Geodesic
Modeling the Cancer Stem Cell Hypothesis
C. Calmelet1 ; A. Prokop2 ; J. Mensah3 ; L. J. McCawley4 ; P. S. Crooke5
1 Department of Mathematics and Statistics, California State University Chico
2 Department of Chemical Engineering ,Vanderbilt University
3 Department of Chemistry, Tennessee State University
4 Department of Cancer Biology, Vanderbilt University
5 Department of Mathematics, Vanderbilt University
Mathematical modelling of natural phenomena, Tome 5 (2010) no. 3, pp. 40-62

Voir la notice de l'article provenant de la source EDP Sciences

Solid tumors and hematological cancers contain small population of tumor cells that are believed to play a critical role in the development and progression of the disease. These cells, named Cancer Stem Cells (CSCs), have been found in leukemia, myeloma, breast, prostate, pancreas, colon, brain and lung cancers. It is also thought that CSCs drive the metastatic spread of cancer. The CSC compartment features a specific and phenotypically defined cell population characterized with self-renewal (through mutations), quiescence or slow cycling, overexpression of anti-apoptotic proteins, multidrug resistance and impaired differentiation. CSCs show resistance to a number of conventional therapies, and it is believed that this explains why it is difficult to completely eradicate the disease and why recurrence is an ever-present threat. A hierarchical phenomenological model is proposed based on eight compartments following the stem cell lineage at the normal and cancer cell levels. As an empirical test, the tumor grading and progression, typically collected in the pathologic lab, is used to correlate the outcome of this model with the tumor development stages. In addition, the model is able to quantitatively account for the temporal development of the population of observed cell types. Two types of therapeutic treatment models are considered, with dose-density chemotherapy (a pulsatile scenario) as well as continuous, metronomic delivery. The drug hit is considered at the stem cell progenitor and early differentiated specialized cell levels for both normal and cancer cells, while the quiescent stem cell and fully differentiated compartments are considered favorable outcome for cancer treatment. Circulating progenitors are neglected in this analysis. The model provides a number of experimentally testable predictions. The relative importance of the cell kill and survival is demonstrated through a deterministic parametric study. The significance of the stem cell compartment is underlined based on this simulation study. This predictive mathematical model for cancer stem cell hypothesis is used to understand tumor responses to chemotherapeutic agents and judge the efficacy.
DOI : 10.1051/mmnp/20105304

C. Calmelet 1 ; A. Prokop 2 ; J. Mensah 3 ; L. J. McCawley 4 ; P. S. Crooke 5

1 Department of Mathematics and Statistics, California State University Chico
2 Department of Chemical Engineering ,Vanderbilt University
3 Department of Chemistry, Tennessee State University
4 Department of Cancer Biology, Vanderbilt University
5 Department of Mathematics, Vanderbilt University 
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C. Calmelet; A. Prokop; J. Mensah; L. J. McCawley; P. S. Crooke. Modeling the Cancer Stem Cell Hypothesis. Mathematical modelling of natural phenomena, Tome 5 (2010) no. 3, pp. 40-62. doi: 10.1051/mmnp/20105304

[1] R.W. Cho, X. Wang X, M. Diehn, K. Shedden, Gy Ghen, G Sherlock, A Gurney, J Lewicki, Mf Clarke Isolation and molecular characterization of cancer stem cells in MMTV-Wnt-1 murine breast tumors Stem Cells 2008 364 71

[2] J. Demongeot, M. Kaufman, R. Thomas Positive feedback circuits and memory C. R. Acad. Sci. III. 2000 69 79

[3] D. Dingli, A. Traulsen, J. Pacheco Stochastics Dynamics of Hematopoietic Tumor Stem Cells Cell Cycle 2007 461 466

[4] V.S. Donnenberg, R.J. Landreneau, A.D. Donnenberg Tumorigenic stem and progenitor cells: implications for the therapeutic index of anti-cancer agents Journal Control Release 2007 385 91

