Gene Expression Microarray Data Analysis for Toxicology Profiling
: When dealing with thousands of genes, all potentially interesting, it is desirable to rank the genes according to their degree of participation in a physiological process. Therefore, genes with the highest Shannon entropy and ERL can be selected as the best toxicity target candidates, permitting p...
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| Vydáno v: | Annals of the New York Academy of Sciences Ročník 919; číslo 1; s. 52 - 67 |
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| Hlavní autoři: | , , , , |
| Médium: | Journal Article |
| Jazyk: | angličtina |
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Oxford, UK
Blackwell Publishing Ltd
01.09.2000
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| ISSN: | 0077-8923, 1749-6632 |
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| Abstract | : When dealing with thousands of genes, all potentially interesting, it is desirable to rank the genes according to their degree of participation in a physiological process. Therefore, genes with the highest Shannon entropy and ERL can be selected as the best toxicity target candidates, permitting preclinical scientists to focus their research and resources on those genes. |
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| AbstractList | : When dealing with thousands of genes, all potentially interesting, it is desirable to rank the genes according to their degree of participation in a physiological process. Therefore, genes with the highest Shannon entropy and ERL can be selected as the best toxicity target candidates, permitting preclinical scientists to focus their research and resources on those genes. When dealing with thousands of genes, all potentially interesting, it is desirable to rank the genes according to their degree of participation in a physiological process. Therefore, genes with the highest Shannon entropy and ERL can be selected as the best toxicity target candidates, permitting preclinical scientists to focus their research and resources on those genes.When dealing with thousands of genes, all potentially interesting, it is desirable to rank the genes according to their degree of participation in a physiological process. Therefore, genes with the highest Shannon entropy and ERL can be selected as the best toxicity target candidates, permitting preclinical scientists to focus their research and resources on those genes. When dealing with thousands of genes, all potentially interesting, it is desirable to rank the genes according to their degree of participation in a physiological process. Therefore, genes with the highest Shannon entropy and ERL can be selected as the best toxicity target candidates, permitting preclinical scientists to focus their research and resources on those genes. A bstract : When dealing with thousands of genes, all potentially interesting, it is desirable to rank the genes according to their degree of participation in a physiological process. Therefore, genes with the highest Shannon entropy and ERL can be selected as the best toxicity target candidates, permitting preclinical scientists to focus their research and resources on those genes. |
| Author | SEILHAMER, J. J. SOMOGYI, R. CUNNINGHAM, M. J. LIANG, S. FURMAN, S. |
