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Tumors carcinogenesis

Ide F, lida N, Nakatsum Y et al. Miee defieient in the nueleotide exeision repair gene XPA have elevated sensitivity to benzo[a]pyrene induetion of lung tumors. Carcinogenesis 2000 21 1263-1265. [Pg.244]

Goodrow, T.L., Nichols, W.W, Storer, R.D., Anderson, M.W. Maronpot, R.R. (1994) Activation of H-ras is prevalent in 1,3-butadiene-induced and spontaneously occurring murine Harderian gland tumors. Carcinogenesis, 15, 2665-2667... [Pg.209]

Wei, M., Wanibuchi, H., Morimura, K. et al. (2002) Carcinogenicity of dimethylarsinic acid in male F344 rats and genetic alterations in induced urinary bladder tumors. Carcinogenesis, 23(8), 1387-97. [Pg.274]

D6. Di llio, C., Del Boccio, G., Aceto, A., Casaccia, R., Mucilli, F., and Federici, G., Elevation of glutathione transferase activity in human lung tumor. Carcinogenesis (London) 9, 335-340 (1988). [Pg.363]

Benzo[fl]pyrene (B[a]P), because of its potency in skin-tumor carcinogenesis and per cigarette MSS yield, was considered the major PAH of concern in tobacco smoke. In 1981, the Surgeon General commented on PAHs [see p. 36 in (4009)] ... [Pg.688]

Gray, J.W. Collins, C. Genome Changes and Gene Expression in Human Solid Tumors. Carcinogenesis. 2000, 21, 443 52. [Pg.208]

Not only is TCDO a potent therapeutic agent in acute radiation syndrome, but treatment using TCDO from days 4—11 after TBI increases the survival rate in rats for up to one year, protects against the development of late GI ulcers, and also reduces the development of y-ray-induced leukemias and malignant epitheHal tumors, but not sarcomas (202). The anticarcinogenic effect of TCDO maybe related to the inhibition of PGs, which promote carcinogenesis, or to immunostimulation, which may result in a more effective elimination of malignant cells. [Pg.496]

Pelin, K. (1994). Asbestos-related malignant mesothelioma Tumor cel characteristics and mechanisms m fibre carcinogenesis. Academic diss.. University of Helsinki. [Pg.339]

A scientifically evaluated and fully referenced data bank, developed and maintained by the National Cancer Institute (NCI). It contains some 8,000 chemical records with carcinogenicity, mutagenicity, tumor promotion, and tumor inhibition test results. Data are derived from studies cited in primaiy journals, current awareness tools, NCI reports, and other special sources. Test results have been reviewed by experts in carcinogenesis and mutagenesis. [Pg.304]

Wattenberg EV (2007) Palytoxin exploiting a novel skin tumor promoter to explore signal transduction and carcinogenesis, Am J Physiol Cell Physiol 292 C24—C32... [Pg.819]

Some authors use the term mutation as a synonym for genetic polymorphism. However, it is recommended to reserve the term mutation for genetic variations acquired within the life span of an organism such as those mutations acquired in tumor tissues during multi-step carcinogenesis. [Pg.948]

Anna CH, Maronpot RR, Pereira MA, et al. 1994. Ras proto-oncogene activation in dichloroacetic acid-, trichloroethylene-and tetrachloroethylene-induced liver tumors in B6C3F, mice. Carcinogenesis 15 2255-2261. [Pg.251]

KATiYAR s K and MUKHTAR H (1997) Inhibition of phorbol ester tumor promoter 12-O-tetradecanoylphorbol-13-acetate-caused inflammatory responses in SENCAR mouse skin by black tea polyphenols . Carcinogenesis, 18 1911-16. [Pg.63]

LU Y p, LOU Y R, xiE J G, YEN p, HUANG M T and coNNEY A H (1997) Inhibitory effect of black tea on the growth of established skin tumors in mice effects on tumor size, apoptosis, mitosis and hromodeoxyuridine incorporation into DNA , Carcinogenesis, 18 (11), 2163-9. [Pg.154]

Tocotrienols are another group of phytochemicals of rice bran which have a chemopreventive effect and have been demonstrated to inhibit breast cancer (Nesaremam et al., 1998). The polysaccharides of rice bran contain a-glucan, the anti-tumor effect of which has been demonstrated by its inhibition of gastrointestinal carcinogenesis (Akeshita et al., 1992). Rice bran agglutinin has been shown to induce apoptosis of cancer cells by the mechanism of cell cycle dysregulation (Miyoshi et al., 2001). [Pg.366]

Both l-nitroso-3,5-dimethylpiperazine and l-nitroso-3,4,5-trimethylpiperazine induced a high incidence of thymic leukemia in rats within 6 months (23). The 4-acetyl derivative of the former induced esophageal tumors in the same time, while the 4-benzoyl derivative was a very much weaker carcinogen, giving rise to only a few tumors of the forestomach after almost 2 years. These contrasting results are difficult to reconcile with any simple mechanism of carcinogenesis. [Pg.98]

Nelson R.L. Chlorophyllin, an antimutagen, acts as a tumor promoter in the rat dimethylhydrazine colon carcinogenesis model. Anticancer Res., 12, 737, 1992. [Pg.49]


See other pages where Tumors carcinogenesis is mentioned: [Pg.189]    [Pg.193]    [Pg.148]    [Pg.418]    [Pg.189]    [Pg.193]    [Pg.148]    [Pg.418]    [Pg.109]    [Pg.491]    [Pg.494]    [Pg.498]    [Pg.374]    [Pg.228]    [Pg.318]    [Pg.319]    [Pg.319]    [Pg.336]    [Pg.319]    [Pg.1075]    [Pg.232]    [Pg.232]    [Pg.233]    [Pg.233]    [Pg.237]    [Pg.238]    [Pg.238]    [Pg.268]    [Pg.135]    [Pg.138]    [Pg.26]    [Pg.94]    [Pg.44]   
See also in sourсe #XX -- [ Pg.200 ]




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