[5] H. Enderling, M. A. Chaplain, A.R. Andersona, J. S. Vaidyab A mathematical model of breast cancer development, local treatment and recurrence Journal of Theoretical Biology 2007 245 259

[6] D. Fang, T. K. Nguyen, K. Leishear, R. Finko, A. N. Kulp, S. Hotz, P. A. Van Belle, X. Xu, D. E. Elder, M. Herlyn A tumorigenic subpopulation with stem cell properties in melanomas Cancer Res. 2005 9328 37

[7] M. Freeman, J.B. Gurdon Regulatory principles of developmental signaling Annu. Rev. Cell. Dev. Biol. 2002 515 39

[8] R. Ganguly, I.K. Puri Mathematical model for the cancer stem cell hypothesis Cell Prolif. 2006 3 14

[9] R. Ganguly, I.K. Puri Mathematical model for chemotherapeutic drug efficacy in arresting tumour growth based on the cancer stem cell hypothesis Cell Prolif. 2007 338 54

[10] R.P. Hill Identifying cancer stem cells in solid tumors: case not proven Cancer Res. 2006 1891 5

[11] M.D. Johnston, C.M. Edwards, W.F. Bodmer, P.K. Maini, S.J. Chapman Mathematical modeling of cell population dynamics in the colonic crypt and in colorectal cancer Proc. Natl. Acad. Sci. 2007 4008 13

[12] E.A. King-Smith, A. Morley Computer simulation of granulopoiesis: normal and impaired granulopoiesis Blood. 1970 254 62

[13] B. Laquente, F. Viűals, J.R. Germĺ Metronomic chemotherapy: an antiangiogenic scheduling Clin. Transl. Oncol. 2007 93 8

[14] M. Leszczyniecka, T. Roberts, P. Dent, S. Grant, P.B. Fisher Differentiation therapy of human cancer: basic science and clinical applications Pharmacol Ther. 2001 105 56

[15] I. Malanchi, J. Huelsken Cancer Stem cells: never Wnt away from the niche Current Opinion in Oncology 2008 41 46

[16] J.A. Marchal, F. Rodršguez-Serrano, R. Madeddu, H. Boulaiz, A. Martinez-Amat, E. Carrillo, O. Caba, J.C. Prados, C. Velez, C. Melguizo, A. Montella, A. Aranega Differentiation: an encouraging approach to anticancer therapy J. Anat. Embryol. 2006 45 64

[17] F. Michor, T.P. Hughes, Y. Iwasa, S. Branford, N. P. Shah, C. L. Sawyers, M. A. Nowack Dynamics of Chronic Myeloid Leukaemia. Nature 2005 1267 1270

[18] J.A. Nilsson, J.L. Cleveland Myc pathways provoking cell suicide and cancer Oncogene. 2003 9007 21

[19] A.B. Pardee Regulatory molecular biology Cell Cycle. 2006 846 52

[20] A.B. Pardee Tumor progression–targets for differential therapy J. Cell Physiol. 2006 589 91

[21] I. Roeder, M. Horn, I. Glauche, A. Hochlaus, M. C. Mueller, M. Loeffler Dynamic modeling of imatinib-treated chronic myeloid leukemia: functional insights and clinical implications Nature Medicine 2006 1181 1184

[22] T. Schatton, N.Y. Frank, M.H Frank Identification and targeting of cancer stem cells Bioessays 2009 1038 49

[23] R. Thomas Laws for the dynamics of regulatory networks Int. J. Dev. Biol. 1998 479 85

[24] M.J. Tindall Modelling the cell cycle and cell movement in multicellular tumour spheroids Bull. Math. Biol. 2007 1147 65

[25] W. C. Lo, C. S. Chou, K. K. Gokoffski, F. Y. Wan, A.D. Lander, A. L. Calof, Q. Nie Feedback regulation in multistage cell lineages Math. Biosci. Eng. 2009 59 82

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