| Author_xml | – sequence: 1 givenname: M. J. surname: CUNNINGHAM fullname: CUNNINGHAM, M. J. email: maryjane@incyte.com organization: Incyte Pharmaceuticals, Incorporated, Palo Alto, California 94304, USA – sequence: 2 givenname: S. surname: LIANG fullname: LIANG, S. organization: Incyte Pharmaceuticals, Incorporated, Palo Alto, California 94304, USA – sequence: 3 givenname: S. surname: FURMAN fullname: FURMAN, S. organization: Incyte Pharmaceuticals, Incorporated, Palo Alto, California 94304, USA – sequence: 4 givenname: J. J. surname: SEILHAMER fullname: SEILHAMER, J. J. organization: Incyte Pharmaceuticals, Incorporated, Palo Alto, California 94304, USA – sequence: 5 givenname: R. surname: SOMOGYI fullname: SOMOGYI, R. organization: Incyte Pharmaceuticals, Incorporated, Palo Alto, California 94304, USA |
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| Cites_doi | 10.1111/j.1749-6632.1996.tb18620.x 10.1016/S0090-9556(24)11826-0 10.1016/S0306-3623(96)00246-7 10.1101/gr.6.7.639 10.1016/S0021-9258(19)50613-5 10.1073/pnas.93.20.10614 10.1016/0378-4274(95)03507-9 10.3109/03602539709037573 10.1006/abbi.1999.1351 10.1080/009841099157269 10.1021/bi00125a027 10.1016/S0021-9258(18)98392-4 10.1006/taap.1996.8007 10.1016/S0306-3623(96)00181-4 10.1093/carcin/17.1.53 10.1021/jm00032a021 |
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| References | Simpson, A.E. 1997. The cytochrome P450 4 (CYP4) family. Gen. Pharmacol. 28: 351-359. Shalon, D., et al. 1996. A DNA microarray system for analyzing complex DNA samples using two-color fluorescent probe hybridization. Genome Res. 6: 639-645. Cummings, B.S., et al. 1999. Cellular distribution of cytochromes P-450 in the rat kidney. Drug Metab. Dispos. 27: 542-548. Christou, M., et al. 1992. Selective suppression of the catalytic activity of cDNA- expressed cytochrome P4502B1 toward polycyclic hydrocarbons in the microsomal membrane: modification of this effect by specific amino acid substitutions. Biochemistry 31: 2835-2841. Cohen, S.D. & E.A. Khairallah. 1977. Selective protein arylation and acetaminophen-induced hepatotoxicity. Drug Metab. Rev. 29: 59-77. Qu, S.X. & N.H. Stacey. 1996. Formation and persistence of DNA adducts in different target tissues of rats after multiple administration of benzo(a)pyrene. Carcinogenesis 17: 53-59. Schena, M., et al. 1996. Parallel human genome analysis: microarray-based expression monitoring of 1000 genes. Proc. Natl. Acad. Sci. U.S.A. 93: 10614-10619. Degawa, M., et al. 1994. Metabolic activation and carcinogen-DNA adduct detection in human larynx. Cancer Res. 54: 4915-4919. Park, S.H. & R.A. Schatz. 1999. Effect of low-level short-term o-xylene inhalation of benzo(a)pyrene (BaP) metabolism and BaP-DNA adduct formation in rat liver and lung microsomes. J. Toxicol. Environ. Health 58: 299-312. Chen, J.X., et al. 1998. Carcinogens preferentially bind at methylated CpG in the p53 mutational hot spots. Cancer Res. 58: 2070-2075. Kaikaus, R.M., et al. 1993. Induction of peroxisomal fatty acid beta-oxidation and liver fatty acid-binding protein by peroxisome proliferators: mediators via the cytochrome P-450IVA1 omega-hydroxylase pathway. J. Biol. Chem. 268: 9593-9603. Tugwood, J.D., et al. 1998. Peroxisome proliferator-activated receptors: structures and function. Ann. N.Y. Acad. Sci. 804: 252-265. Benzo[a]pyrene. 1983. IARC Monogr. Eval. Carcinog. Risk Chem. Hum. 32: 211-224. Sundseth, S.S. & D.J. Waxman. 1992. Sex-dependent expression and clofibrate inducibility of cytochrome P450 4A fatty acid omega-hydroxylases: male specificity of liver and kidney CYP4A2 mRNA and tissue-specific regulation by growth hormone and testosterone. J. Biol. Chem. 267: 3915-3921. Waxman, D.J. 1999. P450 gene induction by structurally diverse xenochemicals: central role of nuclear receptors CAR, PXR, and PPAR. Arch. Biochem. Biophys. 