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
Hlavní autoři: CUNNINGHAM, M. J., LIANG, S., FURMAN, S., SEILHAMER, J. J., SOMOGYI, R.
Médium: Journal Article
Jazyk:angličtina
Vydáno: 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.
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.
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  organization: Incyte Pharmaceuticals, Incorporated, Palo Alto, California 94304, USA
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  surname: FURMAN
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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.
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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.
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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.
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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
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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
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Snippet : When dealing with thousands of genes, all potentially interesting, it is desirable to rank the genes according to their degree of participation in a...
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...
When dealing with thousands of genes, all potentially interesting, it is desirable to rank the genes according to their degree of participation in a...
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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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