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Mathematical modelling of tumour angiogenesis

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Warianty tytułu
PL
Matematyczne modelowanie angiogenezy nowotworowej
Języki publikacji
EN
Abstrakty
EN
Mathematical models are valuable tools for studying the underlying mechanisms of tumour progression. They enable us to explore possible radio-, chemo- and other various therapy combinations that until now have been only a promising hypotheses because of the huge costs of their clinical studies. Here we present a family of mathematical models of tumour angiogenesis, which give an accurate fit to biological data. In addition, after modifications they can describe the effect of anti-angiogenic treatment using various vessel targeting agents, as well as the impact of cytotoxic agents on proliferating cancer cells. We present two ways in which anti-angiogenic treatment can be incorporated into the model. In the first one, the agents directly target tumour vessels, whereas in the second one, they interfere with angiogenic signalling. We illustrate differences between these two approaches by presenting the results of fitting the corresponding models to the biological data.
PL
Modele matematyczne okazały się być cennym narzędziem do badania podstawowych mechanizmów progresji nowotworu. Modele pozwalają nam na badanie możliwości łączenia radioterapii, chemioterapii i innych metod leczenia, co do tej pory, z powodu bardzo wysokich kosztów badań klinicznych, było nieosiągalne. W pracy prezentujemy rodzinę matematycznych modeli angiogenezy nowotworowej, które okazały się dobrze odpowiadać wynikom przeprowadzonych eksperymentów biologicznych. Ponadto, po wprowadzeniu pewnych modyfikacji, modele te skutecznie opisują wpływ terapii antyangiogennej wykorzystującej leki o różnorakim sposobie działania. W pracy przedstawiamy dwa sposoby na uwzględnienie w modelu wpływu leków działających na naczynia krwionośne dostarczające w rejony nowotworu tlen i substancje odżywcze. Pierwszy sposób odnosi się do środków działających bezpośrednio na naczynia guza. Drugi opisuje środki wpływające na proangiogenna sygnalizacje. Różnice miedzy tymi dwoma podejściami ilustrujemy poprzez przedstawienie wyników dopasowywania modeli do danych eksperymentalnych.
Rocznik
Strony
1--12
Opis fizyczny
Bibliogr. 36 poz., rys., tab.
Twórcy
  • College of Inter-Faculty Individual Studies in Mathematics and Natural Sciences The University of Warsaw Zwirki i Wigury 93, 02-089 Warsaw, Poland
Bibliografia
  • [1] Z. Agur, L. Arakelyan, P. Daugulis, and Y. Ginosar, Hopf point analysis for angiogenesis models, Discrete Cont. Dyn. B 4, 29–38, 2004. doi: 10.3934/dcdsb.2004.4.29; MR 2028812.
  • [2] L. Arakelyan, V. Vainstein, and Z. Agur, A computer algorithm describing the process of vessel formation and maturation, and its use for predicting the effects of anti-angiogenic and anti-maturation therapy on vascular tumor growth, Angiogenesis 5, 203–214, 2002. doi:10.1023/A:1023841921971; PMID: 12831061 [PubMed].
  • [3] M. Bodnar and U. Forys, Angiogenesis model with carrying capacity depending on vessel density, J. Biol. Syst. 17, 1–25, 2009. doi: 10.1142/S0218339009002739; MR 2604400.
  • [4] J. Brown and A. Giaccia., The unique physiology of solid tumors: opportunities (and problems) for cancer therapy, Cancer Res. 58, 1408–1416, 1998. PMID: 9537241 [PubMed].
  • [5] O. Casanovas, D. Hicklin, G. Bergers, and D. Hanahan, Drug resistance by evasion of antiangiogenic targeting of VEGF signaling in late-stage pancreatic islet tumors, Cancer Cell 8, 299–309, 2005. doi: 10.1016/j.ccr.2005.09.005; PMID: 16226705 [PubMed].
  • [6] R. Cooke, Dr. Folkman’s War: Angiogenesis and the struggle to defeat cancer, Random House, New York, 2001.