369: 11-23. Nakanishi, Y., et al. 1989. Effects of chronic administration of the peroxisome proliferator, clofibrate, on cytosolic acetyl-CoA hydrolase in rat liver. Biochem. Pharmacol. 45: 1403-1407. Myers, T.G., et al. 1994. Preferred orientations in the binding of 4′-hydroxyacetanilide (acetaminophen) to cytochrome P450 1A1 and 2B1 isoforms as determined by 13C- and 15N-NMR relaxation studies. J. Med. Chem. 37: 860-867. Kadlubar, F.F. & A.F. Badawi. 1995. Genetic susceptibility and carcinogen-DNA adduct formation in human urinary bladder carcinogenesis. Toxicol. Lett. 82/83: 627-632. Amacher, D.E., et al. 1997. Hepatic microsomal enzyme induction, β-oxidation, and cell proliferation following administration of clofibrate, gemfibrozil, or bezafibrate in the CD rat. Toxicol. Appl. Pharmacol. 142: 143-150. Kroger, H., et al. 1997. Protection from acetaminophen-induced liver damage by the synergistic action of low doses of the poly(ADP-ribose) polymerase-inhibitor nicotinamide and the antioxidant N-acetylcysteine or the amino acid l-methionine. Gen. Pharmacol. 28: 257-263. Greenblatt, M.S., et al. 1994. Mutations in the p53 tumor suppressor gene: clues to cancer etiology and molecular pathogenesis. Cancer Res. 54: 4855-4878. 1996; 17 1989; 45 1997; 142 1977; 29 1998; 804 1992; 267 1999; 27 1999; 58 1983; 32 1996; 93 1997; 28 1995; 82/83 1994; 37 1992; 31 1993; 268 1999; 369 1994; 54 1998; 58 1996; 6 Cummings B.S. (e_1_2_6_17_2) 1999; 27 Kaikaus R.M. (e_1_2_6_23_2) 1993; 268 Degawa M. (e_1_2_6_3_2) 1994; 54 e_1_2_6_20_2 Nakanishi Y. (e_1_2_6_13_2) 1989; 45 Benzo[a]pyrene. (e_1_2_6_2_2) 1983; 32 e_1_2_6_7_2 e_1_2_6_18_2 Chen J.X. (e_1_2_6_8_2) 1998; 58 e_1_2_6_19_2 e_1_2_6_4_2 Greenblatt M.S. (e_1_2_6_9_2) 1994; 54 e_1_2_6_6_2 e_1_2_6_5_2 e_1_2_6_12_2 e_1_2_6_24_2 e_1_2_6_10_2 e_1_2_6_22_2 e_1_2_6_11_2 Sundseth S.S. (e_1_2_6_16_2) 1992; 267 e_1_2_6_21_2 e_1_2_6_14_2 e_1_2_6_15_2 |
| References_xml | – reference: Amacher, D.E., et al. 1997. Hepatic microsomal enzyme induction, β-oxidation, and cell proliferation following administration of clofibrate, gemfibrozil, or bezafibrate in the CD rat. Toxicol. Appl. Pharmacol. 142: 143-150. – reference: Qu, S.X. & N.H. Stacey. 1996. Formation and persistence of DNA adducts in different target tissues of rats after multiple administration of benzo(a)pyrene. Carcinogenesis 17: 53-59. – reference: Kroger, H., et al. 1997. Protection from acetaminophen-induced liver damage by the synergistic action of low doses of the poly(ADP-ribose) polymerase-inhibitor nicotinamide and the antioxidant N-acetylcysteine or the amino acid l-methionine. Gen. Pharmacol. 28: 257-263. – reference: Benzo[a]pyrene. 1983. IARC Monogr. Eval. Carcinog. Risk Chem. Hum. 32: 211-224. – reference: Kadlubar, F.F. & A.F. Badawi. 1995. Genetic susceptibility and carcinogen-DNA adduct formation in human urinary bladder carcinogenesis. Toxicol. Lett. 82/83: 627-632. – reference: Schena, M., et al. 1996. Parallel human genome analysis: microarray-based expression monitoring of 1000 genes. Proc. Natl. Acad. Sci. U.S.A. 93: 10614-10619. – reference: Degawa, M., et al. 1994. Metabolic activation and carcinogen-DNA adduct detection in human larynx. Cancer Res. 54: 4915-4919. – reference: Simpson, A.E. 1997. The cytochrome P450 4 (CYP4) family. Gen. Pharmacol. 