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)

Kininase II (KII), identical with angiotensin-I-converting enzyme (E.C. 3.4.15.1) was characterized biochemically and assayed fluorimetrically in bronchoalveolar lavage fluid and serum of 153 patients with several pulmonary disorders. The albumin concentrations of serum and bronchoalveolar lavage fluid (BLF) have also been measured. The pH optimum of KII derived from BLF (LKII) was 8.0. The Michaelis Menten constant was 38.5 mumol/l using benzyloxycarbonyl-phenylalanyl-histidyl-leucine as synthetic substrate. LKII could be inhibited between 80 and 100% by EDTA, phenanthroline, dimercapto-1-propane-sulfonic acid (DMPS), hydroxyquinoline and captopril. The LKII activity (mU/ml BLF) showed no differences in all lung diseases, but the specific LKII (mU/mg albumin) was significantly elevated in sarcoidosis compared to pneumonia (p less than 0.05), fibrosis (p less than 0.05), chronic obstructive bronchitis (p less than 0.005) and lung cancer (p less than 0.01), but not in tuberculosis. This study shows that LKII is measurable in native, unconcentrated BLF and the results indicate that LKII could be useful for diagnosis of pulmonary disorders.
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PMID:Value of determination of kininase II in bronchoalveolar lavage fluid. 302 72

In serum of 530 patients with various lung diseases and in 70 healthy control subjects, kininase I (E.C. 3.4.17.3) and kininase II (E.C. 3.4.15.1) were measured spectrophotometrically using hippuryl-L-arginine for estimation of kininase Ia (KIa), hippuryl-L-lysine for kininase Ib (KIb) and hippuryl-L-histidyl-L-leucine for kininase II (KII). KIa and KIb were significantly elevated (p less than 0.02) in lung cancer and sarcoidosis, compared to tuberculosis and healthy controls. There was an increase (p less than 0.05) in lung cancer in relation to sarcoidosis, chronic obstructive bronchitis, tuberculosis, pulmonary fibrosis and healthy control subjects. KII was significantly elevated in sarcoidosis (p less than 0.0001). According to the histological types of lung cancer, no differences of KIa, KIb and KII have been found. The ratio KIa/KIb X KII was 2.3 in lung cancer and 6.7 in the group with sarcoidosis. These results show that the determination of kininases can be used for diagnosis of lung diseases.
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PMID:Kininase I and II activities in serum of patients with lung diseases. 302 81

The suppressive activity of alveolar macrophages (AM) obtained from bronchoalveolar lavage (BAL), on PHA stimulation of autologous peripheral blood lymphocytes (APL) was evaluated. The effect on lymphocyte stimulation was evaluated by coculturing the AM and APL cells at a ratio of 1:1. PGE2 released by AM during the culture period was measured by a radioimmune assay. The patients included in the study were 11 cases with interstitial lung disease (ILD), 8 cases of lung cancer (CA), and 5 controls (CO). Addition of AM of patients from the CA group resulted in slight suppression of lymphocyte stimulation in 4 cases, slight enhancement in 3 cases and no effect in one case. AM from the CO group induced slight suppression in 4 out of 5 cases. AM from all 11 ILD cases exerted a significant high suppressive activity (65.6% +/- 18.2 - P less than 0.001 by comparison with the CO and CA groups). In ILD cases, a dichotomous pattern was found in regard to relation between high suppressive activity of AM and release of PGE2: in idiopathic pulmonary fibrosis (IPF) patients, high suppressive activity of AM (70.4% +/- 15.4) correlated well with elevated secretion of PGE2: 3.58 +/- 0.26 ng/ml/10(5) cells (P less than 0.02 compared to CO). AM from sarcoidosis patients suppressed PHA stimulation by 61.6% +/- 19.3 but secreted only 0.357 +/- 0.26 ng/ml/10(5) cells of PGE2 (P less than 0.02 compared with the idiopathic pulmonary fibrosis group). Therefore, it seems that other factors, in addition to PGE2, might be involved in the suppressive activity of AM from interstitial lung diseases.
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PMID:Correlation between PGE2 production and suppressor activity of alveolar macrophages from patients with interstitial lung diseases. 316 69

