must fail for tumorigenesis to proceed. It is well known that processes of
DNA repair (e.g. [40, 46]), programmed cell death - apoptosis - (e.g. [19]),
and immune surveillance (e.g. [26, 47]) all act to redress cell mutation. The
immune system is known to be cognitive, and equipped with an array of pos-
sible remediations [3, 12]. It is, then, possible to infer a larger, jointly-acting
‘mutation control’ process incorporating these and other cellular, systemic,
and social mechanisms. This clearly must involve comparison of develop-
ing cells with some internal model of what constitutes a ‘normal’ pattern,
followed by a choice of response: none, repair, programmed cell death, or
full-blown immune attack. The comparison with an internal picture of the
world, with a subsequent choice from a response repertoire, is, as [15, 31]
point out, the essence of cognition.
We are, then, led to propose, in the sense of [56, 57] that a mutual
information may be defined characterizing the interaction of a structured
system of external selection pressures with the ‘language’ of cellular cognition
effecting mutation control. Under the Joint Asymptotic Equipartition or
Rate Distortion Theorems, that mutual information constitutes a splitting
criterion for pairwise linked paths which may itself be punctuated and subject
to sudden phase transitions.
We thus speculate that structured external stress can become jointly and
synergistically linked both with cell mutation and with the cognitive process
which attempts to redress cell mutation, enhancing the former, degrading the
latter, and significantly raising the probability of successful tumorigenesis.
Elsewhere [54] we argue that the staged nature of chronic infectious dis-
eases like malaria, HIV, and tuberculosis represents an information-dynamic
punctuated version of biological interpenetration, in the sense of [33], be-
tween a cognitive ‘immunocultural condensation’ and an adaptive pathogen.
Here we suggest that a larger system of socio-cellular cognition related to the
detection and correction of mutation forms an embedding context of adap-
tation pressures for mutating clones of defective cells (e.g. [8]). Subsequent
learning plateau-analog phase transitions of evolutionary punctuation, in the
sense of [57], constitute the many stages of cancer.
Psychosocial stress and tumorigenesis
As we discuss elsewhere [56, 57], structured psychosocial stress consti-
tutes a determining context for immune cognition or, more generally, the
immunocultural condensation. Here we enlarge the perspective to processes
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