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

Mortality data from cancers of the lung and bladder in England and Wales were analyzed. With the use of detailed information on cigarette consumption, a nonlinear least-squares analysis showed that the differences between males and females in the rates of these cancers could be explained on the basis of differences in smoking habits. Furthermore, estimates of the relative risk due to smoking were obtained. The relative risks of smoking 146,000 cigarettes (equivalent to 20 cigarettes/day for 20 yr) were 4.3 for lung cancer and 2.9 for bladder cancer. These estimates agree with those obtained by other types of epidemiologic studies.
J Natl Cancer Inst 1979 Dec
PMID:Estimation of relative risk from vital data: smoking and cancers of the lung and bladder. 29 7

Phytohemagglutinin (PHA) stimulated lymphocyte protein synthesis was measured in vitro in 21 patients with recently diagnosed, untreated bronchogenic carcinoma and 11 control subjects. In the cancer group absolute protein synthesis was significantly decreased in both baseline and stimulated cultures. The abnormality in protein synthesis was observed despite the fact that there were no differences in vitro DNA synthesis between the two groups. In order to investigate the possibility that a decrease in the number of T-cells was the cause of the impaired protein synthesis in the lung cancer patients, the percentage of circulating E-rosetting forming cells was measured. The mean percentage of rosette forming cells in the cancer patients was 66.8 +/- 2.2 and in the control population was 68.3 +/- 2.6. Our results demonstrate that lymphocyte protein synthesis is abnormal in patients with bronchogenic carcinoma and that the abnormality in protein synthesis is not due to decreased numbers of T-cells. In addition our results suggest that measurement of protein synthesis is a more sensitive assay of lymphocyte function than other standard parameters of cellular immunity.
Cancer 1977 Dec
PMID:Abnormal lymphocyte protein synthesis in bronchogenic carcinoma. 30 35

Cell-to-cell interaction was investigated in various malignant tumor cells (human ovarial tumor, lung cancer, carcinoma of larynx and hamster melanoma cell) and in human lymphoblastoid cells (T-cell (MOLT-4 cell), thymoma cells and B-cells (Burkitt lymphoma cell)). Live lymphoblastoid cells did not adhere to the cell surfaces of tumor cells nor the lymphoblastoid cells were ingested by tumor cells without immunologic and specific treatment. Tumor cells as well as T-cells and B-cells had receptors to concanavalin A on their surfaces, and they showed marked cell binding of tumor cells and lymphoblastoid cells. Moreover, tumor cells that phagocytized lymphoblasts underwent marked cell destruction within 4 hours of cell binding. The cytolytic mechanism of the target tumor cell was probably related to contact with the lymphoblastoid cells and was increased by ingestive activity, and metabolic disturbance by lymphotoxin in tumor cells.
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PMID:Tumor cell phagocytosis and cytotoxicity of lymphoblastoid cells following concanavalin A treatment. 30 16

This paper briefly reviews some mechanisms of tumor immunity and the principles of cancer immunotherapy. Cellular and humoral immunity can both influence tumor cells. Most of the cells belonging to the immune system can act on neoplastic cells. T cells can kill them, macrophages inhibit their growth, and K cells through their Fc receptor also destroy antibody-coated tumor cells. Cancer patients have usually depressed cellular immune functions. The goal of immunotherapy is to amplify the immune reactions in order to destroy the tumor cells. The modalities of immunotherapy are described. They may become important as adjuvant therapy. Immunotherapy has already been successfully in skin cancers, lung cancer and acute myeloblastic leukemia.
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PMID:Cancer immunotherapy. 30 38

Cohorts of 1974 gold miners and 213 coal miners in Western Australia surveyed for respiratory symptoms, smoking habits, occupational history and radiographic evidence of pneumoconiosis have been followed up for 13-14 years. Overall, neither group had a significantly higher mortality than expected from the experience of Western Australian men in general. Lung cancer mortality was relatively high in the gold miners (59 deaths observed, 40.8 expected) but weakly and inconclusively related to the extent of their underground mining experience. Cigarette smoking may explain the excess of lung cancer in the gold miners because the prevalence of the habit in the latter (66.3%) was higher than in the coal miners (58.7%) or in other men in Western Australia (53.2%). Radiographic evidence of silicosis was present in 21.7% of the gold miners but did not appear to have contributed substantially to their mortality. The coal miners showed a lower than expected rate of lung cancer but an excess of deaths from all other forms of cancer (11 observed, 5.6 expected). This excess was not attributable to any one cancer site and cannot be explained readily.
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PMID:Mortality in gold and coal miners in Western Australia with special reference to lung cancer. 31 11

