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Readings

  1. Abu-Asab, M., M. Chaouchi, and H. Amri, Evolutionary medicine: A meaningful connection between omics, disease, and treatment. Proteomics Clin Appl, 2008. 2(2): p. 122-134.
  2. Anderson, C. The end of theory: will the data deluge make the scientific method obsolete? Edge  2008; Available from: http://www.edge.org/3rd_culture/anderson08/anderson08_index.html.
  3. Axelrod, R., D.E. Axelrod, and K.J. Pienta, Evolution of cooperation among tumor cells. Proc Natl Acad Sci U S A, 2006. 103(36): p. 13474-9.
  4. Brash, D.E., Cellular proofreading. Nat Med, 1996. 2(5): p. 525-6.
  5. Brash, D.E., et al., Colonization of adjacent stem cell compartments by mutant keratinocytes. Semin Cancer Biol, 2005. 15(2): p. 97-102.
  6. Coffey, D.S., Self-organization, complexity and chaos: the new biology for medicine. Nat Med, 1998. 4(8): p. 882-5.
  7. Coffey, D.S., Similarities of prostate and breast cancer: Evolution, diet, and estrogens. Urology, 2001. 57(4 Suppl 1): p. 31-8.
  8. Deisboeck, T.S., et al., In silico cancer modeling: is it ready for prime time? Nat Clin Pract Oncol, 2009. 6(1): p. 34-42.
  9. Ewald, P.W., Evolutionary medicine and the causes of chronic disease, in Human Evolution, M.P. Muehlenbein, Editor. 2009 anticipated, Cambridge University Press: Cambridge, UK.
  10. Feinberg, A.P., Epigenetics at the epicenter of modern medicine. JAMA, 2008. 299(11): p. 1345-50.
  11. Feinberg, A.P., R. Ohlsson, and S. Henikoff, The epigenetic progenitor origin of human cancer. Nat Rev Genet, 2006. 7(1): p. 21-33.
  12. Fong, J.H., et al., Modeling the evolution of protein domain architectures using maximum parsimony. J Mol Biol, 2007. 366(1): p. 307-15.
  13. Frank, S.A., Dynamics of cancer: incidence, inheritance, and evolution. Princeton series in evolutionary biology. 2007, Princeton, N.J.: Princeton University Press. xi, 378 p.
  14. Frank, S.A. and M.A. Nowak, Cell biology: Developmental predisposition to cancer. Nature, 2003. 422(6931): p. 494.
  15. Galipeau, P.C., et al., NSAIDs modulate CDKN2A, TP53, and DNA content risk for progression to esophageal adenocarcinoma. PLoS Med, 2007. 4(2): p. e67.
  16. Gatenby, R.A. and R.J. Gillies, A microenvironmental model of carcinogenesis. Nat Rev Cancer, 2008. 8(1): p. 56-61.
  17. Gonzalez-Garcia, I., R.V. Sole, and J. Costa, Metapopulation dynamics and spatial heterogeneity in cancer. Proc Natl Acad Sci U S A, 2002. 99(20): p. 13085-9.
  18. Gupta, G.P. and J. Massague, Cancer metastasis: building a framework. Cell, 2006. 127(4): p. 679-95.
  19. Heng, H.H., Cancer genome sequencing: the challenges ahead. Bioessays, 2007. 29(8): p. 783-94.
  20. Heng, H.H., et al., Stochastic cancer progression driven by non-clonal chromosome aberrations. J Cell Physiol, 2006. 208(2): p. 461-72.
  21. Hinow, P., et al., The DNA binding activity of p53 displays reaction-diffusion kinetics. Biophys J, 2006. 91(1): p. 330-42.
  22. Knudson, A.G., Chasing the cancer demon. Annu Rev Genet, 2000. 34: p. 1-19.
  23. Knudson, A.G., Two genetic hits (more or less) to cancer. Nat Rev Cancer, 2001. 1(2): p. 157-62.
  24. Maley, C.C., et al., Genetic clonal diversity predicts progression to esophageal adenocarcinoma. Nat Genet, 2006. 38(4): p. 468-73.
  25. Merlo, L.M., et al., Cancer as an evolutionary and ecological process. Nat Rev Cancer, 2006. 6(12): p. 924-35.
  26. Michor, F., Mathematical models of cancer stem cells. J Clin Oncol, 2008. 26(17): p. 2854-61.
  27. Michor, F., et al., Dynamics of chronic myeloid leukaemia. Nature, 2005. 435(7046): p. 1267-70.
  28. Michor, F., Y. Iwasa, and M.A. Nowak, Dynamics of cancer progression. Nat Rev Cancer, 2004. 4(3): p. 197-205.
  29. Nowak, M.A., Evolutionary dynamics : exploring the equations of life. 2006, Cambridge, Mass.: Belknap Press of Harvard University Press. xi, 363 p.
  30. Pawelek, J.M. and A.K. Chakraborty, Fusion of tumour cells with bone marrow-derived cells: a unifying explanation for metastasis. Nat Rev Cancer, 2008. 8(5): p. 377-86.
  31. Rubin, H., What keeps cells in tissues behaving normally in the face of myriad mutations? Bioessays, 2006. 28(5): p. 515-24.
  32. Rubin, H., Cell-cell contact interactions conditionally determine suppression and selection of the neoplastic phenotype. Proc Natl Acad Sci U S A, 2008. 105(17): p. 6215-21.
  33. Shibata, D. and S. Tavare, Counting divisions in a human somatic cell tree: how, what and why? Cell Cycle, 2006. 5(6): p. 610-4.
  34. Tarafa, G., et al., Mutational load distribution analysis yields metrics reflecting genetic instability during pancreatic carcinogenesis. Proc Natl Acad Sci U S A, 2008. 105(11): p. 4306-11.
  35. Wang, Z. and T. Deisboeck, Computational modeling of brain tumors: discrete, continuum or hybrid? Scientific Modeling and Simulation, 2008. 15(1): p. 381-393.
  36. Ye, C.J., et al., The dynamics of cancer chromosomes and genomes. Cytogenet Genome Res, 2007. 118(2-4): p. 237-46.
  37. Zhang, L., et al., Simulating brain tumor heterogeneity with a multiscale agent-based model: Linking molecular signatures, phenotypes and expansion rate. Mathematical and Computer Modelling, 2009. 49(1-2): p. 307-319.
  38. Zhang, L., et al., Multiscale agent-based cancer modeling. J Math Biol, 2009. 58(4-5): p. 545-59.

 

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