angiogenesis, vascular growth. We conjectured about it, in a previ-
ous work [35], where apparent fluctuations related to the joint
action of the host and immune system on tumor cells may cause
an adverse outcome causing a type of stochastic resonance effect.
This leads to a change in the fractal dimension of the tumor
interface and consequently a certain number of active cells in the
tumor interface could escape which could lead to vascular growth.
It is an acceptable explanation of why a tumor in a latent phase,
stationary state [36], can go to a critical state, reach macroscopic
dimensions, vascular phase, and subsequently invade distant
organs, metastasis, despite actions of the immune system, and the
host [37, 38].
It is important to note that whereas it is possible to predict
when tumors reach latency, as in a first approximation occurs, it is
virtually impossible to predict when a tumor metastasizes [39],
given the highly random character of the action of the immune
system and the host.
In the vascular phase, the tumor acquires macroscopic dimen-
sions, invading much of the host and adjacent organs, that is to say,
the nonequilibrium self-organized tumor system acquires a higher
level of hierarchy and apparently robust as it is known that in most
cases after surgical removal there of, micro-metastasis is found [40].
The process of metastasis [41] appears abruptly as a reminiscent
of hard, first-order transitions, in these cases, the chances of survival
are lower compared to the previous stages, because they exhibit a
higher robustness and a higher level of hierarchy. The tumor now
competes with the different levels of hierarchical and functional
organization of the body (those which play vital roles), so it is
considered like a cancer tumor, given its ability to metastasize [42].
The pioneering work of Prigogine and Lefever [43], consider-
ing the stability of tumor growth in the presence of cytotoxic cells,
revealed that cancer growth can be described by a phase transition,
like a second-order phase transition. Moreover, Delsanto et al. [44]
developed a dynamical system model for the analysis of phase
transition from tumor growth to latency, while Sole ́showed that
tumors have a behavior close to a limit of instability, as well as the
tumor cell populations [45]. Davies et al. [46] argued that the
transition from health cells to malignant cells can be described by
a phase transition of the first order.
In order to describe the dynamics of avascular process based
empirically on the evidence discussed above, we have proposed the
following heuristic mechanism [21] sustained by a chemical net-
work modelðÞ 1 Nþx! 2 x
ðÞ 2 2 x!ncp
ðÞ 3 Hþx!ncp134 Sheyla Montero et al.