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Query: UMLS:C0242379 (lung cancer)
 71,905 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We have found growth-promoting activity for vascular endothelial cells in the conditioned medium of a human lung cancer cell line, T3M-11. Purification and characterization of the growth-promoting activity have been carried out using ammonium sulfate precipitation and gel-exclusion chromatography. The activity migrated as a single peak just after ribonuclease. It did not bind to a heparin affinity column. These results suggest that the activity is not a heparin-binding growth factor (including fibroblast growth factors) or a vascular endothelial growth factor. To identify the molecule exhibiting the growth-promoting activity, a cDNA encoding the growth factor was isolated through functional expression cloning in COS-1 cells from a cDNA library prepared from T3M-11 cells. The nucleotide sequence encoded by the cDNA proved to be identical with that of insulin-like growth factor II.
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PMID:Isolation of a cDNA for a growth factor of vascular endothelial cells from human lung cancer cells: its identity with insulin-like growth factor II. 773 Jan 45

This paper reviews recent advances in the methods for assessing the quality of life of patients with lung cancer and recent applications of quality-of-life measures in lung cancer clinical trials. In terms of methodology, there exist today a number of self-report quality-of-life questionnaires that are valid, reliable, and sufficiently brief to be of practical use in clinical research settings. Application of these measures in lung cancer clinical trials has contributed to the evaluation of: 1) long-versus short-duration chemotherapy, four- versus two-drug combinations, intensive versus standard chemotherapy, and continuous versus bolus injection chemotherapy in the treatment of small cell lung cancer; 2) high versus low radiation doses in the treatment of non-small cell lung cancer; 3) megestrol acetate and hydrazine sulfate as supportive treatment for small cell lung cancer and non-small cell lung cancer patients receiving chemotherapy; 4) granulocyte colony-stimulating factor in small cell lung cancer patients receiving dose-intensified chemotherapy; and 5) the rehabilitation needs of lung cancer survivors. Future efforts should be directed toward achieving higher levels of compliance with clinical trial-based quality-of-life studies, and the development of techniques for integrating quality of life and clinical outcomes for purposes of cost-effectiveness evaluations.
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PMID:Quality-of-life and cost-effectiveness assessment in lung cancer. 775 77

Time-series, cross-sectional, and prospective cohort studies have observed associations between mortality and particulate air pollution but have been limited by ecologic design or small number of subjects or study areas. The present study evaluates effects of particulate air pollution on mortality using data from a large cohort drawn from many study areas. We linked ambient air pollution data from 151 U.S. metropolitan areas in 1980 with individual risk factor on 552,138 adults who resided in these areas when enrolled in a prospective study in 1982. Deaths were ascertained through December, 1989. Exposure to sulfate and fine particulate air pollution, which is primarily from fossil fuel combustion, was estimated from national data bases. The relationships of air pollution to all-cause, lung cancer, and cardiopulmonary mortality was examined using multivariate analysis which controlled for smoking, education, and other risk factors. Although small compared with cigarette smoking, an association between mortality and particulate air pollution was observed. Adjusted relative risk ratios (and 95% confidence intervals) of all-cause mortality for the most polluted areas compared with the least polluted equaled 1.15 (1.09 to 1.22) and 1.17 (1.09 to 1.26) when using sulfate and fine particulate measures respectively. Particulate air pollution was associated with cardiopulmonary and lung cancer mortality but not with mortality due to other causes. Increased mortality is associated with sulfate and fine particulate air pollution at levels commonly found in U.S. cities. The increase in risk is not attributable to tobacco smoking, although other unmeasured correlates of pollution cannot be excluded with certainty.
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PMID:Particulate air pollution as a predictor of mortality in a prospective study of U.S. adults. 788 54

In this study, we report on two patients diagnosed with active pulmonary tuberculosis who later developed complications of lung cancer. In both instances, lung cancer was not detected until after cessation of tuberculostatic drugs. Both patients were initially considered to be experiencing exacerbation of pulmonary tuberculosis. Patient 1 was a 77-year-old female. A roentgenogram of her chest revealed a cavitary lesion with infiltration into the right lung field. Her sputum tested positive for acid-fast bacilli. Although she was treated with isoniazid (INH), rifampicin (RFP) and streptomycin sulfate (SM), the RFP and INH treatments had to be discontinued due to liver dysfunction. Her general condition was deteriorated, and pleural effusion appeared on a subsequent chest roentgenogram. Primary squamous-cell lung cancer was confirmed by conducting a transbronchial biopsy. Patient 2 was a 59-year-old male. A roentgenogram of his chest revealed multiple cavitary lesions with infiltration into the bilateral lung field. His sputum also tested positive for acid-fast bacilli. Although he was treated with INH, RFP and SM, INH and RFP treatment had to be discontinued due to liver dysfunction and high fever. The shadow infiltrating the left lung field subsided, but a massive shadow appeared in the right lung field. Primary small-cell lung cancer was confirmed after conducting a sputum cytology. The patients was then administered cisplatin and etoposide. Patient 1 was diagnosed with lung cancer five months after being admitted to the hospital, and Patient 2 ten months after admission. Both patients succumbed due to lung cancer at seven and 26 months, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Study of two cases of active pulmonary tuberculosis complicated by lung cancer]. 818 86

