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)

A range finding study for experimental induction of pulmonary fibrosis in which female Syrian golden hamsters received five subcutaneous injections of 0.8, 0.6, 0.4, 0.2 or 0 mg of N-methyl-N-nitrosourethane (MNUR) once a week or once per two weeks revealed most of the animals of the 0.8 mg group to die of acute pulmonary injury due to MNUR while typical interstitial pneumonia was induced in the 0.6 mg group. Based on these results hamsters were given five subcutaneous injections of 0.6 mg/animal of MNUR once per two weeks and then reared without any treatment for 12 weeks. Marked interstitial edema and intraalveolar infiltration of macrophages due to alveolar capillary damage were seen in treated animals at week 1, and secondary diffuse fibrotic thickening of the alveolar septa, as evidenced by increased type III collagen demonstrated immunohistochemically, was marked thereafter. The content of hydroxyproline in the lung was significantly increased from week 4. The present study indicates that lung injuries attributable to primary damage of alveolar capillaries progress to diffuse alveolar fibrosis in hamsters treated with MNUR, suggesting that this animal model might be of advantage for pathogenetic analysis of the relationship between pulmonary fibrosis and lung cancer development.
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PMID:Experimental induction of pulmonary fibrosis in Syrian golden hamsters by N-methyl-N-nitrosourethane. 789 38

Asbestos-related diseases continue to be sources of controversy for epidemiologist, clinician, and pathologist. Most investigators agree that the different fiber types behave differently in the lung, with chrysotile being rapidly removed, and amphibole persisting. These differences in biologic behavior probably account for the much greater disease potential of amphibole (amosite and crocidolite) compared with chrysotile asbestos, particularly in regard to mesothelioma induction in man. Asbestosis is defined as diffuse interstitial fibrosis of the lung caused by asbestos exposure, and this is the only condition to which the term asbestosis should be applied. The classical pathologic diagnostic criteria for asbestosis, namely the presence of diffuse interstitial fibrosis resembling usual interstitial pneumonia, and asbestos bodies visible in ordinary tissue sections, have proved to withstand the test of time. Cases without asbestos bodies visible in routine or iron-stained tissue sections almost never turn out to be asbestosis. It should be remembered that workers with asbestos exposure develop all of the interstitial lung diseases to which the remainder of the populace is subject; some of these conditions are treatable and should not be misdiagnosed as asbestosis, which is not treatable. There is strong epidemiologic and pathologic evidence that the only association of asbestos exposure and lung cancer is the association of asbestosis and lung cancer. Thus, a lung cancer should only be attributed to asbestos exposure when asbestosis is present on clinical or pathologic grounds. The histologic type and location of the tumor are irrelevant in this regard. Analytical electron microscopy indicates that chrysotile asbestos does induce mesothelioma in man, but that extremely high levels of retained fibers, levels as high as those seen in cases of asbestosis, are required for this event to occur. The weight of the evidence suggests that exposure of the general population to the very low levels of chrysotile that are found in some public building (levels not greatly different from ambient air) will never produce mesothelioma, asbestosis, or lung cancer because these diseases all appear to require quite high-level occupational chrysotile exposure. Even if one accepts the ideas (probably wrong) that any level of asbestos exposure carries a risk of cancer, and that mathematical extrapolation of risk from high-level occupational exposure to low-level building exposure is scientifically valid, the calculated risks are much smaller than real everyday risks such as driving to work. Thus, exposure to asbestos at environmental levels appears to produce no real dangers to health.
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PMID:Asbestos-related disease in the workplace and the environment: controversial issues. 810 99

The presence of the HTLV-I gene in peripheral blood mononuclear cells was studied by polymerase chain reaction in 42 patients including 16 with lung cancer, 12 with diffuse panbronchiolitis (DPB), 11 with idiopathic interstitial pneumonia (IIP), and 3 with pneumoconiosis and hematological malignancy. Sequences equal to a part of the pX gene were found in 44% of the lung cancer cases, 50% of the DPB cases, 55% of the IIP cases, and 100% of the cases of pneumoconiosis and leukemia. In the lung cancer cases, detection of the pX gene was frequently associated with the existence of diffuse interstitial pulmonary shadows. The pX gene was detected in 100% of patients with anti-HTLV-I antibody, 50% of patients with HTLV-I-related reaction and 14% of patients who tested seronegative. It may be inferred from the results that respiratory diseases that produce diffuse interstitial pulmonary shadows are closely associated with HTLV-I infection and that the HTLV-I-related reaction to the immunofluorescent test might reflect the latent infection state of HTLV-I.
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PMID:Detection of the pX gene of human T-lymphotropic virus type I in respiratory diseases with diffuse interstitial pulmonary shadows and lung cancer. 812 9