28: 351-359. – reference: Tugwood, J.D., et al. 1998. Peroxisome proliferator-activated receptors: structures and function. Ann. N.Y. Acad. Sci. 804: 252-265. – reference: Waxman, D.J. 1999. P450 gene induction by structurally diverse xenochemicals: central role of nuclear receptors CAR, PXR, and PPAR. Arch. Biochem. Biophys. 369: 11-23. – reference: Nakanishi, Y., et al. 1989. Effects of chronic administration of the peroxisome proliferator, clofibrate, on cytosolic acetyl-CoA hydrolase in rat liver. Biochem. Pharmacol. 45: 1403-1407. – reference: Christou, M., et al. 1992. Selective suppression of the catalytic activity of cDNA- expressed cytochrome P4502B1 toward polycyclic hydrocarbons in the microsomal membrane: modification of this effect by specific amino acid substitutions. Biochemistry 31: 2835-2841. – reference: Myers, T.G., et al. 1994. Preferred orientations in the binding of 4′-hydroxyacetanilide (acetaminophen) to cytochrome P450 1A1 and 2B1 isoforms as determined by 13C- and 15N-NMR relaxation studies. J. Med. Chem. 37: 860-867. – reference: Chen, J.X., et al. 1998. Carcinogens preferentially bind at methylated CpG in the p53 mutational hot spots. Cancer Res. 58: 2070-2075. – reference: Cummings, B.S., et al. 1999. Cellular distribution of cytochromes P-450 in the rat kidney. Drug Metab. Dispos. 27: 542-548. – reference: Park, S.H. & R.A. Schatz. 1999. Effect of low-level short-term o-xylene inhalation of benzo(a)pyrene (BaP) metabolism and BaP-DNA adduct formation in rat liver and lung microsomes. J. Toxicol. Environ. Health 58: 299-312. – reference: Shalon, D., et al. 1996. A DNA microarray system for analyzing complex DNA samples using two-color fluorescent probe hybridization. Genome Res. 6: 639-645. – reference: Sundseth, S.S. & D.J. Waxman. 1992. Sex-dependent expression and clofibrate inducibility of cytochrome P450 4A fatty acid omega-hydroxylases: male specificity of liver and kidney CYP4A2 mRNA and tissue-specific regulation by growth hormone and testosterone. J. Biol. Chem. 267: 3915-3921. – reference: Kaikaus, R.M., et al. 1993. Induction of peroxisomal fatty acid beta-oxidation and liver fatty acid-binding protein by peroxisome proliferators: mediators via the cytochrome P-450IVA1 omega-hydroxylase pathway. J. Biol. Chem. 268: 9593-9603. – reference: Greenblatt, M.S., et al. 1994. Mutations in the p53 tumor suppressor gene: clues to cancer etiology and molecular pathogenesis. Cancer Res. 54: 4855-4878. – reference: Cohen, S.D. & E.A. Khairallah. 1977. Selective protein arylation and acetaminophen-induced hepatotoxicity. Drug Metab. Rev. 29: 59-77. – volume: 267 start-page: 3915 year: 1992 end-page: 3921 article-title: Sex‐dependent expression and clofibrate inducibility of cytochrome P450 4A fatty acid omega‐hydroxylases: male specificity of liver and kidney CYP4A2 mRNA and tissue‐specific regulation by growth hormone and testosterone publication-title: J. Biol. Chem. – volume: 58 start-page: 2070 year: 1998 end-page: 2075 article-title: Carcinogens preferentially bind at methylated CpG in the p53 mutational hot spots publication-title: Cancer Res. – volume: 17 start-page: 53 year: 1996 end-page: 59 article-title: Formation and persistence of DNA adducts in different target tissues of rats after multiple administration of benzo(a)pyrene publication-title: Carcinogenesis – volume: 804 start-page: 252 year: 1998 end-page: 265 article-title: Peroxisome proliferator‐activated receptors: structures and function publication-title: Ann. N.Y. Acad. Sci. – volume: 32 start-page: 211 year: 1983 end-page: 224 article-title: IARC Monogr publication-title: Eval. Carcinog. Risk Chem. Hum. – volume: 