This paper reviews the available literature regarding the work environment in pulp and paper mills and the risk for malignant diseases. An increased risk for lung cancer among pulp and paper mill workers has been reported. Most studies are inconclusive with regard to considerations of etiologic agents. However, maintenance workers seem to be at an increased risk for lung cancer, as well as for malignant mesothelioma, indicating that this occupational group was (is) exposed to asbestos. Workers exposed to chlorine compounds also seem to run an increased risk for lung cancer. An increased risk for malignant lymphomas among pulp mill workers is a constant finding. The increased risk is observed both among sulfite and sulfate workers, indicating a common exposure. Such an exposure could be wood dust, terpenes, or preservatives present in the wood. An increased risk for leukemias has been found in many studies carried out on pulp and paper workers, but the studies do not permit any conclusions about etiologic factors. In some studies an increased risk for stomach cancer has been found. However, the socioeconomic status of the workers is strongly related to stomach cancer, and factors, such as dietary habits, have not been taken into account in any of the reviewed studies. Hence, no further conclusions can be drawn regarding etiologic agents.
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PMID:Health effects of working in pulp and paper mills: malignant diseases. 890 14

Successful lung cancer management has been hindered by the limited efficacy of dietary and pharmacologic interventions to prevent or reverse cancer-associated weight loss. The addition of total parenteral nutrition to chemotherapy in early trials was associated with survival detriment. Dietary counseling and enteral supplement use are common strategies that, when evaluated in randomized trials, do not improve anthropometrics or clinical outcome in lung cancer. Pharmacologic agents including corticosteroids, cyproheptadine, growth hormone, hydrazine sulfate, dronabinol, and pentoxyphylline also have failed to improve even anthropometric parameters in this condition. Megestrol acetate use is associated with appetite stimulation and non-fluid weight gain but, when evaluated in small cell lung cancer patients receiving defined chemotherapy, failed to improve global quality of life, and survival and was associated with toxicity. New strategies for nutrition-based interventions in lung cancer cachexia must consider their potential influence on tumor growth as well as on nutritional status. Recent lung cancer prognostic analyses have identified gender differences in outcome and weight loss that suggest potential targets for combined hormonal and nutrition interventions. Emerging information regarding the influence of specific fatty acids on tumor growth and cachexia development have identified additional approaches for future evaluation.
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PMID:Recent implications of weight loss in lung cancer management. 885 Feb 20

In order to improve the diagnosis of lung carcinoma, in which a complicated histologic pattern is present, the immunohistochemistry of 119 adenocarcinomas, 65 squamous cell carcinomas, 12 small cell carcinomas, 18 large cell carcinomas, and 15 metastatic adenocarcinoma in the lung were evaluated using a monoclonal antibody, KM195, against lung carcinoma, and compared with the immunohistochemical results using anti-human cytokeratin (CAM 5.2) and other monoclonal antibodies. Formalin-fixed, paraffin-embedded tissues were stained using the labeled streptavidin-biotin method. Extracts from fresh tissue homogenate, after fractionation by sodium dodecyl sulfate-polyacrylamide gel electrophoresis, were transferred by Western blotting and stained with KM195. The anti-lung adenocarcinoma, murine, monoclonal antibody KM195 (IgG), was positive in 107 of 119 adenocarcinomas (90%), in 15 of 18 large cell carcinoma (83%), in three of 65 squamous cell carcinomas (5%), 13 of 15 (87%) metastatic adenocarcinoma in the lung, and was negative in 12 small cell carcinomas (P < 0.001). KM195-bound protein of primary and metastatic adenocarcinoma in the lung cases concentrated at about 40 kDa. In contrast, CAM 5.2 was positive in 52 of 67 (78%) adenocarcinomas, 10 of 62 (16%) squamous cell carcinomas, and was negative in six small cell carcinomas. These results suggest that the immunohistochemistry for KM195 may be a more useful marker over CAM 5.2 for the diagnosis of pulmonary adenocarcinoma.
Lung Cancer 1996 Aug
PMID:KM195 as an immunohistochemical marker of adenocarcinoma of the lung. 886 22

