Chalmers Conferences, 9th European Conference on Mathematical and Theoretical Biology

Find the Glass Phase Transition Properties in a multi-cell model for tumorogenesis
Yuting Lou

Last modified: 2014-03-31


This research focuses on the design of a computational model for a multi-cell system and an original understanding of cancer initiation from the perspective of glass phase transition. Since the cancer is considered to be a disease resulting from both the genetic deficiency and system dysfunction, it may well be a multi-scale emergent phenomenon. If a cell can be viewed as a correlation of molecules outside and inside it, the initiation of tumor can be understood as an everlasting stronger correlation throughout the time and space, which is a typical feature of glass phase transition. Therefore, my goal is to find the control parameter and calculate dynamic susceptibility in this system in order to prove the conjecture that the cancer initiation is a process of glass phase transition.

In this study, I set up a framework to investigate the phase transition property of tumorogenesis. The model includes three dynamics, namely the micro-environment, cell membrane receptors and inner cell signaling pathway. Different dynamics have interplay among each other: the receptor dynamics is decided by a cell cycle function which evolves along with the inner cell genetic modes; and the receptor dynamics will decide the cell behavior which will cause the change of micro-environment. A distinct feature of my model is that genetic modes inside every cell is modeled by a coarse-grained Boolean representation of signaling pathways that control whether the growth, proliferation, R-point, G2 checkpoint, and adhesion of a cell is dysfunctional. The effectiveness of model system is demonstrated through a series of simulations of the process for the system to reach different equilibrium states, representing the wound healing scenario as well as the tumorogenesis.


glass phase transition; tomorogenesis; signaling pathway;