Biology Reference
In-Depth Information
When growth stops, it is quite simply because the system has
reached a state of equilibrium in respect of the quantitative values
of its parameters. Disruption to the overall equilibrium of the
system leads to proliferation being resumed.
To illustrate this we performed another simulation experiment.
In the first instance, we allowed a bilayer of stabilised cells to form
until it stopped growing (Fig. 26A). Then we modified the value
of one parameter involved in cell autostabilisation (the parameter
C
0
of the function that determines the probability of a cell chang-
ing its type; see the caption for Fig. 23). We progressed gradu-
ally until we found the limit which destabilises the structure
without destroying it completely. As can be seen in Fig. 26, we
found ourselves looking at localised limited resumption of prolif-
eration, by cell budding from the bilayer. This resumption of
proliferation, which can be produced at different locations on the
bilayer depending on its shape, creates cell masses which are
released into the environment (Figs. 26B, C, D). Similar results
can be obtained if other parameters are modified, for example,
those affecting the quantities of molecules present in the cell
environment.
This simulation experiment suggests that cancer may arise from
such disruption to the equilibrium between the selective action of
the microenvironment and that of autostabilisation of the cell
types, i.e. the stochastic expression of the underlying genes on
which the synthesis of the molecules
a
and
b
in the model implic-
itly depends. In an actual organism, the action of a carcinogenic
agent which fixes on a protein could modify its properties of diffu-
sion into the tissues or its fixing on the DNA. Modifications such
as these would lead in turn to upsetting the concentrations of this
molecule in the tissues or destabilisation of the expression of genes,
resulting in imbalance permitting cell proliferation to resume. This
conception of control of proliferation does not mean that DNA
mutation has no role to play
per se
. Such mutation could produce
identical effects by modifying the properties of a protein.
Obviously a real organism is much more complicated than our
cell bilayer and disruption of the equilibrium of this nature could
