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  1. [1] S. Dawling, N. Roodi, R.L. Mernaugh, X. Wang, and F.F. Parl, Catechol-O-methyltransferase (COMT)-mediated metabolism of catechol estrogens: comparison of wild-type and variant COMT isoforms, Cancer Research, 61(18), 2001, 6716–6722.
  2. [2] I.H. Hanna, S. Dawling, N. Roodi, F.P. Guengerich, andF.F. Parl, Cytochrome P450 1B1 (CYP1B1) pharmacogenetics:association of polymorphisms with functional differences inestrogen hydroxylation activity, Cancer Research, 60(13), 2000, 3440–3444.
  3. [3] J.L. Staudinger, Disease, drug metabolism, and transporter interactions, Pharmaceutical Research, 30(9), 2013, 2171–2173.
  4. [4] U.M. Zanger and M. Schwab, Cytochrome P450 enzymesin drug metabolism: regulation of gene expression, enzymeactivities, and impact of genetic variation, Pharmacology and Therapeutics, 138(1), 2013, 103–141.
  5. [5] P.S. Crooke, C. Justenhoven, H. Brauch, S. Dawling,N. Roodi, K.S. Higginbotham, W.D. Plummer, P.A. Schuyler,M.E. Sanders, D.L. Page, J.R. Smith, W.D. Dupont,and F.F. Parl, Estrogen metabolism and exposure in agenotypic-phenotypic model for breast cancer risk prediction, Cancer Epidemiology, Biomarkers and Prevention, 20(7), 2011, 1502–1515.
  6. [6] F.F. Parl, K.M. Egan, C. Li, and P.S. Crooke, Estrogenexposure, metabolism, and enzyme variants in a model forbreast cancer risk prediction, Cancer Information, 7(5), 2009, 109–121.
  7. [7] S.C. Philip, D.R. Marylyn, L.H. David, D. Sheila, R. Nady, and F.P. Fritz, Estrogens, enzyme variants, and breast cancer: a risk model, Cancer Epidemiology Biomarkers & Prevention, 15(9), 2006, 1620–1629.
  8. [8] E.L. Cavalieri and E.G. Rogan, Unbalanced metabolism ofendogenous estrogens in the etiology and prevention of human cancer, Journal of Steroid Biochemistry and Molecular Biology, 125(3–5), 2011, 169–180.
  9. [9] A.M. Feist and B.O. Palsson, The growing scope of applications of genome-scale metabolic reconstructions using Escherichia coli, Nature Biotechnology, 26(6), 2008, 659–667.
  10. [10] O. Folger, L. Jerby, C. Frezza, E. Gottlieb, E. Ruppin, and T. Shlomi, Predicting selective drug targets in cancer through metabolic networks, Molecular Systems Biology, 7(501), 2011, 501–501.
  11. [11] J.D. Orth and I. Thiele, What is flux balance analysis?, Nature Biotechnology, 28(3), 2010, 245–248.
  12. [12] N.C. Duarte, S.A. Becker, N. Jamshidi, I. Thiele, M.L. Mo, T.D. Vo, R. Srivas, and B.O. Palsson, Global reconstruction of the human metabolic network based on genomic and bibliomic data, Proceedings of National Acadmic of Sciences: United States of America, 104(6), 2007, 1777–1782.
  13. [13] A.M. Feist, M.J. Herrgard, I. Thiele, J.L. Reed, andB.O. Palsson, Reconstruction of biochemical networks inmicroorganisms, Nature Reviews Microbiology, 7(2), 2009,129–143.
  14. [14] J.T. Dean, M.L. Rizk, Y. Tan, K.M. Dipple, and J.C. Liao, Ensemble modelling of hepatic fatty acid metabolism with a synthetic glyoxylate shunt, Biophysical Journal, 98(8), 2010, 1385–1395.
  15. [15] T. Khazaei, et al., Ensemble modelling of cancer metabolism, Frontiers in Physiology, 3(5), 2012, 1–14.
  16. [16] L.M. Tran, M.L. Rizk, and J.C. Liao, Ensemble modelling of metabolic networks, Biophysical Journal, 95(12), 2008, 5606–5617.
  17. [17] S. Schnell and C. Mendoza, The condition for pseudo-first-order kinetics in enzymatic reactions is independent of the initial enzyme concentration, Biophysical Chemistry, 107(2), 2004, 165–174.
  18. [18] J. Srividhya and S. Schnell, Why substrate depletion has apparent first-order kinetics in enzymatic digestion, Computational Biology and Chemistry, 30(3), 2006, 209–214.
  19. [19] Biochemistry: the chemical reactions of living cells (San Diego, California, USA: Harcourt/Academic Press, 2001).
  20. [20] N.W. Gaikwad, L. Yang, E.G. Rogan, and E.L. Cavalieri,Evidence for NQO2-mediated reduction of the carcinogenicestrogen ortho-quinones, Free Radical Biology and Medicine,46(2), 2009, 253–262.
  21. [21] F.F. Parl, S. Dawling, N. Roodi, and P.S. Crooke, Estrogen metabolism and breast cancer: a risk model, Annals of the New York Academy of Sciences, 1155(2), 2009, 68–75.
  22. [22] J.L. Bolton and G.R. Thatcher, Potential mechanisms of estrogen quinone carcinogenesis, Chemical Research in Toxicology, 21(1), 2008, 93–101.
  23. [23] E. Cavalieri, D. Chakravarti, J. Guttenplan, E. Hart, J. Ingle, R. Jankowiak, P. Muti, E. Rogan, J. Russo, R. Santen, and T. Sutter, Catechol estrogen quinones as initiators of breast and other human cancers: implications for biomarkers of susceptibility and cancer prevention, Biochimica et Biophysica Acta, 1766(1), 2006, 63–78.
  24. [24] D.L. Hachey, S. Dawling, N. Roodi, and F.F. Parl, Sequential action of phase I and II enzymes cytochrome p450 1B1 and glutathione S-transferase P1 in mammary estrogen metabolism, Cancer Research, 63(23), 2003, 8492–8499.
  25. [25] M. Rahman, C. Hayes Sutter, G.L. Emmert, and T.R. Sut-ter, Regioselective 2-hydroxylation of 17β-estradiol by rat cytochrome P4501B1, Toxicology and Applied Pharmacology, 216(3), 2006, 469–478.
  26. [26] D.E. Stack, G. Li, A. Hill, and N. Hoffman, Mechanisticinsights into the Michael addition of deoxyguanosine to catechol estrogen-3,4-quinones, Chemical Research in Toxicology, 21(7), 2008, 1415–1425.
  27. [27] S. Dawling, D.L. Hachey, N. Roodi, and F.F. Parl, Invitro model of mammary estrogen metabolism: structuraland kinetic differences between catechol estrogens 2- and4-hydroxyestradiol, Chemical Research in Toxicology, 17(9),2004, 1258–1264.

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