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 cohort of 54,128 men who worked in Ontario mines was observed for mortality between 1955 and 1986. Most of these men worked in nickel, gold, or uranium mines; a few worked in silver, iron, lead/zinc, or other ore mines. If mortality that occurred after a man had started to mine uranium was excluded, an excess of carcinoma of the lung was found among the 13,603 Ontario gold miners in the study (standardised mortality ratio (SMR) 129, 95% confidence interval (95% CI) 115-145) and in men who began to mine nickel before 1936 (SMR 141, 95% CI 105-184). The excess mortality from lung cancer in the gold miners was confined to men who began gold mining before 1946. No increase in the mortality from carcinoma of the lung was evident in men who began mining gold after the end of 1945, in men who began mining nickel after 1936, or in men who mined ores other than gold, nickel, and uranium. In the gold mines each year of employment before the end of 1945 was associated with a 6.5% increase in mortality from lung cancer 20 or more years after the miner began working the mines (95% CI 1.6-11.4%); each year of employment before the end of 1945 in mines in which the host rock contained 0.1% arsenic was associated with a 3.1% increase in lung cancer 20 years or more after exposure began (95% CI 1.1-5.1%); and each working level month of exposure to radon decay products was associated with a 1.2% increase in mortality from lung cancer five or more years after exposure began (95% CI 0.02-2.4%). A comparison of two models shows that the excess of lung cancer mortality in Ontario gold miners is associated with exposure to high dust concentrations before 1946, with exposure to arsenic before 1946, and with exposure to radon decay products. No association between the increased incidence of carcinoma of the lung in Ontario gold miners and exposure to mineral fibre could be detected. It is concluded that the excess of carcinoma of the lung in Ontario gold miners is probably due to exposure to arsenic and radon decay products.
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PMID:Carcinoma of the lung in Ontario gold miners: possible aetiological factors. 166 86

The association between silicosis and lung cancer mortality was estimated in 9,912 (369 silicotics and 9,543 nonsilicotics) white male metal miners. These miners were examined by the U.S. Public Health Service during 1959-1961 and were followed through 1975. Miners were excluded from this study if they were employed in a mine during 1959-1961 that used diesel equipment underground. The ores that were mined consisted of copper, lead-zinc, iron, mercury, lead silver, gold and gold-silver, tungsten, and molybenum. The standardized mortality ratio (SMR, U.S. white male rates) for lung cancer was 1.73 (95% CI: .94-2.90) in silicotics and 1.18 (95% CI: .98-1.42) in nonsilicotics. Additionally, SMRs were higher in silicotics than in nonsilicotics, even in most subgroups stratified by cigarette smoking habit, type of ore mined, years of service in an underground job, radon exposure group, or year of hire. When lung cancer mortality between silicotics and nonsilicotics was compared, the age-adjusted rate ratio (95% CI) was 1.56 (.91-2.68), and the age- and smoking-adjusted rate ratio was 1.96 (.98-3.67). Corresponding figures for miners who were employed in mines with low levels of radon exposure were 1.90 (.98-3.67) and 2.59 (1.44-4.68), respectively. These findings indicate that lung cancer mortality risk was increased in silicotics, and this probably did not result from chance or bias. However, confounding from radon exposure could not be ruled out. The findings indicate that further follow-up of this cohort is needed.
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PMID:Silicosis and lung cancer in U.S. metal miners. 200 98

Previous studies have demonstrated that monoclonal antibody TFS-4 recognizes a cell surface antigen with a molecular weight of 124,000 expressed selectively on small-cell lung cancer but not on non-small-cell lung cancers and that it cross-reacts with human brain. The antigenic determinant on small-cell lung cancer and that on brain shared common characteristics, i.e., trypsin sensitivity, heat lability, and neuraminidase resistance, suggesting that they are similar peptides (T. Okabe et al., Cancer Res., 44: 5273-5278, 1984; J-i. Watanabe et al., Cancer Res., 47:826-829, 1987). In order to elucidate the nature of this unique antigen recognized by TFS-4, we have purified the antigen to homogeneity from human brain. The antigen was solubilized from brain with 0.5% Nonidet P-40, precipitated with 50% ammonium sulfate, and subsequently purified by sequential chromatographies, i.e., diethylaminoethyl-Sepharose ion exchange, immunoaffinity, and gel permeation high-pressure liquid chromatography. The antigenic reactivity was assessed by immunoblotting using TFS-4 as a primary antibody. The purified antigen showed a single protein band with a molecular weight of 124,000 on sodium dodecylsulfate-polyacrylamide gel electrophoresis detected by a silver staining technique. The results suggest that the antigen on brain tissues is structurally related to the molecule expressed on small-cell lung cancer.
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PMID:Isolation of small cell lung cancer-associated antigen from human brain. 243 35

