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)

Two types of assay systems to measure the effect of radiation on immune competence are described. The first, transformation, is measured by blast formation or uptake and incorporation of tritiated thymidine by lumphocytes. This measure is affected by a number of known cell responses to radiation such as division delay and delay in DNA synthesis. The second, called Bactec, is designed to measure lymphocyte metabolic acitivty. Data gathered on 37 patients with lung cancer show that the Bactec system provides a better index of the patient's immune status before and after radiation therapy.
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PMID:Transformation delay of lymphocytes in patients undergoing radiation therapy. 18 17

Most humans in the United States have been infected with BK virus (BKV), a human papovavirus. Because BKV has oncogenic properties, we have investigated whether it may be a cause of human cancer. Basic principles of tumor virology imply that BKV-induced tumors should contain BKV DNA sequences. Therefore, we assayed (by molecular hybridization) DNA from human tumors and malignant cell lines for BKV DNA, using BKV [(32)P]DNA as probe. The BKV [(32)P]DNA was labeled in vitro (nick translation) to specific activities of 1 to 2 x 10(8) cpm/mug. The BKV DNA used to prepare our probes had the properties expected of authentic BKV genomes, including density of superhelical DNA, sedimentation velocity in alkaline and neutral sucrose gradients, production of one fragment by endonuclease EcoRI cleavage and four fragments by endonuclease Hin II + III cleavage and reassociation properties. From these studies we conclude that our BKV probes hybridized well, and represented bona fide BKV DNA. Using three different BKV [(32)P]DNA probes, i.e., from three distinct plaque isolates, we have analyzed DNA from BKV-transformed cells, normal human tissues, and a large number of human tumors. All human DNAs (cell lines, normal tissues, tumors) hybridized 5% with BKV DNA. Hybridization analysis of BKV-transformed hamster cell DNA indicated 5-6 copies of at least 88% of the BKV genome per cell. No BKV DNA sequences were detected (above the normal 5% hybridization to all human DNAs) in the following normal human tissues: 10 kidney (BKV is usually isolated from urine), 3 spleen, 13 lung, 23 colon, 2 rectum, 1 ileum, and 1 skin. No BKV-specific DNA was found in 166 tumors, including 5 carcinomas (Ca) of stomach, 3 Ca small intestine, 26 Ca colon, 9 Ca rectum, 31 Ca lung, 9 adenocarcinomas and 5 oat cell carcinomas of lung, 17 melanomas, 5 Ca prostate, 4 Ca bladder, 6 Wilms tumors, 4 hypernephromas, 15 Ca kidney, 7 brain tumors, 5 Hodgkin lymphomas, 10 lymphomas (immunosuppressed patients have a high incidence of lymphomas), 2 reticulum cell sarcomas (spleen), and 3 skin tumors. We have also analyzed 7 human malignant cell lines (melanoma, lung, rhabdomyosarcoma, and glioblastomas), including several clones of a lung melanoma line; no BKV DNA sequences were detected. Because our probes could detect one copy of BKV DNA if only 10% of the cells were tumor cells, our results are very strong evidence that the tumors we analyzed did not have a BKV etiology. The tumors we tested represent about 50% of all cancers in the United States; there is no evidence that BKV is involved in the etiology of these types of tumors.
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PMID:Analysis of human tumors and human malignant cell lines for BK virus-specific DNA sequences. 20 40

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.
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PMID:Abnormal lymphocyte protein synthesis in bronchogenic carcinoma. 30 35

The quantity of antibodies to double-stranded DNA (ds-DNA) in 53 pleural effusions from 48 patients was measured by means of a modified Farr technique. In 10 samples, binding of ds-DNA was greater than 5 mg/l (range 6--14 mg/l), five samples being from patients with systemic lupus erythematosus (SLE), four from patients with lung cancer, and one from a patient with pulmonary tuberculosis. After treatment of pleural effusion samples with DNase, there was a marked increase of ds-DNA binding in the SLE group (n = 5), but none in the lung cancer group (n = 7) or in 4 patients with pleural effusions of various origin. In pleural fluid, demonstration of antibodies to ds-DNA and anti-ds-DNA-ds-DNA complexes, unmasked by DNase, may prove valuable when differentiating clinical conditions with pleural effusions.
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PMID:Systemic lupus erythematosus and DNA antibodies in pleural effusions. 31 Jan 56

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.
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PMID:The C1q binding test for soluble immune complexes: clinical correlations obtained in patients with cancer. 32 5