  • [7] A. d’Onofrio and A. Gandolfi, Tumour eradication by antiangiogenic therapy: analysis and extensions of the model by Hahnfeldt et al.(1999), Math. Biosci. 191, 159–184, 2004. doi:10.1016/j.mbs.2004.06.003; MR 2090896; Zbl 1004.92023; PMID: 15363652 [PubMed].
  • [8] A. d’Onofrio and A. Gandolfi, A family of models of angiogenesis and anti-angiogenesis anti-cancer therapy, Math. Med. Biol. 26, 63–95, 2009. doi: 10.1093/imammb/dqn024; Zbl 1157.92024; PMID: 19033598 [PubMed].
  • [9] A. Ergun, K. Camphausen, and L.Wein, Optimal scheduling of radiotherapy and angiogenic inhibitors, Bull. Math. Biol. 65, 407–424, 2003. doi: 10.1016/S0092-8240(03)00006-5; PMID:12749532 [PubMed].
  • [10] J. Folkman, Tumor angiogenesis: therapeutic implications, N. Engl. J. Med. 285, 1182–1184, 1971. doi: 10.1056/NEJM197111182852108; PMID: 4938153 [PubMed].
  • [11] K. Fujita, D. Sano, M. Kimura, Y. Yamashita, M. Kawakami, Y. Ishiguro, G. Nishimura, H. Matsuda, and M. Tsukuda, Anti-tumor effects of bevacizumab in combination with paclitaxel on head and neck squamous cell carcinoma, Oncol. Rep. 18, 47–51, 2007. PMID:17549344 [PubMed].
  • [12] B. Gompertz, On the nature of the function expressive of the law of human mortality, and on a new mode of determining the value of life contingencies, Phil. Trans. R. Soc. B 115, 513–583, 1825. doi: 10.1098/rstl.1825.0026.
  • [13] H. P. Greenspan, Models for the growth of a solid tumor by diffusion, Stud. Appl. Math. 51, 317–340, 1972. Zbl 0257.92001.
  • [14] P. Hahnfeldt, D. Panigrahy, J. Folkman, and L. Hlatky, Tumor development under angiogenic signaling: a dynamical theory of tumor growth, treatment response, and postvascular dormancy, Cancer Res. 59, 4770–4775, 1999. PMID: 10519381 [PubMed].
  • [15] R. K. Jain, Normalization of tumor vasculature: an emerging concept in antiangiogenic therapy, Science 307, 58–62, 2005. doi: 10.1126/science.1104819; PMID: 15637262 [PubMed].
  • [16] R. K. Jain, Taming vessels to treat cancer, Sci. Am. 298, 56–63, 2008. doi:10.1038/scientificamerican0108-56; PMID: 18225696 [PubMed]
  • [17] T. B. Kepler and T. C. Elston, Stochasticity in transcriptional regulation: origins, consequences, and mathematical representations, Biophys. J. 81, 3116–3136, 2001. doi:10.1016/S0006-3495(01)75949-8; PMID: 11720979 [PubMed].
  • [18] R. Kerbel, Tumor angiogenesis, N. Engl. J. Med. 358, 2039–2049, 2008. doi: 10.1056/NEJMra0706596; PMID: 18463380 [PubMed].
  • [19] M. Leach, K. Brindle, J. Evelhoch, J. Griffiths, M. Horsman, A. Jackson, G. Jayson, I. Judson, M. Knopp, R. Maxwell, et al., The assessment of antiangiogenic and antivascular therapies in early-stage clinical trials using magnetic resonance imaging: issues and recommendations, Br. J. Cancer 92, 1599–1610, 2005. doi: 10.1038/sj.bjc.6602550; PMID: 15870830 [PubMed].
  • [20] A. K. Laird, Dynamics of tumor growth, Brit. J. Cancer 18, 490–502, 1964. doi:10.1038/bjc.1964.55; PMID: 14219541 [PubMed].
  • [21] U. Ledzewicz and H. Schättler, Analysis of optimal controls for a mathematical model of tumour anti-angiogenesis, Optim. Contr. Appl. Met. 29, 41–58, 2008. doi: 10.1002/oca.814; MR 2397499.
  • [22] U. Ledzewicz and H. Schättler, Antiangiogenic therapy in cancer treatment as an optimal control problem, SIAM J. Control Optim. 46, 1052–1079, 2007. doi: 10.1137/060665294; MR 2338438; Zbl 05288515.