Tumor cell nucleoli obtained from pleural effusions of 26 patients with different morphologic types of lung cancer were evaluated by silver staining. Distinct heterogeneity of tumor cell populations, with regard to the number of nucleoli as well as their functional activity in respect to ribosomal RNA synthesis, were shown to be the most common feature of all the tumors studied, regardless of their morphologic variants. One likely cause of heterogeneity in Ag nucleolar organized region (NOR) pattern of tumor cells may be due to chromosomal losses and gains from the karyotypes of acrocentric chromosomes with active NORs. Another possible cause for heterogeneity in nucleolar activity might be due to different reactions of tumor cells towards some humoral and cellular factors of pleural fluid including T-lymphocytes.
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PMID:[Characteristics of the silver-stained nucleoli of tumor cells from the pleural fluid of lung cancer patients]. 243 30

The mortality experience of 1392 lead-zinc-silver miners (Gorno, Northern Italy) employed in the period 1/1/1950-31/12/1980 and followed-up to 31/12/1986 was examined. Two separate estimates of the radon exposure level are available: 0.60 and 0.36 working levels respectively. The silica exposure level was not assessed. Vital status was ascertained for 95.6% of the cohort members and their mortality was compared with expected deaths based on national rates. Significant excess mortality from esophageal cancer, stomach cancer, lung cancer, respiratory tuberculosis, respiratory diseases and deaths from external causes was found among underground miners. Surface workers show significantly increased mortality from liver and bile ducts cancer, hepatic cirrhosis, respiratory tuberculosis and respiratory diseases. Based on the 16.4 excess lung cancer cases among underground miners and their cumulative radon exposure, an attributable risk estimate ranging from 9.78 and 16.31 cases per million person-years and WLM (Working Level Month) was calculated.
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PMID:[Mortality among lead-zinc miners in Val Seriana]. 263 Aug 93

After treating human lung adenocarcinoma cells by Na2SeO3 (1 microgram/ml) for 24 hours, its mitotic index decreased by 50%. The reduction rate was directly proportional to selenite concentration (1-5 micrograms/ml). In the meantime, the labelling index, growth rate and progression of the cell cycle were also inhibited. In contrast to the above observation, there was no marked change in the cell count, mitotic index, labelling index and the average silver granule number in the human embryonic lung diploid cells treated by Na2SeO3 (1-5 micrograms/ml) for 1-3 days. When human embryonic lung diploid cells were mix-cultured with human lung adenocarcinoma cells in the presence of 5 micrograms/ml Na2SeO3 for 24 hours, the former maintained a normal morphology, while the lung cancer cells showed heavily vacuolated cytoplasms and distorted nuclei.
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PMID:[Different effects of selenium on proliferation of human lung adenocarcinoma cells and human embryonic lung diploid cells in vitro]. 345 35

Until now, measurement of human antitumor immunity to organ-specific cancer neoantigen (OSN) by the leukocyte adherence inhibition (LAI) assay depended on using crude extracts of cancer. In this study, a new method is presented to generate and to isolate a highly enriched OSN from spent medium of a lung cancer cell line, NCI-H69, grown in chemically defined medium. Production of large quantities of OSN with minimal contamination by extraneous proteins was possible. Four physicochemical steps were used to give a 1000-fold enrichment of OSN activity: anion-exchange and molecular-sieve chromatography; Blue Sepharose affinity chromatography; and finally anion-exchange high-pressure liquid chromatography. The enriched OSN isolates showed dose-response antigenicity when tested in LAI assay with leukocytes from lung cancer patients but had no antigenicity with leukocytes from control subjects or patients having malignant melanoma, colon cancer, or pancreatic cancer. Cross-reactive antigenicity was observed with leukocytes from patients with breast cancer and slight reactivity with leukocytes from bladder cancer patients. The final isolate from the four-step separation procedure as well as the isolates produced using additional separation techniques consistently had antigenicity at less than 10 ng in blocking LAI and 500 ng in the direct assay and showed components with molecular weights of about 62,000 +/- 3,000 (SD) (p62), 40,000 +/- 3,000 (p40), and 25,000 +/- 1,000 (p25) by sodium dodecyl sulfate-polyacrylamide gel electrophoresis. The OSN isolates on two-dimensional gels showed p40 to have microheterogeneity (seven spots), with a pl from 6.2 to 7.6, and p62 and p25 as even more basic streaks. The polypeptide bearing the antigenic determinant was not purified, although we tried to separate p62, p40, and p25 to determine whether they carried the OSN determinant. The results of this study are important in showing that an isolate of an organ-specific tumor antigen containing 5 to 13 components, as determined by highly sensitive silver stains and radiolabeled patterns on single and two-dimensional gels, can be used successfully in LAI to measure tumor immune responses.
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PMID:An isolated enriched organ-specific cancer neoantigen of human lung cancer for leukocyte adherence inhibition assays. 388 36

