Tumor growth is a fundamental scientic and societal problem. While
much work has been done in the mathematics community on tumor
modeling, the state-of-the-art in modeling and numerical simulation
lags behind the current understanding of the biophysical processes.
From a materials science perspective, a cancerous tumor is a
complex, multiscaled material. There can be strong nonlinear coupling
between the nanoscale (genetics), the microscale (cell-signals)
and the macroscale (tumor mass).
The goal of our work is to develop a mathematically rigorous, and
biologically-justified model of solid tumors that is capable
of describing growth through all the known phases of evolution
from avascular multicell spheriods to angiogenesis to invasion of malignant
tumors.
Tumor growth and tumor-induced angiogenesis
Case 1. Vessels are initiated randomly about 200 microns from the tumor
to mimic tumor-induced angiogenesis from a dense background
of microvasculature. The random initiation is biased by
the level of tumor angiogenic factors (e.g., vascular endothelial
cell growth factor, VEGF). The tumor grows in a compact shape
because of the nearly isotropic neovasculature distribution.
Case 2. Vessels are initiated randomly about 200 microns from the tumor
to mimic tumor-induced angiogenesis from a dense background
of microvasculature. The random initiation is biased by
the level of tumor angiogenic factors (e.g., vascular endothelial
cell growth factor, VEGF). The difference between this and
the above simulation is that here, vessels are crushed by the
proliferation pressure induced by the tumor. As a result, both
the vessels and the tumor regress periodically. Effectively, this
induces nearly periodic angiogenic cycles as the regression is
associated with increased release of tumor angiogeneic factors.
More details, results and images coming soon...
Collaborators:
Vittorio Cristini UT Health Sci. Center at Houston, M.D. Anderson Cancer Center
Steven Wise UT Knoxville
Fang Jin UC Irvine
Yao-Li Chuang UTHSCH
Herman Frieboes UCI