Aerofoil Sections: Results from Wind-Tunnel Investigations, by Friedrich Wilhelm Riegels

By Friedrich Wilhelm Riegels

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M. , 5-Methylcytosine as an endogenous mutagen in the human LDL receptor and p53 genes, Science, 249, 1288, 1990. , Modulation of benzo[a]pyrene diolepoxide-DNA adduct levels in human white blood cells by CYP1A1, GSTM1, and GSTT1 polymorphism, Carcinogenesis, 21, 35, 2000. , Urinary aflatoxin biomarkers and risk of hepatocellular carcinoma, Lancet, 339, 943, 1992. , Modulation of gene expression and endocrine response pathways by 2,3,7,8tetrachlorodibenzo-p-dioxin and related compounds, Pharmacol.

Lab. Clin. , 119, 598, 1992. , Proc. Natl. Acad. Sci. USA, 98, 10,469, 2001. Hanahan, D. , The hallmarks of cancer, Cell, 100, 57, 2000. , p53 tumor suppressor gene: from the basic research laboratory to the clinic — an abridged historical perspective, Carcinogenesis, 17, 1187, 1996a. , Structure and function of the p53 tumor suppressor gene: clues for rational cancer therapeutic strategies, J. Natl. , 88, 1442, 1996b. , Approaches to cancer prevention based on an understanding of N-nitrosamine carcinogenesis, Proc.

The interaction of bcl-2 and Bax proteins determines their ratio and hence, cell survival or death following apoptotic stimulus. 3). 3 MOLECULAR AND CELLULAR EVENTS OF CARCINOGENESIS DURING PROGRESSION A number of oncogenes and tumor suppressor genes are genetically altered in cancer cells, and those alterations accumulate in a stepwise manner during tumor progression (Yokota, 2000). This is evidenced by a greater number of genetic alterations in late-stage than in early-stage tumors. Moreover, the frequencies of alterations in a particular set of genes may be higher in late-stage than in early-stage tumors, whereas the frequencies in another set of genes may be high in both early- and late-stage tumors.

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