  • [23] U. Ledzewicz and H. Schättler, Optimal and suboptimal protocols for a class of mathematical models of tumor anti-angiogenesis, J. Theor. Biol. 252, 295–312, 2008. doi:10.1016/j.jtbi.2008.02.014; MR 2948532; PMID: 18371982 [PubMed].
  • [24] L. Loeb, A mutator phenotype in cancer, Cancer Res. 61, 3230–3239, 2001. PMID: 11309271 [PubMed].
  • [25] N. Mantzaris, S. Webb, and H. Othmer, Mathematical modeling of tumor-induced angiogenesis, J. Math. Biol. 49, 111–187, 2004. doi: 10.1007/s00285-003-0262-2; MR 2145689; Zbl 1109.92020; PMID: 15293017 [PubMed].
  • [26] M. O’Reilly, T. Boehm, Y. Shing, N. Fukai, G. Vasios, W. Lane, E. Flynn, J. Birkhead, B. Olsen, and J. Folkman, Endostatin: an endogenous inhibitor of angiogenesis and tumor growth, Cell 88, 277–285, 1997. doi: 10.1016/S0092-8674(00)81848-6; PMID: 9008168 [PubMed].
  • [27] M. O’Reilly, L. Holmgren, Y. Shing, C. Chen, R. Rosenthal, M. Moses, W. Lane, Y. Cao, E. Sage, and J. Folkman, Angiostatin: a novel angiogenesis inhibitor that mediates the suppression of metastases by a Lewis lung carcinoma, Cell 79, 315–328, 1994. doi: 10.1016/0092-8674(94)90200-3; PMID: 7525077 [PubMed].
  • [28] M. Piotrowska and U. Forys, Analysis of the Hopf bifurcation for the family of angiogenesis models, J. Math. Anal. Appl. 382, 180–203, 2011. doi: 10.1016/j.jmaa.2011.04.046; MR 2805506; Zbl 1109.92020.
  • [29] J. Poleszczuk, M. Bodnar, and U. Forys, New approach to modeling of antiangiogenic treatment on the basis of Hahnfeldt et al. model, Math. Biosci. Eng. 8, 591–603, 2011. doi:10.3934/mbe.2011.8.591; MR 2793501; Zbl 1259.34011; PMID: 21631148 [PubMed].
  • [30] J. Poleszczuk and U. Forys, Angiogenesis process with vessel impairment for Gompertzian and logistic type of tumour growth, Appl. Math.(Warsaw) 36, 313–331, 2009. doi:10.4064/am36-3-5; MR 2545966; Zbl 1184.92022.
  • [31] J. Poleszczuk and U. Forys, Derivation of the Hahnfeldt et al. model (1999) revisited, In Proceedings of the XVI National Conference Applications of Mathematics to Biology and Medicine, 87–92, 2010.
  • [32] J. Poleszczuk and I. Skrzypczak, Tumour angiogenesis model with variable vessels’ effectiveness, Appl. Math.(Warsaw) 38, 33–49, 2011. doi: 10.4064/am38-1-3; MR 2774269; Zbl 1221.92051.
  • [33] L. Preziosi, Cancer Modelling and Simulation, CRC Press, 2003.
  • [34] A. Swierniak, Comparison of six models of antiangiogenic therapy, Appl. Math.(Warsaw) 36(3), 333–348, 2009. doi: 10.4064/am36-3-6; MR 2545967; Zbl 1179.93101.
  • [35] A. Swierniak and A. d’Onofrio, Control problems related to tumor angiogenesis In IEEE Industrial Electronics-IECON2006, Paris, November 6-10, 677–681, 2006. doi:10.1109/IECON.2006.347815.
  • [36] A. Swierniak, G. Gala, A. d’Onofrio, and A. Gandolfi, Optimization of anti-angiogenic therapy as optimal control problem, In Proc 4th IASTED Conf. on Biomechanics, ACTA Press (ed. M. Doblar´e), 56–60, 2006.
Typ dokumentu
Bibliografia
Identyfikator YADDA
bwmeta1.element.baztech-d28c9b6f-dad3-4b72-acba-03b4cf47d206
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