Citation: |
[1] |
M. R. Arkin and J. A. Wells, Small-molecule inhibitors of protein-protein interactions: progressing towards the dream, Nat. Rev. Drug Discov., 3 (2004), 301-317.doi: 10.1038/nrd1343. |
[2] |
T. Asaki, Y. Sugiyama, T. Hamamoto, M. Higashioka, M. Umehara, H. Naito and T. Niwa, Design and synthesis of 3-substituted benzamide derivatives as Bcr-Abl kinase inhibitors, Bioorg. Med. Chem. Lett., 16 (2006), 1421-1425.doi: 10.1016/j.bmcl.2005.11.042. |
[3] |
D. E. Axelrod, K. A. Baggerly and M. Kimmel, Gene amplification by unequal sister chromatid exchange: probabilistic modeling and analysis of drug resistance data, J. Theor. Biol., 168 (1994), 151-159.doi: 10.1006/jtbi.1994.1095. |
[4] |
N. T. J. Bailey, "The Elements of Stochastic Processes with Applications to the Natural Sciences," Wiley, New York, 1964. |
[5] |
N. Bellomo, N. K. Li and P. K. Maini, On the foundations of cancer modelling: Selected topics, speculations, and perspectives, Math. Models Methods Appl. Sci., 18 (2008), 593-646.doi: 10.1142/S0218202508002796. |
[6] |
Nicola Bellomo, Mark Chaplain and Elena De Angelis (eds.), "Selected Topics on Cancer Modeling: Genesis - Evolution - Immune Competition - Therapy," Boston, Birkhauser, 2008. |
[7] |
D. Bonnet and J. E. Dick, Human acute myeloid leukemia is organized as a hierarchy that originates from a primitive hematopoietic cell, Nat. Med., 3 (1997), 730-737.doi: 10.1038/nm0797-730. |
[8] |
H. A. Bradeen, C. A. Eide, T. O'Hare, K. J. Johnson, S. G.Willis, F. Y. Lee, B. J. Druker and M. W. Deininger, Comparison of imatinib mesylate, dasatinib (BMS-354825), and nilotinib (AMN107) in an N-ethyl-N-nitrosourea (ENU)-based mutagenesis screen: high efficacy of drug combinations, Blood, 108 (2006), 2332-2338.doi: 10.1182/blood-2006-02-004580. |
[9] |
H. M. Byrne, T. Alarcon, M. R. Owen, S. D. Webb and P. K. Maini, Modelling aspects of cancer dynamics: A review, Philos. Trans. R. Soc. Lond. Ser. A Math. Phys. Eng. Sci., 364 (2006), 1563-1578. |
[10] |
A. J. Coldman and J. H. Goldie, Role of mathematical modeling in protocol formulation in cancer chemotherapy, Cancer Treat. Rep., 69 (1985), 1041-1048. |
[11] |
A. J. Coldman and J. H. Goldie, A stochastic model for the origin and treatment of tumors contain- ing drug-resistant cells, Bull. Math. Biol., 48 (1986), 279-292. |
[12] |
R. S. Day, Treatment sequencing, asymmetry, and uncertainty: Protocol strategies for combination chemotherapy, Cancer Res., 46 (1986), 3876-3885. |
[13] |
M. W. Deininger, Optimizing therapy of chronic myeloid leukemia, Experimental Hematol., 35 (2007), 144-154.doi: 10.1016/j.exphem.2007.01.023. |
[14] |
M. W. Deininger and B. J. Druker, Specific targeted therapy of chronic myelogenous leukemia with imatinib, Pharmacol. Rev., 55 (2003), 401-423.doi: 10.1124/pr.55.3.4. |
[15] |
T. S. Deisboeck, L. Zhang, J. Yoon and J. Costa, In silico cancer modeling: Is it ready for prime time?, Nat. Clin. Pract. Oncol., 6 (2009), 34-42.doi: 10.1038/ncponc1237. |
[16] |
M. Eigen, and P. Schuster, "The Hypercycle: A Principle of Natural Self-Organization," Springer-Verlag, Berlin, New York, 1979. |
[17] |
S. Faderl, M. Talpaz, Z. Estrov and H. M. Kantarjian, Chronic myelogenous leukemia: biology and therapy, Ann. Intern. Med., 131 (1999), 207-219. |
[18] |
