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Bronchial carcinoma

ACTH-secreting non-pituitary tumors (ectopic ACTH syndrome)—15% of cases of endogenous Cushing s syndrome usually from small cell lung carcinoma, bronchial carcinoids, pheochromocytoma, or thymus, pancreatic, ovarian, or thyroid tumor. The tumor is usually disseminated (difficult to localize). [Pg.693]

Neoplasm Carcinoma Bronchial adenoma Bronchial carcinoid Metastatic disease Endometriosis... [Pg.264]

Lomustine (2-chlorethyl-3 cyclohexyl-1 -nutrosourea, CCNU, Fig 3) is a nitrosourea for oral application. It is used for the treatment of Hodgkin s lymphomas, brain tumors and bronchial carcinomas at a dose of 3.5 mg/kg (130 mg/m2) repeated in 6-8 weeks intervals. [Pg.56]

Cancer treatment is a multimodality treatment, i.e., surgery is combined with radiotherapy and antineoplastic chemotherapy. The latter treatment mode is used mainly for cancers which have disseminated. Different forms of cancer differ in their sensitivity to chemotherapy with antineoplastic agents. The most responsive include lymphomas, leukemias, choriocarcinoma and testicular carcinoma, while solid tumors such as colorectal, pancreatic and squamous cell bronchial carcinomas generally show a poor response. The clinical use of antineoplastic agents is characterized by the following principles. [Pg.157]

Hellman GM et al. Gene expression profiling of cultured human bronchial epithelial and lung carcinoma cells. Toxicol Sci 2001 61 154-163. [Pg.114]

Intestinal pseudoobstruction is also part of paraneoplastic syndromes. The anti-/zu antibodies are useful to indicate this condition, as shown in bronchial small cell carcinoma [171], In pheochromocytoma [172] and carcinoid [173] neuromediators affecting small bowel motility are produced by the tumor cells. Intestinal pseudoobstruction has also been reported in neuroblastoma [174],... [Pg.14]

Thus, oxygen radical production by leukocytes can be responsible for cancer development. However, the levels of leukocyte oxygen radical generation depend on the type of cancer. For example, PMNs and monocytes from peripheral blood of patients with lung cancer produced a diminished amount of superoxide [169], Timoshenko et al. [170] observed the reduction of superoxide production in bronchial carcinoma patients after the incubation of neutrophils with concanavalin A or human lectin, while neutrophils from breast cancer patients exhibited no change in their activity. Chemotherapy of lung and colorectal carcinoma patients also reduced neutrophil superoxide production. Human ALL and AML cells produced, as a rule, the diminished amounts of superoxide in response to PMA or FMLP [171], On the other hand total SOD activity was enhanced in AML cells but diminished in ALL cells, while MnSOD in AML cells was very low. It has been proposed that decreased superoxide production may be responsible for susceptibility to infections in cancer patients. [Pg.927]

Nickel water-soluble salts were also reported to induce chromosome aberrations in CHO cells [444, 445] and in mouse mammary carcinoma cells [260, 446], Changes in growth control and chromosome aberrations in human bronchial cells were demonstrated in vitro after exposure to nickel sulphate the changes were insufficient to cause the cells to be tumourigenic [447], Nickel chloride was unable to produce chromosome aberrations in vivo in mammalian male germ cells [448],... [Pg.220]

F. Trump, and C. C. Harris. 1991. Human bronchial epithelial cells transformed by the c-raf-1 and c-myc protooncogenes induce multidifferentiated carcinomas in nude mice A model for lung carcinogenesis. Cancer Res 51 3793-3801. [Pg.637]

Exposed female mice had significant compound-related increases in nasal carcinomas (NTP 1982 Stinson et al. 1981). The incidences of combined alveolar/bronchiolar carcinoma and adenoma were significantly increased in the lungs of high-dose male and female mice as compared with control animals. In addition to these tumors, adenomatous polyps were present in tracheal, bronchial, and bronchiolar lumens (NTP 1982). [Pg.32]

Bronchogenic carcinoma (Table 3.3) is a thoracic neoplastic disease that has been associated with the inhalation of inorganic mineral fibers malignancy that arises in the bronchial epithelium. The carcinoma may be a squamous cell or adenocarcinoma, a small- or large-cell carcinoma, may or may not contain asbestos fibers, and may or may not be associated with asbestosis. [Pg.137]

