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Pulmonary cancer

Dufresne A, Loosereewanich P, Armstrong B, et al. 1996. Inorganic particles in the lungs of five aluminum smelter workers with pleuro-pulmonary cancer. Am Ind Hyg Assoc J 57 370-375. [Pg.307]

The level of pentosidine of nondiabetic pulmonary cancer patients in treatment with the antineoplastic drug, cisplatin, has been found to be higher than in healthy subjects,443 when the protein from urine, plasma, and erythrocyte membranes was examined by HPLC. Urine pyrraline was unaffected. This work implies a whole field of study of the interactions of medication with the Maillard reaction. [Pg.123]

Haguenoer JM, Dubois G, Frimat P, et al. 1981. [Mortality due to bronch-pulmonary cancer in a factory producing pigments based on lead and zinc chromates]. In Prevention of occupational cancer -International Symposium, Occupational Safety and Health Series 46. Geneva, Switzerland International Labour Office, 168-176. (French)... [Pg.424]

In smokers who also consume alcohol, beta-carotene supplementation promotes pulmonary cancer and possibly cardiovascular complications. [Pg.3650]

The two trials also showed that beta-carotene supplementation increased the incidence of pulmonary cancer in smokers. Because heavy smokers are commonly heavy drinkers it was supposed that alcohol might have contributed to the increased incidence of lung cancer. Subsequent analysis showed that there was indeed a relation between the incidence of pulmonary cancer and the amount of alcohol consumed. [Pg.3650]

Numerous chemicals have been identified as capable of causing pulmonary cancer in both animals and humans. The International Agency for Research on Cancer (lARC) states that there are adequate experimental inhalation studies in animals for several chemicals. Table 4 lists chemicals that cause lung... [Pg.2274]

Yoshimura H. 1982. [The influence of air pollution on the development of pulmonary cancer, with special reference to gasoline engine.] Jpn H Hyg 37 848- 865. (Japanese)... [Pg.163]

In addition, genomic data, molecular and cellular phenotype data, and clinical phenotype data are accepted from the scientific community at large. NIH PGRN currently funds clinical and basic pharmacokinetic and pharmacogenomic research in the cardiovascular, pulmonary, cancer, pathways, metabolic, and transporter domains. [Pg.56]

Taking these factors into consideration, the intravenous administration of Hpoplex may represent a promising gene dehvery method to treat pulmonary diseases. Simple gene delivery can be an effective approach for the treatment of lung diseases, including pulmonary metastasis of tumor cells. Indeed, the intravenous administration of interferon (IFN)-/9- and interleukin (IL)-12-encoding pDNA has been shown to provide effective treatment in a murine pulmonary cancer metastasis model [27, 28]. [Pg.1511]

Overexpression of FASN in tumor cells is induced at the transcriptional level by receptor tyrosine kinase (RTK)-stimulation of Ras and Akt (Fig. 7.2B). Keratinocyte growth factor (KGF) can induce the Akt- and cJun N-terminal kinase (JNK)-dependent expression of FASN in pulmonary cancer cells (Chang et ah, 2005). Epidermal growth factor (EGF) has also been shown to increase FASN in prostate cancer cells (Swinnen et ah, 2000a). [Pg.178]

As - cerebral lesions - pulmonary cancer chronic bronchitis -hemoglobi- nuria hematuria kidney cancer -hepatopor-tal sclerosis liver cancer - anemia leukopenia tachycardia... [Pg.261]

An isoform of fibronectin containing field ED-D is overexpressed in fetal and neoplastic tissue, and during the vascular proliferation. Tarli et al. (1999) synthesized an iodinated antibody anti ED-D. The iodinated labeled antibody I-labeled dimeric L19 [L19(scFv)(2)] has been localized in different tumors colorectal cancer, pulmonary cancer and gliobastoma (Santimaria et al., 2003). [Pg.754]

Many isolated steroidal saponins have been shown to be either cytostatic or cytotoxic to HL-60 human leukemia cell lines [43]. Lee et al. reported the in vitro tumor activity of saponins in different cancer cell line and suggested that it could be a good candidate for treatment of pulmonary cancer cells [88]. [Pg.212]

The major health effect of nickel and its compounds is contact allergy and allergic contact dermatitis as a result of skin exposure to nickel ions, Ni(II). Inhalation exposure to soluble nickel and nickel oxides/sulfides has caused nasal and pulmonary cancer in workers in nickel refineries although there are no convincing data on carcinogenicity for metallic nickel dust in humans. Exposure to nickel or nickel compounds via routes other than inhalation has not been shown to increase the cancer risk in humans (Aitio 1995). Inhalation of nickel compounds may induce asthma however, nickel-induced asthma is rare. [Pg.525]

Observations of excess nasal and pulmonary cancers in people working with nickel oxide or high-temperature roasting of nickel-copper matte resulted in the suspi-... [Pg.704]

Pulmonary cancer Neuroendocrine tumour (i.e. carcinoids) Hepatocellular and cholangiocellular cancer tissue tumour Renal cell cancer Osseous cancer... [Pg.295]

D.H. Jeong, S.K. Kim, Y.S. Lee, M.H. Cho, Target-specific near-IR induced drug release and photothermal therapy with accumulated Au/Ag hollow nanoshells on pulmonary cancer cell membranes. Biomaterials 45, 81 (2015)... [Pg.207]


See other pages where Pulmonary cancer is mentioned: [Pg.432]    [Pg.456]    [Pg.161]    [Pg.456]    [Pg.205]    [Pg.474]    [Pg.521]    [Pg.460]    [Pg.2273]    [Pg.459]    [Pg.362]    [Pg.262]    [Pg.261]    [Pg.261]    [Pg.263]    [Pg.323]    [Pg.544]    [Pg.226]    [Pg.49]   
See also in sourсe #XX -- [ Pg.205 ]




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