The early epidemiological data indicated different carcinogenic risks from inhalation of different nickel compounds, but it was not clear what characteristics governed the intrinsic carcinogenic hazard of the various nickel compounds. Based on the earlier results, all soluble and insoluble nickel compounds were assumed to have the same carcinogenic mechanism albeit different potencies. Recent in vivo and in vitro studies challenged this assumption. In this paper an attempt is made to integrate the most relevant human, animal, and in vitro data into a general model that can help understand the different carcinogenic potentials of the various nickel compounds. In this perspective, it is recognized that there are two main components that could contribute to the development of lung cancer via exposure to certain nickel compounds. The first component corresponds to the heritable changes (genetic or epigenetic) derived from the direct or indirect actions of nickel compounds. The second component may be the promotion of cell proliferation elicited by certain nickel compounds. The different contributions of three nickel compounds to these two components are presented. This paper emphasizes the importance of recognizing the individuality of the different nickel species in reaching regulatory decisions and the fact that different risk assessment considerations may apply for compounds that appear to produce immortality and cancer by genetic/epigenetic mechanisms (like nickel subsulfide), compounds that may present a threshold for the induction of tumors in rats (like high-temperature nickel oxide), or compounds that may only have an enhancing effect on carcinogenicity (like nickel sulfate).
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PMID:Carcinogenicity assessment of selected nickel compounds. 907 3

We have previously reported on the secretion of a family of high Mr plasminogen activators (PAs) by a human lung cancer cell line [Harvey et al. (1991) Biochim. Biophys. Acta 1078, 360-368]. We have now extended these studies to several human cancer cell lines and a human embryonic lung cell line. In the present study with HPL-SK-1 lung cancer, A431 epidermoid cancer, ovarian carcinoma, and embryonic lung cell lines, we show that the 900- and the 660-kDa PAs are disulfide-bonded multiprotein oligomeric complexes. They are functionally and immunologically related to human urinary PA (uPA). Their size and PA activity are not destroyed by strong denaturants such as 8 M urea or 2% sodium dodecyl sulfate (SDS), suggesting that the uPA moiety is covalently associated with the rest of the molecule. It is only under strong denaturing conditions with 1.4 M beta-mercaptoethanol and 2% SDS that the uPA moiety could be released as a 21- to 23-kDa fragment along with two major polypeptide chains of 70 and 40 kDa, respectively. The presence of the uPA active center in the reduced PA660 was demonstrated by [3H]diisopropylphosphorofluoridate labeling and by Western blot using a monoclonal antibody to uPA B chain. N-terminal amino acid sequencing of the 70- and 40-kDa polypeptides, respectively, showed homology to the neural cell adhesion molecule and the beta chain of haptoglobin. A minor fragment of 18 kDa obtained under strong reduction conditions was also sequenced and shown to share homology with the alpha chain of haptoglobin. Western blot analysis of the reduced PAs with monoclonal antibody to the neural cell adhesion molecule and rabbit anti-haptoglobin confirmed the homologies obtained by the sequence data. Further, immobilized monoclonal antibodies to the neural cell adhesion molecule, uPA B chain, and rabbit anti-haptoglobin bound the multiprotein complexes with uPA activity, from A431, ovarian cancer, and embryonic lung cell lines. The bound material, after dissociation, exhibited PA activity that was inhibited by monoclonal antibody to the uPA B chain. These data suggest that in tumor and embryonal cell lines, in addition to proper folding and assembly of proteins by intramolecular disulfide bond formation in the endomembrane compartment, intermolecular disulfide bonds could also occur, producing multiprotein oligomers as in the present case. Formation of such oligomers may have a selective advantage for such cells in the focalization of proteolytic activity through the interaction of the neural cell adhesion molecule domain with the extracellular matrix and in immunosuppression of lymphocytes by the haptoglobin portion of the complex.
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PMID:Cancer cells release a covalent complex containing disulfide-linked domains from urinary plasminogen activator, neural cell adhesion molecule, and haptoglobin alpha and beta chains. 930 1

Rats and other rodents are exposed by inhalation to identify agents that might present hazards for lung cancer in humans exposed by inhalation. In some cases, the results are used in attempts to develop quantitative estimates of human lung cancer risk. This report reviews evidence for the usefulness of the rat for evaluation of lung cancer hazards from inhaled particles. With the exception of nickel sulfate, particulate agents thought to be human lung carcinogens cause lung tumors in rats exposed by inhalation. The rat is more sensitive to carcinogenesis from nonfibrous particles than mice or Syrian hamsters, which have both produced false negatives. However, rats differ from mice and nonhuman primates in both the pattern of particle retention in the lung and alveolar epithelial hyperplastic responses to chronic particle exposure. Present evidence warrants caution in extrapolation from the lung tumor response of rats to inhaled particles to human lung cancer hazard, and there is considerable uncertainty in estimating unit risks for humans from rat data. It seems appropriate to continue using rats in inhalation carcinogenesis assays of inhaled particles, but the upper limit of exposure concentrations must be set carefully to avoid false-positive results. A positive finding in both rats and mice would give greater confidence that an agent presents a carcinogenic hazard to man, and both rats and mice should be used if the agent is a gas or vapor. There is little justification for including Syrian hamsters in assays of the intrapulmonary carcinogenicity of inhaled agents.
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PMID:Relevance of particle-induced rat lung tumors for assessing lung carcinogenic hazard and human lung cancer risk. 940 Jul 48


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