Biology Reference
In-Depth Information
proliferate. This means that cells ceasing to multiply is the result
of the joint action of mechanisms of interdependence for prolifera-
tion, i.e. selection and autostabilisation. Interdependence prevents
the multiplication of cells that lack substrate because they are too
far away from the source of it, whilst autostabilisation fixes these
cells as the type they have acquired and prevents growth of the
other cell type.
Through this combined action of the two mechanisms, continu-
ation of overall growth of the structure is inhibited. We have
checked the relevance of this analysis by alternately deleting
autostabilisation and interdependence of cells for proliferation from
the model. In both situations total loss of the properties of organi-
sation is observed. Cells no longer cease proliferating spontaneously.
This produces infinitely alternating areas of RED and GREEN cells
which are only restricted by the size of the matrix (Fig. 27C). In as
far as the two processes of interdependence and autostabilisation
themselves depend on the quantitative value of all the parameters
of the model, growth arrest is the result of equilibrium between the
values of these parameters. If we distort these values one by one, it
is possible to induce a loss of organisation properties in the bilayer.
Figure 27A shows the example of distortion of the speed of diffu-
sion. Here, the cell population is again growing infinitely with cells
of the RED and GREEN types overlapping.
6.4.4
A new conception of cancer
The results of the simulations suggest cancer could be seen in a new
light. In conventional theory, the genetic programme not only reg-
ulates the differentiation of cells through the signals it emits but
also their proliferation. The multiplication of a cell is activated or
inhibited by appropriate signals. In the Darwinian model, the func-
tioning logic is quite different. There is no difference between the
cell system in a state of growth and the quiescent system which
might be connected with the action of a signal controlling multipli-
cation. In the simulations, the cells cease to proliferate sponta-
neously without any functioning rule for the model stipulating this.