E. A. Gaffney, The application of mathematical modelling to aspects of adjuvant chemotherapy scheduling, J. Math. Biol., 48 (2004), 375-422.doi: 10.1007/s00285-003-0246-2. |
[19] |
E. A. Gaffney, The mathematical modelling of adjuvant chemotherapy scheduling: incorporating the effects of protocol rest phases and pharmacokinetics, Bull. Math. Biol., 67 (2005), 563-611.doi: 10.1016/j.bulm.2004.09.002. |
[20] |
C. W. Gardiner, "Handbook of Stochastic Methods: For Physics, Chemistry and the Natural Sciences," Springer, 2004. |
[21] |
Shea N. Gardner and Michael Fernandes, New tools for cancer chemotherapy: Computational assistance for tailoring treatments, Mol. Cancer Ther., 2 (2003), 1079-1084. |
[22] |
R. A. Gatenby, J. Brown and T. Vincent, Lessons from applied ecology: Cancer control using an evolutionary double bind, Cancer Res., 69 (2009), 7499-7502.doi: 10.1158/0008-5472.CAN-09-1354. |
[23] |
J. H. Goldie and A. J. Coldman, A mathematic model for relating the drug sensitivity of tumors to their spontaneous mutation rate, Cancer Treat. Rep., 63 (1979), 1727-1733. |
[24] |
J. H. Goldie and A. J. Coldman, A model for resistance of tumor cells to cancer chemotherapeutic agents, Math. Biosci., 65 (1983), 291-307.doi: 10.1016/0025-5564(83)90066-4. |
[25] |
J. H. Goldie and A. J. Coldman, Quantitative model for multiple levels of drug resistance in clinical tumors, Cancer Treat. Rep., 67 (1983), 923-931. |
[26] |
J. H. Goldie and A. J. Coldman, "Drug Resistance in Cancer: Mechanisms and Models," Cambridge University Press, 1998.doi: 10.1017/CBO9780511666544. |
[27] |
J. H. Goldie, A. J. Coldman and G. A. Gudauskas, Rationale for the use of alternating non-cross-resistant chemotherapy, Cancer Treat. Rep., 66 (1982), 439-449. |
[28] |
L. E. Harnevo and Z. Agur, Drug resistance as a dynamic process in a model for multistep gene amplification under various levels of selection stringency, Cancer Chemother. Pharmacol., 30 (1992), 469-476.doi: 10.1007/BF00685599. |
[29] |
A. A. Katouli and N. L. Komarova, The worst drug rule revisited: Mathematical modeling of cyclic cancer treatments, Bull. Math Bio., (2010), 1-36.doi: 10.1007/s11538-010-9539-y. |
[30] |
M. Kimmel and D. N. Stivers, Time-continuous branching walk models of unstable gene amplification, Bull. Math. Biol., 56 (1994), 337-357. |
[31] |
M. Kimmel, A. Swierniak and A. Polanski, Infinite-dimensional model of evolution of drug resistance of cancer cells, Jour. Math. Syst. Est. Contr., 8 (1998), 1-16. |
[32] |
N. L. Komarova, Stochastic modeling of drug resistance in cancer, J. Theor. Biol., 239 (2006), 351-366.doi: 10.1016/j.jtbi.2005.08.003. |
[33] |
N. L. Komarova, A. A. Katouli and D. Wodarz, Combination of two but not three current targeted drugs can improve therapy of chronic myeloid leukemia, PLoS ONE, 4 (2009), e4423.doi: 10.1371/journal.pone.0004423. |
[34] |
N. L. Komarova and D. Wodarz, Drug resistance in cancer: Principles of emergence and prevention, Proc. Natl. Acad. Sci. U.S.A., 102 (2005), 9714-9719.doi: 10.1073/pnas.0501870102. |
[35] |
L. Norton and R. Day, Potential innovations in scheduling of cancer chemotherapy, in "Important Advances in Oncology" (Vincent T. Devita, Samuel Hellman, and Steven A. Rosenberg, eds.), Lippincott, Williams & Wilkins, Philadelphia, 1985, 57-72. |
[36] |
