Anna Konstorum

Research Data Scientist

Predicting mechanism of biphasic growth factor action on tumor growth using a multi-species model with feedback control.


Journal article


A. Konstorum, S. Sprowl, M. Waterman, A. Lander, J. Lowengrub
Journal of coupled systems and multiscale dynamics, 2013

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APA   Click to copy
Konstorum, A., Sprowl, S., Waterman, M., Lander, A., & Lowengrub, J. (2013). Predicting mechanism of biphasic growth factor action on tumor growth using a multi-species model with feedback control. Journal of Coupled Systems and Multiscale Dynamics.


Chicago/Turabian   Click to copy
Konstorum, A., S. Sprowl, M. Waterman, A. Lander, and J. Lowengrub. “Predicting Mechanism of Biphasic Growth Factor Action on Tumor Growth Using a Multi-Species Model with Feedback Control.” Journal of coupled systems and multiscale dynamics (2013).


MLA   Click to copy
Konstorum, A., et al. “Predicting Mechanism of Biphasic Growth Factor Action on Tumor Growth Using a Multi-Species Model with Feedback Control.” Journal of Coupled Systems and Multiscale Dynamics, 2013.


BibTeX   Click to copy

@article{a2013a,
  title = {Predicting mechanism of biphasic growth factor action on tumor growth using a multi-species model with feedback control.},
  year = {2013},
  journal = {Journal of coupled systems and multiscale dynamics},
  author = {Konstorum, A. and Sprowl, S. and Waterman, M. and Lander, A. and Lowengrub, J.}
}

Abstract

A large number of growth factors and drugs are known to act in a biphasic manner: at lower concentrations they cause increased division of target cells, whereas at higher concentrations the mitogenic effect is inhibited. Often, the molecular details of the mitogenic effect of the growth factor are known, whereas the inhibitory effect is not. Hepatoctyte Growth Factor, HGF, has recently been recognized as a strong mitogen that is present in the microenvironment of solid tumors. Recent evidence suggests that HGF acts in a biphasic manner on tumor growth. We build a multi-species model of HGF action on tumor cells using different hypotheses for high dose-HGF activation of a growth inhibitor and show that the shape of the dose-response curve is directly related to the mechanism of inhibitor activation. We thus hypothesize that the shape of a dose-response curve is informative of the molecular action of the growth factor on the growth inhibitor.