Today it is believed that mast cells (MC) are important not only in IgE-mediated reactions, but also in delayed hypersensitivity reactions, and that their functions are mediated by factors released by T lymphocytes. Recent studies have shown their presence in bronchoalveolar lavage (BAL) of patients with asthma and interstitial lung disease. MC have been identified by us in the BAL of patients with sarcoidosis and lung cancer, and in controls. A statistically significant correlation has been found between MC and lymphocytes, CD3+ and CD4+ cells present in BAL, thus supporting the hypothesis of interactions between T lymphocytes and MC in immune reactions at the alveolar level.
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PMID:Mast cells in bronchoalveolar lavage in sarcoidosis: correlation with alveolar lymphocytes. 323 5

Cytomorphologic characteristics of bronchial epithelium have been examined in 58 patients with central lung cancer (42 patients in stage T1N0M0 and 16 in stage T1N1M0 and 84 patients with nonneoplastic diseases (tuberculosis, hamartoma, sarcoidosis, or chronic nonspecific inflammation), using smears from bronchial mucosa, imprints from tissue pieces biopsied on bronchoscopy, scrapings from lesions and surrounding tissues, and transthoracic puncture samples. In 34 of the 58 cancer patients, the changes in bronchial epithelium were categorized as moderate to severe dysplasia. A scheme summarizing malignant transformation of bronchial epithelium is proposed. It is shown that bronchial epithelial dysplasia can be recognized by cytologic examination, which may be used to advantage in screening subjects for early detection of lung cancer.
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PMID:[Cytologic characteristics of bronchial epithelial dysplasia from the viewpoint of the early detection of lung cancer]. 366 58

In vivo animal studies support the concept that monocytes and macrophages are important in the immune surveillance of oncogenesis and that in vitro activated murine macrophages are cytocidal for tumour cells. In this study, the tumour cell cytotoxic activity of human peripheral blood monocytes was examined by measuring the inhibition of 3H-thymidine uptake in the human cancer cell line, established in our laboratory from human squamous cell lung cancer. The monocytes from 8 of the 31 lung cancer patients (26%) showed a percentage growth inhibition of less than 69.8%, which exceeded the 95% confidence limits of the percentage growth inhibition observed with healthy control monocytes. On the other hand, among the 16 sarcoidosis and the 8 tuberculosis cases no value was below 69.8%. However, there was no significant difference between the growth inhibition and the clinical stages or histological type. When OK-432, a Streptococcal agent, was administered in vivo to patients with lung cancer, an elevation of the growth inhibition was observed in 7 out of 8 patients. It was confirmed that the tumour cell cytostatic activity of the monocyte is suppressed in patients with lung cancer, and these monocyte deficits hinder the inhibition of tumour growth and metastasis.
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PMID:Decreased monocyte-mediated cytostasis of human cancer cell in patients with lung cancer. 385 93

Bronchoalveolar lavage (BAL) is a powerful tool with which the immunology of the lung in health and disease can be studied. This technique has been successfully used to characterize localized humoral and cell-mediated responses in sarcoidosis and a number of other interstitial pneumonitides. In contrast, BAL in patients with lung cancer has resulted in some confusion regarding the extent and type of local and systemic immunity in these patients. This review summarizes some of the data obtained from these patients via BAL, but does not attempt to explain the reported discrepancies. The objective of this review is rather to identify gaps which exist in our knowledge of the environmental factors influencing pulmonary immunity in primary lung cancer.
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PMID:Bronchoalveolar lavage and the immunology of primary lung cancer. 388 17