A. S. Novozhilov, G. P. Karev and E. V. Koonin, Biological applications of the theory of birth-and-death processes, Brief. Bioinformatics, 7 (2006), 70-85.doi: 10.1093/bib/bbk006. |
[37] |
M. E. O'Dwyer, M. J. Mauro and B. J. Druker, Recent advancements in the treatment of chronic myelogenous leukemia, Annu. Rev. Med., 53 (2002), 369-381. |
[38] |
T. O'Hare, C. A. Eide, J. W. Tyner, A. S. Corbin, M. J. Wong, S. Buchanan, K. Holme, K. A. Jessen, C. Tang, H. A. Lewis, R. D. Romero, S. K. Burley and M. W. Deininger, SGX393 inhibits the CML mutant BcrAblT315I and preempts in vitro resistance when combined with nilotinib or dasatinib, Proc. Natl. Acad. Sci. U.S.A., 105 (2008), 5507-5512.doi: 10.1073/pnas.0800587105. |
[39] |
K. Peggs and S. Mackinnon, Imatinib mesylate-the new gold standard for treatment of chronic myeloid leukemia, N. Engl. J. Med., 348 (2003), 1048-1050.doi: 10.1056/NEJMe030009. |
[40] |
A. Quintas-Cardama, H. Kantarjian, L. V. Abruzzo and J. Cortes, Extramedullary BCR-ABL1-negative myeloid leukemia in a patient with chronic myeloid leukemia and synchronous cytogenetic abnormalities in Philadelphia-positive and negative clones during imatinib therapy, Leukemia, 21 (2007), 2394-2396.doi: 10.1038/sj.leu.2404865. |
[41] |
A. Quints-Cardama, H. Kantarjian and J. Cortes, Flying under the radar: The new wave of BCR-ABL inhibitors, Nat. Rev. Drug Discov., 6 (2007), 834-848.doi: 10.1038/nrd2324. |
[42] |
T. Reya, S. J. Morrison, M. F. Clarke and I. L. Weissman, Stem cells, cancer, and cancer stem cells, Nature, 414 (2001), 105-111.doi: 10.1038/35102167. |
[43] |
S. Sanga, J. P. Sinek, H. B. Frieboes, M. Ferrari, J. P. Fruehauf and V. Cristini, Mathematical modeling of cancer progression and response to chemotherapy, Expert Rev. Anticancer Ther., 6 (2006), 1361-1376.doi: 10.1586/14737140.6.10.1361. |
[44] |
S. Soverini, S. Colarossi, A. Gnani, G. Rosti, F. Castagnetti, A. Poerio, I. Iacobucci, M. Amabile, E. Abruzzese, E. Orlandi, F. Radaelli, F. Ciccone, M. Tiribelli, R. di Lorenzo, C. Caracciolo, B. Izzo, F. Pane, G. Saglio, M. Baccarani and G. Martinelli, Contribution of ABL kinase domain mutations to imatinib resistance in different subsets of Philadelphia-positive patients: by the GIMEMA Working Party on Chronic Myeloid Leukemia, Clin. Cancer Res., 12 (2006), 7374-7379.doi: 10.1158/1078-0432.CCR-06-1516. |
[45] |
G. W. Swan, Role of optimal control theory in cancer chemotherapy, Math. Biosci., 101 (1990), 237-284.doi: 10.1016/0025-5564(90)90021-P. |
[46] |
A. Swierniak, M. Kimmel and J. Smieja, Mathematical modeling as a tool for planning anticancer therapy, Eur. J. Pharmacol., 625 (2009), 108-121.doi: 10.1016/j.ejphar.2009.08.041. |
[47] |
A. Swierniak and J. Smieja, Cancer chemotherapy optimization under evolving drug resistance, Nonlin. Anal., 47 (2001), 375-386.doi: 10.1016/S0362-546X(01)00184-5. |
[48] |
E. Weisberg, P. W. Manley, S. W. Cowan-Jacob, A. Hochhaus and J. D. Griffin, Second generation inhibitors of BCR-ABL for the treatment of imatinib-resistant chronic myeloid leukaemia, Nat. Rev. Cancer, 7 (2007), 345-356.doi: 10.1038/nrc2126. |
[49] |
D. Wodarz and N. L. Komarova, "Computational Biology of Cancer: Lecture Notes and Mathematical Modeling," World Scientific, 2005. |
[50] |
J. Zhang, P. L. Yang and N. S. Gray, Targeting cancer with small molecule kinase inhibitors, Nat. Rev. Cancer, 9 (2009), 28-39.doi: 10.1038/nrc2559. |