Dust particles inhaled in tobacco smoke, together with bronchial mucus, must be removed from the airways by the ciliated epithelium. Ciliary activity, however, is depressed by tobacco smoke mucociliary transport is impaired. This depression favors bacterial infection and contributes to the chronic bronchitis associated with regular smoking. Chronic injury to the bronchial mucosa could be an important causative factor in increasing the risk in smokers of death from bronchial carcinoma. [Pg.112]

Statistical surveys provide an impressive correlation between the number of cigarettes smoked a day and the risk of death from coronary disease or lung cancer. Statistics also show that, on cessation of smoking, the increased risk of death from coronary infarction or other cardiovascular disease declines over 5-10 years almost to the level of non-smokers. Similarly, the risk of developing bronchial carcinoma is reduced. [Pg.112]

Fjellbirkeland L, Bjerkvig R, Laerum OD (1998) Non-smaU-cell lung carcinoma cells invade human bronchial mucosa in vitro. In Vitro Cell Dev Biol Anim 34 333-340... [Pg.252]

Kollmeier H, Seemaim JW, Muller KM, et al. 1987. Increased chromium and nickel content in lung tissue and bronchial carcinoma. Am J Ind Med 11 659-669. [Pg.240]

DoU, Richard, and Richard Peto. 1978. Cigarette Smoking and Bronchial Carcinoma Dose and Time Relationships Among Regular Smokers and Lifelong Non-smokers. Journal of Epidemiology and Community Health 22 303-13. [Pg.87]

In a survey of chemical plants (without prior hypothesis) in the German Democratic Republic, nine cancer cases were found in a factory where the main process was dimerization of acetaldehyde and where the main exposures were to acetaldol (3-hydroxybu-tanal), acetaldehyde, butyraldehyde, crotonaldehyde (IARC, 1995) and other higher, condensed aldehydes, as well as to traces of acrolein (lARC, 1985). Of the cancer cases, five were bronchial tumours and two were carcinomas of the oral cavity. All nine patients were smokers. The relative frequencies of these tumours were reported to be higher than those expected in the German Democratic Republic. [The Working Group noted the mixed exposure, the small number of cases and the poorly defined exposed population.]... [Pg.321]

As previously summarized, four cases of bronchial carcinoma were reported in men exposed occupationally to dimethyl sulfate (IARC, 1974). Additional case reports have since appeared a case of pulmonary carcinoma in a man exposed for seven years to small amounts of dimethyl sulfate but to larger amounts of bis(chloromethyl)ether and chloromethyl methyl ether (lARC, 1987b), and a case of choroidal melanoma in a man exposed for six years to dimethyl sulfate (IARC, 1987a). [Pg.576]

No epidemiological studies were available to the Working Group. A small number of cases of, mainly, bronchial carcinoma has been reported. [Pg.583]

In one epidemiological study of 138 workers exposed to vinylidene chloride in the United States, no excess of cancer was found, but follow-up was incomplete, and nearly 40% of the workers had less than 15 years latency since first exposure (lARC, 1986). In a study in the Federal Republic of Germany of 629 workers exposed to vinylidene chloride, seven deaths from cancer (five bronchial carcinomas) were reported this number was not in excess of the expected value. Two cases of bronchial carcinoma were foimd in workers, both of whom were 37 years old, whereas 0.07 were expected for persons aged 35-39 years (Thiess et al., 1979). The limitations of these two studies preclude assessment of the carcinogenicity of the agent to humans. No specific association was found between exposure to vinylidene chloride and an excess of lung cancer observed in a synthetic chemicals plant in the United States. [Pg.1164]

Korallus U, Lange H, Neiss A, et al. 1982. Relationships between hygienic measures and the bronchial carcinoma mortality in the chromate producing industry. Arb Soz Prev 17 159-167. [Pg.433]

Langard S, Norseth T. 1975. A cohort study of bronchial carcinomas in workers producing chromate pigments. Br J Ind Med 32 62-65. [Pg.436]


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See also in sourсe #XX -- [ Pg.112 ]




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