The Authors have tested serum levels of alpha-1-antitrypsin (A1AT), phosphohexose-isomerase (GPI) and carcinoembryonic antigen (CEA) in 133 patients affected with primary lung cancer, not treated with any drug, and in 183 patients affected with not neoplastic lung diseases or healthy, to control the utility of these markers in the early diagnosis of lung cancer. In many patients all the tests have been made at the same time. The three tumoral markers have been also examined in connection with the histological kinds of lung cancer. Results show that is suitable to test GIP and A1AT at the same time because they are percentually more pathological; serum levels of CEA, that are not very elevated in the pathological cases, seem in correlation with the histological kind of cancer.
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PMID:[Serum levels of GPI, AAT and CEA in primary lung neoplasms and chronic bronchopneumopathies]. 31 40

A review is presented of the various factors important in the identification of carcinogenic disease from occupational and environmental exposure to asbestos and vinyl chloride. The long lapsed period, usually of 20 or more years from first exposure to these materials, is discussed, as well as the requirement for sufficiently long observation periods in prospective epidemiological studies. The multiple-factor etiology of lung cancer involving cigarette smoking and asbestos exposure is illustrated. The risks of asbestos-related cancers to other than those directly working with the material are discussed in a variety of circumstances, and finally the effectiveness of control procedures for vinyl chloride and asbestos are compared.
Cancer 1977 Apr
PMID:Cancer following occupational exposure to asbestos and vinyl chloride. 32 44

There is much experimental data which indicates that ionizing radiation is a very potent carcinogenic agent. Most types of carcinoma can be produced by radiation. Carcinoma is apparently induced through a single or a series of mutations in somatic cells. Radiologists have excess leukemia and other malignancy from external x-ray; uranium and other miners have excess lung cancer from internal alpha radiation; luminous dial painters have excess osteogenic sarcomas; and uranium mill workers appear to have excess lymphomas. A large number of persons are now exposed occupationally to radiation from nuclear reactors, and from various uses of radioisotopes. For the induction of most types of cancers from radiation it appears that the risk is between 0.5 and 2 cancers per rem per million person years. Epidemiological techniques are essential in determining risks of this low magnitude. Other agents may inhibit or enhance the carcinogenicity of radiation.
Cancer 1977 Apr
PMID:Occupational exposure to radiation as a cancer hazard. 32 45

Sera from 134 selected patients with various types of cancer were tested for soluble antigen-antibody complexes by the C1q binding method. Sera from 85 healthy blood bank donors served as normal controls. C1q binding activity (C1q BA) values above the 95th percentile for healthy subjects were found in 83% of sera from patients with neoplastic diseases. The incidence of abnormal C1q BA values among patients with malignant melanoma was 83%, with breast cancer 74%, with colon cancer 75%, with lung cancer 88%, with leukemia and lymphoma 85%, and with miscellaneous tumors 94%. High C1q BA values were found most frequently in sera of patients who had been diagnosed relatively recently (within 5 mo) and who had evident residual disease after surgical treatment. Recurrence or progression of tumor growth occurred significantly more frequently in lung cancer patients with high C1q BA. DNA was not detected in cancer patients' sera and treatment with DNase did not decrease in C1q BA. C1q BA in sera could not be explained by the presence of antiglobulin antibodies. Sucrose density gradient ultracentrifugation studies of the serum C1q BA in 4 cancer patients showed that the major binding activity was found between 19S and 7S.
J Natl Cancer Inst 1977 May
PMID:The C1q binding test for soluble immune complexes: clinical correlations obtained in patients with cancer. 32 5

Several data justify the suspension that air pollution may contribute to cancer risk. These observations are: high risk of lung cancer in coal gas workers; higher incidence of lung cancer in urbanized regions as compared with rural ones and higher incidence in highly industrialized countries as compared with less industrialized; observations in migrant populations; data of comparative pathology. Specific studies of the association between lung cancer and air pollution taking into consideration confounding variables failed to give conclusive evidence of a causal relationship. Obviously the role of air pollution for cancerogenesis in the lung is far less important than inhalation of tobacco smoke. Furthermore there are some findings suggesting a causal association of particulate air pollution and malignant neoplasms of the stomach and prostate.
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PMID:[Air pollution and cancer (author's transl)]. 33 5


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