KL-6, a circulating mucin-like glycoprotein, is a pulmonary adenocarcinoma-associated antigen and is also regarded as an indicator of disease activity of interstitial pneumonitis. KL-6 has extensive heterogeneous antigenic determinants and consists of multiple heterogeneous antigen molecules. We have searched for circulating KL-6-associated glycoproteins with superior diagnostic value to KL-6 as a tumor marker for pulmonary adenocarcinoma. A new murine monoclonal antibody EH-123 reacting with an asialosugar chain on KL-6 was established. A new KL-6-associated molecule detected by a bimonoclonal bideterminant sandwich assay using the EH-123 antibody as a catcher and horseradish peroxidase-labeled KL-6 as a tracer was designated as CAM 123-6. In 59% (22 of 37) of patients with pulmonary adenocarcinoma, serum levels of CAM 123-6 were abnormally elevated and the positive rate increased with the progression of clinical stage. Elevated levels were not detected in normal individuals or in patients with benign lung diseases, other histologic types of lung cancer, gastric cancer, colon cancer or breast cancer. CAM 123-6 was more specific to pulmonary adenocarcinoma than carcinoembryonic antigen (CEA), but the sensitivity of CAM 123-6 for pulmonary adenocarcinoma was similar to that of CEA. CAM 123-6 is a promising candidate as a serum tumor marker for pulmonary adenocarcinoma.
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PMID:A new serum tumor marker, CAM 123-6, highly specific to pulmonary adenocarcinoma. 814 2

We reported two cases of idiopathic interstitial pneumonia (IIP) who developed acute exacerbation after bronchoalveolar lavage (BAL). One case was a 67-year-old male who presented with dry cough and exertional dyspnea. He was diagnosed as IIP and transbronchial lung biopsy revealed alveolitis. BAL was performed after administration of prednisolone. He complained of severe dyspnea after BAL and was diagnosed as having an acute exacerbation of IIP. In spite of extensive treatment including pulse therapy with methylprednisolone, he died. The other case was a 57-year-old male noted to have a chest X-ray abnormality who presented with dry cough and dyspnea on exertion. He was diagnosed as having IIP and primary lung cancer. BAL was performed to evaluate the activity of IIP, and respiratory distress subsequently became severe. After BAL, he developed an acute exacerbation of IIP and died in spite of treatment. In both cases, peripheral white blood cell counts were increased just before BAL. It was suggested that this condition might participate in acute exacerbation of IIP. It should be kept in mind that some patients with IIP may develop acute exacerbation after BAL.
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PMID:[Two cases of IIP which developed acute exacerbation after bronchoalveolar lavage]. 816 6

It has been generally accepted that lung fibrosis as in idiopathic interstitial pneumonia (IIP) is frequently associated with the development of lung cancer. This observation implies that the mechanism involved in carcinogenesis and/or enhanced proliferation of cancer cells is common to the fibrosing process. However, there are few studies reported on the pathogenesis of associated lung cancer except for several studies assessed from the point of view of surgical pathology. This study was undertaken to learn whether BAL fluid, which reflects the local milieu of the fibrosing process, enhances the proliferation of human lung cancer cell line Lu-99, Lu-65 and rat lung fibroblasts as assessed by 3H-thymidine incorporation. BAL fluid was obtained from patients with IIP (n = 8) and normal volunteers (n = 8). BAL fluids from patients with IIP enhanced the mean incorporation of 3H-thymidine of Lu-99 up to 3.6 times (p < 0.01) compared to that of normal volunteers. Furthermore, the mean incorporation of Lu-65 was increased up to 1.8 times (p < 0.05) by BAL fluids from patients with IIP. In contrast, BAL fluids from patients caused no significant increase of the mean incorporation of rat lung fibroblasts as compared to normal BAL fluids. The enhancing activities on the growth of cancer cell line Lu-99, Lu-65 were eluted in several fractions by high performance liquid chromatography using Superose 12. These observations indicate that the BAL fluid of IIP patients contains factors enhancing the growth of cancer cells.
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PMID:[Pathogenesis of development of lung cancer in idiopathic interstitial pneumonia--growth factors in bronchoalveolar lavage fluid]. 825 13

