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)

To define the clinical characteristics of multiple lung cancer (LC) associated with idiopathic pulmonary fibrosis (IPF), we reviewed 154 LC patients associated with IPF: 23 patients with synchronous multiple LC (IPF-multiple LC group) and 131 with single LC (IPF-single LC group), and these were compared with 4,931 patients with LC from 1975 to 1977 in Japan (whole LC group). In the IPF-single and IPF-multiple LC groups, most tumors were observed in male patients (91% and 96%), smokers (94% and 100%), and in peripheral regions of the lung (91% and 98%). The incidence of occurrence in the lower lobes, where a fibrotic shadow was prominent, was significantly higher in the IPF-LC groups (58% and 67%) than for the whole LC group (37%). The distribution of histologic types in the IPF-single LC group was similar to that of the whole LC group. However, the incidence of small cell carcinoma was significantly higher in the IPF-multiple LC group (33%) than for the IPF-single LC (14%) and whole LC (12%) groups. These results indicate that the features characteristic to synchronous multiple LC in patients with IPF are as follows: (1) male patients; (2) smokers; (3) small cell carcinoma histologic type; (4) lower lobes; and (5) peripheral type, all of which show a high rate of occurrence.
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PMID:Clinical characteristics of synchronous multiple lung cancer associated with idiopathic pulmonary fibrosis. A review of Japanese cases. 758 14

A total of 117 patients with pulmonary interstitial diseases (PID) were examined. The functional activity of alveolar macrophages was assayed in the lavage fluid and in lung tissue biopsy specimens from the generation of active oxygen forms, the secretion of tumor necrosis factor, fibronectin, expression of c-fos- and c-sis-oncoprotein. The stereotypic value for various PID was the development of alveolitis running in 2 stages: 1) early one, including exudative inflammation and 2) late one, involving sclerotic changes up to the formation of the honeycomb lung. This results in the block of the blood-air barrier and progression of respiratory failure and hypoxia in patients. The morphogenesis of fibrosing alveolitis is formed of alveolar septal damages caused by etiological agents of various nature, which is frequently unclear, by active forms of oxygen, lipid peroxidation products, proteases, tumor necrosis factor, which are produced by activated alveolar macrophages and polymorphonuclear leukocytes. The alveolar macrophage that secretes growth factors, c-fos- and c-sis-oncoproteins plays the key role in the progression of sclerotic changes. Lung cancer may develop at the end of fibrosing alveolitis at the stage of the honeycomb lung.
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PMID:[Intercellular interactions in morphogenesis of initial lesions and sclerosis in interstitial lung diseases]. 762 80

Prostaglandin E2 (PGE2) inhibits fibroblast proliferation and collagen synthesis. In this study, we compared lung fibroblasts isolated from patients with idiopathic pulmonary fibrosis (F-IPF) and from patients undergoing resectional surgery for lung cancer (F-nl) with respect to their capacity for PGE2 synthesis and their expression and regulation of cyclooxygenase (COX) proteins. Basal COX activity, assessed by quantitating immunoreactive PGE2 synthesized from arachidonic acid, was twofold less (P < 0.05) in F-IPF than F-nl. In F-nl, incubation with the agonists PMA, LPS, or IL-1 increased COX activity and protein expression of the inducible form of COX, COX-2, and these responses were inhibited by coincubation with dexamethasone. By contrast, F-IPF failed to demonstrate increases in COX-2 protein expression or COX activity in response to these agonists. Under conditions of maximal induction, COX activity in F-IPF was sixfold less than that in F-nl (P < 0.05). Our data indicate that F-IPF have a striking defect in their capacity to synthesize the antiinflammatory and antifibrogenic molecule PGE2, apparently because of a diminished induction of COX-2 protein. This reduction in the endogenous capacity of F-IPF to down-regulate their function via PGE2 may contribute to the inflammatory and fibrogenic response in IPF. Moreover, we believe that this represents the first description of a defect in COX-2 expression in association with a human disease.
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PMID:Cultured lung fibroblasts isolated from patients with idiopathic pulmonary fibrosis have a diminished capacity to synthesize prostaglandin E2 and to express cyclooxygenase-2. 770 93