369 start-page: 11 year: 1999 end-page: 23 article-title: P450 gene induction by structurally diverse xenochemicals: central role of nuclear receptors CAR, PXR, and PPAR publication-title: Arch. Biochem. Biophys. – volume: 82/83 start-page: 627 year: 1995 end-page: 632 article-title: Genetic susceptibility and carcinogen‐DNA adduct formation in human urinary bladder carcinogenesis publication-title: Toxicol. Lett. – volume: 29 start-page: 59 year: 1977 end-page: 77 article-title: Selective protein arylation and acetaminophen‐induced hepatotoxicity publication-title: Drug Metab. Rev. – volume: 27 start-page: 542 year: 1999 end-page: 548 article-title: Cellular distribution of cytochromes P‐450 in the rat kidney publication-title: Drug Metab. Dispos. – volume: 45 start-page: 1403 year: 1989 end-page: 1407 article-title: Effects of chronic administration of the peroxisome proliferator, clofibrate, on cytosolic acetyl‐CoA hydrolase in rat liver publication-title: Biochem. Pharmacol. – volume: 142 start-page: 143 year: 1997 end-page: 150 article-title: Hepatic microsomal enzyme induction, β‐oxidation, and cell proliferation following administration of clofibrate, gemfibrozil, or bezafibrate in the CD rat publication-title: Toxicol. Appl. Pharmacol. – volume: 58 start-page: 299 year: 1999 end-page: 312 article-title: Effect of low‐level short‐term ‐xylene inhalation of benzo(a)pyrene (BaP) metabolism and BaP‐DNA adduct formation in rat liver and lung microsomes publication-title: J. Toxicol. Environ. Health – volume: 6 start-page: 639 year: 1996 end-page: 645 article-title: A DNA microarray system for analyzing complex DNA samples using two‐color fluorescent probe hybridization publication-title: Genome Res. – volume: 93 start-page: 10614 year: 1996 end-page: 10619 article-title: Parallel human genome analysis: microarray‐based expression monitoring of 1000 genes publication-title: Proc. Natl. Acad. Sci. U.S.A. – volume: 54 start-page: 4915 year: 1994 end-page: 4919 article-title: Metabolic activation and carcinogen‐DNA adduct detection in human larynx publication-title: Cancer Res. – volume: 54 start-page: 4855 year: 1994 end-page: 4878 article-title: Mutations in the p53 tumor suppressor gene: clues to cancer etiology and molecular pathogenesis publication-title: Cancer Res. – volume: 31 start-page: 2835 year: 1992 end-page: 2841 article-title: Selective suppression of the catalytic activity of cDNA‐ expressed cytochrome P4502B1 toward polycyclic hydrocarbons in the microsomal membrane: modification of this effect by specific amino acid substitutions publication-title: Biochemistry – volume: 37 start-page: 860 year: 1994 end-page: 867 article-title: Preferred orientations in the binding of 4′‐hydroxyacetanilide (acetaminophen) to cytochrome P450 1A1 and 2B1 isoforms as determined by C‐ and N‐NMR relaxation studies publication-title: J. Med. 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| SubjectTerms | Acetaminophen - pharmacology Animals Benzo(a)pyrene - pharmacology Clofibrate - pharmacology Drug-Related Side Effects and Adverse Reactions - genetics Entropy Gene Expression - drug effects Gene Expression Profiling Liver - drug effects Liver - metabolism Liver - pathology Male Oligonucleotide Array Sequence Analysis Organ Size - drug effects Rats Rats, Sprague-Dawley RNA, Messenger - analysis RNA, Messenger - genetics Toxicity Tests - methods |
| Title | Gene Expression Microarray Data Analysis for Toxicology Profiling |
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