Cultured human diploid skin fibroblasts incubated with [G-3H]benzo(a)pyrene yielded about 10 times more H2O-=soluble benzo(a)pyrene metabolites and DNA adducts of stationary growth phase than did proliferating cultures. This increased formation could be blocked by alpha-naphthoflavone. Trichloropropenoxide and cyclohexenoxide, inhibitors of the epoxide hydratase, inhibited predominantly the formation of DNA adducts. Cultures from older individuals formed significantly more benzo(a)pyrene metabolites and DNA adducts, but control cultures from patients with either lung cancer or melanoma did not. The age influence was not apparent when the ratio of DNA adducts to H2O-soluble metabolites was determined for each individual cell line. However, the proportion of DNA-bound material in the cells from patients with lung cancer was significantly increased compared to cells from melanoma patients or healthy individuals.
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PMID:Metabolism and formation of DNA adducts of benzo(a)pyrene in human diploid fibroblasts. 42 49

A very large variation (44-fold) was observed in the ability of short-term organ cultures of peripheral lung tissue from lung-cancer patients to metabolize the environmental carcinogen benzo(alpha)pyrene to organic solvent-soluble metabolites. The amounts of benzo(alpha)pyrene (2 microM) metabolized ranged from little (1%) to almost total (96.2%) metabolism within 24 h of culture. Previous work by Kellerman et al. (1973) has suggested a relationship between susceptibility to lung cancer and the indicibility of aryl hydrocarbon hydroxylase activity in cultured human lymphocytes. The metabolic fate of carcinogenic polycyclic aromatic hydrocarbons in the respiratory tract in vivo is undoubtedly more closely mimicked by short-term organ culture of human lung than by cultured lymphocytes. Thus the very wide interindividual variation observed in pulmonary metabolism of benzo(alpha)pyrene in this study and the large variations in covalent binding to human bronchial DNA observed by Harris et al. (1976) strongly suggest that there may be little basis for screening humans for variations in lymphocyte aryl hydrocarbon hydroxylase activity as a means of assessing their susceptibility to lung cancer.
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PMID:Large interindividual variations in metabolism of benzo(alpha)pyrene by peripheral lung tissue from lung cancer patients. 48 61

Aryl hydrocarbon hydroxylase (AHH) inducibility was studied in cultured lymphocytes from 21 healthy control subjects and from 15 lung cancer patients selected for radiation therapy. AHH inducibility of the patients was measured prior to, during and at the end of radiation therapy. Four of 15 patients had values comparable to the healthy controls. Cellular DNA and protein measurements of cultured lymphocytes were the same for patients and healthy controls. There was no significant difference in the percentage of lymphoblast formation and percentage of cell survival between the two groups. Radiation therapy reduces the number of lymphocytes in vivo and the amount of lymphoblast formation in vitro. AHH inducibulity is signifcantly lowered by radiation in the patients who had very high inducibility at pre-treatment level. DNA and protein contents of cultured lymphocytes did not change during radiation therapy.
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PMID:Aryl hydrocarbon hydroxylase inducibility in lung cancer patients undergoing radiotherapy. 52 67

A radiometric assay for the determination of AHH activity in lymphocytes is described. Subjects included eleven male patients with histologically verified lung cancer (nine squamous cell carcinoma and two adenocarcinoma) and eleven age- and sex-matched controls. Lung cancer patients exhibited considerably greater variation and elevated levels of both AHH activity per se and AHH activity adjusted for total cellular DNA than control individuals. Methodology for AHH determinations and implications for lung cancer epidemiology and control are discussed.
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PMID:Aryl-hydrocarbon hydroxylase activity in lymphocytes from lung cancer patients and normal controls. 101 43

The studies reported here demonstrate some of the factors affecting the binding of benzo(a)pyrene (BP) to macromolecules in cultured human bronchial mucosa. Bronchial specimens were obtained at either surgy or "immediate" autopsy from patients with and without lung cancer. Grossly normal-appearing pieces of bronchus were cultured in a chemically defined medium, i.e., CMRL 1066 medium containing 1 mug insulin per ml, 0.1 mug beta-retinyl acetate per ml,, 0.1 mug hydrocortisone hemisuccinate per ml, 2 mM L-glutamine, 100 units penicillin G per ml, and 100 mug streptomycin per ml. After 7 days, explant cultures were exposed to [3H]BP, usually for 24 hr, and then binding to total cellular macromolecules was studied by autoradiography, and binding to DNA was measured following isolation of DNA from bronchial mucosal cells. The extent of binding of [3H]BP was dependent on dose of BP, length of exposure to [3H]BP, and temperature. By autoradiography, bronchial epithelial cells bound more [3H]BP than stromal fibroblasts. Both 7,8-benzoflavone and butylated hydroxytoluene appeared to reduce the level of [3H]BP bound to DNA, while nicotine apparently did not alter the level of binding. These studies demonstrate that the bronchial mucosa, an important human cancer target tissue, has the capability to form metabolites of BP which bind to macromolecules including DNA. In addition, 7,8-benzoflavone and butylated hydroxytoluene, both known to alter the microsomal metabolism of BP, reduce the level of [3H]BP bound to DNA.
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PMID:Binding of (3H)benzo(a)pyrene to DNA in cultured human bronchus. 2809 25


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