Despite the large numbers of T-cells present in the lungs in fibrosing alveolitis, their pathogenetic role is poorly understood. If these cells are involved in pathogenesis, they are more likely to express the CD45RO+ memory phenotype. To test this hypothesis, open lung biopsies from patients with fibrosing alveolitis associated with systemic sclerosis (FASSc) were compared with grossly normal lung taken from the periphery of lobes resected for lung cancer. Biopsies from eight patients with FASSc were compared with tissue from seven cancer controls. Paraffin sections were stained with a polyclonal anti-CD3 antibody for T-lymphocytes, monoclonal anti-CD45 antibody for leucocyte common antigen, and monoclonal anti-CD45RO antibody for primed T-lymphocytes. Staining was assessed quantitatively by computerized image analysis: in each case, the number of immunopositive cells was related to alveolar wall area and alveolar wall length. Mean alveolar wall thickness was increased in patients with FASSc (60.7 +/- 24.0 microns) compared with cancer controls (15.7 +/- 5.3 microns). Patients with FASSc had greater numbers of CD45+, CD3+ and CD45RO+ cells.mm-1 alveolar wall length compared with the controls. CD45RO+ cells made up 77% (median) of the CD3+ cells in FASSc, and their numbers per unit alveolar wall length were positively associated with alveolar wall thickness (r = 0.61). In conclusion, in fibrosing alveolitis of systemic sclerosis, most interstitial T-lymphocytes express the phenotype of memory cells; these cells are likely to be involved in the persistent inflammatory process.
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PMID:Fibrosing alveolitis in systemic sclerosis: increase in memory T-cells in lung interstitium. 775 62

Fibrosis is a pathological process characterized by the replacement of normal tissue by mesenchymal cells and the extracellular matrix produced by these cells. The sequence of events leading to fibrosis of an organ involves the subsequent processes of injury with inflammation and disruption of the normal tissue architecture, followed by tissue repair with accumulation of mesenchymal cells in the area of derangement. The same sequence of events occurs in wound healing with normal granulation tissue and scar formation, but, while normal scar formation is very localized and transient, in contrast, in fibrosis, the repair process is exaggerated and usually widespread and can be chronic. Inflammatory cells (mainly mononuclear phagocytes), platelets, endothelial cells, and type II pneumocytes play a direct and indirect role in tissue injury and repair. The evaluation of three human fibrotic lung diseases, two diffuse [idiopathic pulmonary fibrosis (IPF), and the adult respiratory distress syndrome (ARDS)], and one focal (tumor stroma in lung cancer), has shown that several cytokines participate to the local injury and inflammatory reaction [interleukin-1 (IL-1), interleukin-8 (IL-8), monocyte chemotactic protein-1 (MCP-1), tumor necrosis factor-alpha (TNF-alpha)], while other cytokines are involved in tissue repair and fibrosis [platelet-derived growth factor (PDGF), insulin-like growth factor-1 (IGF-1), transforming growth factor-beta (TGF-beta), and basic-fibroblast growth factor (b-FGF)]. A better understanding of the cytokines and cytokine networks involved in lung fibrosis leads to the possibility of new therapeutic approaches.
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PMID:Cytokines in human lung fibrosis. 867 88

Fibrosis is a disorder characterized by a qualitative and quantitative alteration of the deposition of extracellular matrix with accumulation of mesenchymal cells in replacement of normal tissue. The sequence of events leading to fibrosis of an organ involves the subsequent processes of injury with inflammation and disruption of the normal tissue architecture, followed by tissue repair with accumulation of mesenchymal cells in this area. A similar sequence of events occurs in wound healing with formation of normal, limited and transient granulation tissue, while in fibrosis, a maladaptive repair leads to an extensive, exaggerated process with functional impairment. Inflammatory cells (mainly mononuclear phagocytes), platelets, endothelial cells, and type II pneumocytes play a direct and indirect role in tissue injury and repair. The evaluation of several human fibrotic lung diseases, five diffuse (idiopathic pulmonary fibrosis (IPF); adult respiratory distress syndrome (ARDS); coal workers' pneumoconiosis (CWP); Hermansky-Pudlak syndrome (HPS); systemic sclerosis (SS)) and two focal (tumour stroma in lung cancer; and obliterative bronchiolitis (OB) after lung transplantation), has shown that several cytokines participate in the local injury and inflammatory reaction (interleukin-1 (IL-1), interleukin-8 (IL-8), monocyte chemotactic protein-1 (MCP-1), and tumour necrosis factor-alpha (TNF-alpha)), while other cytokines are involved in tissue repair and fibrosis (platelet-derived growth factor (PDGF), insulin-like growth factor-1 (IGF-1), transforming growth factor-beta (TGF-beta), and basic-fibroblast growth factor (b-FGF)). A better understanding of the cytokines and cytokine networks involved in lung fibrosis leads to the possibility of new therapeutic approaches.
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PMID:The role of cytokines in human lung fibrosis. 868 Mar 82