A 64-year-old male was admitted to Oita Medical University Hospital because of primary lung cancer. After the anticancer chemotherapy, the patient developed a high fever. His chest X-ray showed diffuse reticular shadows bilaterally, which were considered to be a drug induced pneumonia, then pulse therapy with corticosteroid was performed. With this treatment, the diffuse reticular shadows disappeared. One month later, however, a severe interstitial pneumonia developed, and the patient died of respiratory failure. Autopsy findings demonstrated cytomegalovirus (CMV) and Pneumocystis carinni pneumonia. The polymerase chain reaction (PCR) for CMV in mononuclear cells in the blood was positive through out his hospitalization. In the sera, however, it was negative at the time of admission, then became positive 10 days before the onset of pneumonia. In addition, the PCR for P. carinni on the swab became positive as well. These results imply that PCR can be used for diagnosis of CMV and P. carinii infections from sera or swabs.
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PMID:[A case of cytomegalovirus pneumonia and Pneumocystis carinii pneumonia with lung cancer--diagnosis by the polymerase chain reaction]. 827 Aug 3

A phase II trial of menadione [2.5 gm/m2 as a continuous intravenous (i.v.) infusion over 48 hours] followed by mitomycin C (10-20 mg/m2 i.v. bolus) administered every 4 to 6 weeks was performed in 23 patients with advanced lung cancer. Menadione, a vitamin K analog which lowers intracellular pools of reduced glutathione (GSH), was combined with mitomycin C in an attempt to overcome thiol-mediated resistance to alkylating agent chemotherapy. The median age of patients entered on this trial was 62 years; performance status ranged from 60-90%. Two of the 23 patients (9%; 95% confidence interval, 1% to 28%) had objective responses lasting 3.5 months and 13 months respectively, while 4 additional patients developed short unconfirmed responses (lacking follow-up response data to estimate response duration). Median survival for all patients was 5.5 months. Treatment with mitomycin C and menadione was well tolerated except for hematologic toxicity and cardiac events of unclear relationship to the study drugs. Thirty-one percent of treatment courses were complicated by grade 3 or 4 hematologic toxicity including one episode of hemolytic anemia. One patient developed interstitial pneumonitis. Two patients developed a decrease in left ventricular ejection fraction: one patient remained asymptomatic, but the other patient developed congestive heart failure. Although only 9% of patients had confirmed objective responses, 28% (5 of 18) of the patients with non-small cell lung cancer demonstrated biological activity (tumor regression fulfilling the criteria for objective response on a single occasion but 3 patients lacking a follow-up measurement to document response duration) to this combination of mitomycin C and menadione. We conclude that further studies of chemomodulation in non-small cell lung cancer are appropriate.
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PMID:Mitomycin C and menadione for the treatment of lung cancer: a phase II trial. 861 79

Among 102 patients with idiopathic interstitial pneumonia (IIP), 22 with lung cancer who were treated from 1981 to 1994 were studied retrospectively. As controls, 248 patients with lung cancer only who were treated from 1991 to 1992 were also studied. Lung cancer developed in 6 of 85 patients after IIP was diagnosed (7.1%). The time from the onset of IIP to the onset of lung cancer was 7.7 years. In 17 patients both IIP and lung cancer were present on admission. In general, patients with IIP and lung cancer were heavy smokers. In patients with IIP and lung cancer, %VC was higher than in those with IIP alone, and 20 cancers (90.0%) were in peripheral lung fields. Seventeen patients received anticancer chemotherapy, irradiation, or both. Five patients (29.4%) died of respiratory failure due to progression of pneumonitis after the therapy. The prognosis for patients with IIP and lung cancer was very poor.
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PMID:[Characteristics and management of patients with lung cancer and idiopathic interstitial pneumonia]. 874 30

There were 83 cases of usual interstitial pneumonia (UIP) in 3712 consecutive autopsy cases during 1972 to 1992 in Toranomon Hospital. Primary lung cancer had arisen in 40 cases of UIP in that period. The prevalence of lung cancer (48.2%) in UIP was significantly higher than that of lung cancers (9.1%) in the age-matched general population without UIP (P < 0.001). The prevalence of association of multiple lung cancer in UIP (20.0%) was also significantly increased. Thus, UIP showed a remarkable potency to develop lung cancers. The lung cancer cases in UIP had obvious smoking habits. Both the rates of smokers and the quantity of smoking were significantly increased in the lung cancer cases in UIP (P < 0.05). There was a distinct anatomical distribution of lung cancer in UIP. Most cancers in UIP (98%) arose in the peripheral area of the lung (P < 0.001, compared to lung cancer cases without UIP) with close relation to the honeycombing lesion. Studies on surgical specimens with small cancers showed that most tumors in UIP arose in the border area between honeycombing and the non-fibrotic area. Thus, the front of the remodeling of the lung is suspected to be a potential field of developing lung cancer. The chronic inflammatory process resulting in the remodeling of the lung may play an important part in the development of lung cancer in UIP under the circumstance of heavy smoking.
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PMID:Lung cancer associated with usual interstitial pneumonia. 880 97


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