Cell proliferation in 211 primary non-small cell lung carcinomas was assessed by using an immunostaining of proliferating cell nuclear antigen (PCNA) and a silver staining of argyrophilic nucleolar organizer region (Ag-NOR). More than 5% PCNA positive cells was designated PCNA(+), and less than 5% was PCNA(-). A mean number or more of the Ag-NOR was a high Ag-NOR count, and less than the mean number was a low Ag-NOR count. The proportion of the tumors with PCNA(+) and high Ag-NOR counts showed an increase in patients in an advanced stage of the disease (P < 0.05). In 125 patients with stage I disease, the 5-year survival rate was 20% in patients with PCNA(+) and high Ag-NOR counts, compared with 47% in those with either PCNA(+) or high Ag-NOR counts and 76% in those with PCNA(-) and low Ag-NOR counts (P < 0.05). Our data suggest that the tumors with PCNA(+) and high Ag-NOR counts have a high proliferative activity. The combination analysis of PCNA and Ag-NOR may be useful in assessing prognosis in lung cancer, even in stage I disease.
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PMID:Proliferating cell nuclear antigen expression and argyrophilic nucleolar organizer regions as factors influencing prognosis of surgically treated lung cancer patients. 810 90

Macrophages have been suggested to play a major role in the immune response to cancer. They have also been suggested to stimulate the formation of tumor stroma and to promote tumor vascularization. The availability of the op/op mouse, which has no endogenous colony-stimulating factor 1 (CSF-1) and which possesses a profound macrophage deficiency, provides a new model to verify these notions. Subcutaneous growth of transplantable Lewis lung cancer (LLC) is markedly impaired in the op/op mice compared with normal littermates. Treatment of tumor-bearing op/op mice with human recombinant CSF-1 corrects this impairment. Histological analysis of tumors grown in op/op and normal mice revealed marked differences. Tumors grown in op/op mice display a decreased mitotic index and pronounced necrosis, particularly hemorrhagic. Moreover, particularly in the op/op tumors, peculiar sinusoid-like abortive vessels (not filled with blood) have been observed. These tumors, in contrast to tumors grown in normal mice, are almost deprived of regular arteries and veins. In contrast to tumors grown in normal mice, they exhibit almost no Sirius red-stained collagenous fibers and Gomori silver-stained reticular fibers. Our data suggest that the CSF-1-dependent macrophage subpopulation missing in op/op mice plays a primary role in supporting tumor stroma formation and tumor vascularization in murine LLC tumors.
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PMID:Impaired tumor growth in colony-stimulating factor 1 (CSF-1)-deficient, macrophage-deficient op/op mouse: evidence for a role of CSF-1-dependent macrophages in formation of tumor stroma. 854 87

The prognostic value of the number of nucleolar organizer regions (NORs) (DNA loops in the nucleus) in tumor cells from various kinds of malignancies has been widely studied in recent years. During the period 1989 to 1992, a total of 73 primary lung tumors was examined for the number of NORs by silver staining AgNOR proteins on the stump smear of resected specimens in this hospital. The relations of the mean number of AgNOR per cell with other factors such as sex, age, habit of smoking, performance status, tumor location, tumor size, pathological stage, histological type, degree of differentiation, and whether histologically vascular or lymphatic invasion were analysed. It was found that the mean number of AgNOR was significantly different between positives and negatives of histologically vascular or lymphatic invasion (6.4 +/- 0.4 vs 5.5 +/- 0.2) (p < 0.05). Both single and multiple-variate analysis of patient survival revealed that the mean number of AgNOR was a significant prognostic factor, as were pathological stage, histological type, and performance status of the patient. Patients with a higher mean number of AgNOR (> 7) had a significantly worse prognosis compared with those with less AgNOR (< or = 7) (median survival 28 versus 43 months) (p < 0.05). It was concluded that the mean number of AgNOR of tumor cells is a significant prognostic factor in surgically treated lung cancer patients.
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PMID:Nucleolar organizer regions as a prognostic factor in surgically treated lung cancer patients. 889 64


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