The potential difficulties offered by the presence of a solitary pulmonary nodule in a patient with rheumatoid arthritis are illustrated by a male non-smoker with clinical, serologic and radiographic rheumatoid arthritis, active and fibrosing alveolitis and a new lung nodule. This nodule proved to be squamous cell carcinoma without the typical risk factors. The findings of a solitary pulmonary density or nodule in a patient with rheumatoid arthritis provides no assurance that the lesion is benign. Both necrobiotic nodules and lung cancer may present as solitary pulmonary nodules in patients with this autoimmune disease.
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PMID:Rheumatoid arthritis and the pulmonary nodule. 901 4

The cause of digital clubbing is unknown. Hepatocyte growth factor (HGF) is a pleotrophic factor which has various biological effects. We measured serum HGF in 12 patients with digital clubbing; the underlying diseases of these patients were: lung cancer, 2; cystic fibrosis, 2; idiopathic pulmonary fibrosis, 3; lung cancer with idiopathic pulmonary fibrosis, 1; chronic hepatitis, 1; interstitial pneumonia with collagen disease, 2; and bronchiectasis, 1; nine hundred and fifty-seven normal volunteers and 17 lung cancer patients without clubbing served as the control. As a result, the serum HGF concentration in patients with digital clubbing (0.47 +/- 0.29 ng/ml) was significantly higher when compared to that of lung cancer patients without digital clubbing (0.15 +/- 0.04, p < 0.01). Therefore, we suggest that HGF may play a role in the formation of digital clubbing.
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PMID:Hepatocyte growth factor and digital clubbing. 905

Significant numbers of syncytial cells were observed in the bronchoalveolar lavage fluid (BALF) of a 42-year-old patient who had SLE with interstitial pneumonia. Electron microscopic study of the BALF cells and positive reverse transcriptase activity in the supernatant of the cultured cells revealed unknown retroviral particles in the BALF cells. No antibodies to known human retroviruses or proviral sequences were detected. Type C retroviral particles and positive reverse transcriptase activity were also observed in co-cultured U937 cells. To evaluate the pathogenic role of unknown type C retroviral particles, screening for antibodies to this retroviral particle was performed by immunofluorescence in 26 patients with idiopathic pulmonary fibrosis, 17 patients with SLE, 22 patients with lung cancer, and 58 healthy volunteers. Serum antibody to this putative type C retrovirus was detected in 24% of SLE patients, 27% of idiopathic pulmonary fibrosis patients, none of the lung cancer patients and 2% of healthy volunteers. Although no direct evidence of this virus as the pathogen for SLE could be demonstrated, a possible role in the development of SLE and interstitial pneumonia might be suggested.
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PMID:Syncytial cell formation in vivo by type C retroviral particles in the systemic lupus erythematosus (SLE) lung. 906 20

We investigated whether intraalveolar inflammatory cells such as alveolar macrophages or lymphocytes produced the gene product of a type-C human endogenous retrovirus (HERV), HERV-E 4-1, which might initiate an immune response resulting in interstitial lung disease. We evaluated HERV-E 4-1 Env protein production by bronchoalveolar lavage fluid (BALF) cells and PBL in 109 patients with sarcoidosis, idiopathic pulmonary fibrosis (IPF), lung cancer, and rheumatoid lung disease as well as 26 normal control individuals. Production of HERV-E 4-1 Env protein by alveolar macrophages was observed using indirect immunofluorescence in 3 IPF patients and 3 sarcoidosis patients (6/135). No peripheral blood lymphocytes showed HERV-E 4-1 Env protein production. Antibodies to HERV-E 4-1 Env protein were detected in the BALF of all six patients by immunoblot analysis, while none of the normal control individuals showed HERV-E 4-1 Env protein antibody in the BALF. All examined BALF cells showed HERV-E 4-1 env mRNA transcript expression by reverse transcription-polymerase chain reaction. No significant influence of point mutation or DNA polymorphism on HERV-E 4-1 Env protein production was recognized. In conclusion, local production of HERV-E 4-1 Env protein and defective tolerance of HERV gene products with resultant antibody production may contribute to the pathogenesis of IPF or sarcoidosis in some patients.
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PMID:Alveolar macrophages produce the Env protein of a human endogenous retrovirus, HERV-E 4-1, in a subgroup of interstitial lung diseases. 911 54


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