The functions of human pulmonary alveolar macrophages (PAMs) have been relatively little studied compared with those of their circulating counterparts, blood monocytes. This study examined the ability of human PAMs to kill primary human tumor cell cultures and control normal fibroblasts in vitro. PAMs were derived by bronchial lavage from patients with lung cancer of various histological types and stages, patients with acute or chronic noncancerous pulmonary disorders, and subjects with a presumed illness who proved to be normal. After extensive washing, the PAMs were cocultured with [3H]proline-labeled tumor cells, principally lung cancers and melanomas, at various effector:target ratios for 60 hr. Cytotoxicity was measured by comparing radioactivity associated with the remaining adherent tumor cells cultured in the presence or absence of PAMs. Twenty-eight of 42 preparations of PAMs from 42 individuals were cytotoxic to one or more short-term primary tumor cultures. All 28 specimens from patients with lung cancer or chronic pulmonary disease were cytotoxic; all of the 14 PAM preparations lacking cytotoxicity were from individuals with acute pulmonary disorders or who were proved free of pulmonary disease. PAMs were cytotoxic even at effector:target ratios of 2.5:1 or 1.25:1. Fibroblasts were unaffected at any ratio. Sarcoidosis patients in remission had noncytotoxic PAMs, whereas the disease in relapse was characterized by cytotoxic PAMs. Serial study of 2 patients confirmed a loss of reactivity during remission. Smoking did not correlate with the presence or absence of spontaneous cytotoxicity and did not influence the degree of cytotoxicity in "reactors." Partially purified alpha-interferon enhanced the killing of cytotoxic PAMs in 10 of 21 instances but did not induce cytotoxicity in 9 tests on nonreactive PAMs. We conclude that human PAMs from patients with lung cancer or chronic pulmonary diseases, including active sarcoidosis, were cytotoxic to several recently explanted tumor cell cultures. PAMs from acute pulmonary dysfunctions and those from patients with inactive sarcoidosis were not spontaneously cytotoxic.
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PMID:Cytotoxic activity of human pulmonary alveolar macrophages. 396 51

Lung cancer and chronic interstitial pneumonia associated with systemic sarcoidosis was detected in a 66-year-old woman at autopsy. Histologically, hyalinized sarcoid lesions were scattered in cervical lymph nodes, thoracic lymph nodes, abdominal lymph nodes, and spleen. Scattered non-caseating epithelioid cell granulomas with giant cells were observed in both lungs demoting cancer and chronic interstitial pneumonia. A tumor mass occupying right hilar portion was well-differentiated squamous cell carcinoma involving right upper lobe and right hilar lymph nodes. In the lower lobe of the left lung, a small nodule of poorly differentiated squamous cell carcinoma was detected. Alveolar septa, especially in both lower lobes of the lungs were thickened diffusely with fibrosis, edema, and inflammatory cell infiltration. Alveolar cavities contained hyaline membrane and large mononuclear cells. Atypical bronchiolar epithelial proliferation and squamous metaplasia associated with squamous cell carcinoma were detected. The clinical and pathological characteristics among eight reported cases of lung cancer associated with sarcoidosis and three reported cases of interstitial pneumonia associated with sarcoidosis were reviewed separately. There is no report describing both lung cancer and chronic interstitial pneumonia associated with sarcoidosis.
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PMID:Lung cancer and chronic interstitial pneumonia associated with systemic sarcoidosis. 400 90

An increased incidence of lung cancer and epithelial metaplasia or hyperplasia which is felt to be as a precursor of cancer, has been reported in patients with idiopathic pulmonary fibrosis (IPF). In this study, carcinoembryonic antigen (CEA) in bronchoalveolar lavage (BAL) fluid was measured in 53 control patients, 31 patients with sarcoidosis, 10 patients with hypersensitivity pneumonitis, 16 patients with primary lung cancer and 26 patients with histologically confirmed IPF. High ratio of CEA to albumin (Alb), exceeding mean + 2SD of nonsmoking control patients, were found in 8 (25%) out of 32 smoking control patients, 4 (44%) out of 9 nonsmoking patients with IPF, 8 (62%) out of 13 smoking patients with IPF, 3 (75%) out of 4 smoking patients with IPF and lung cancer and 13 (81%) out of 16 patients with primary lung cancer, although BAL was performed at the noncancerous parts of the lung in the cases of lung cancer. Furthermore, it was confirmed that CEA increased in BAL fluid in these subjects were different from nonspecific cross-reacting antigen (NCA) which was detectable in the normal lung. Thus we consider that the increase of CEA/Alb ratio in BAL fluid is a possible marker of these early histological disorders in the lung, and also suggests a greater risk of malignant change in the clinical course of IPF.
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PMID:Carcinoembryonic antigen in bronchoalveolar lavage fluid in patients with idiopathic pulmonary fibrosis. 406 59


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