plateaus’ [57] representing the punctuated interpenetration between muta-
tion control and clones of mutated cells constitute the stages of disease.
Such stages arise in the context of an embedding culture which, to use a
Rate Distortion argument, literally writes an image of itself on all aspects of
the disease.
The synergistic effects of structured external stress on both mutation
and the selection pressure facing mutated cell clones implies that reduc-
tionist magic bullets and ‘life style’ approaches will be of severely limited
effect for marginalized human populations in the absence of highly proactive
socioeconomic, political, and related interventions. Cancer plays a multidi-
mensional chess across interacting levels of biological and social organization.
To counter cancer, we’ll need to play the same. Only in the full context of
such broad ‘biological control’ can individual-oriented strategies contribute
significant impact.
‘Social exposures’ are far more than incidental cofactors in tumorigene-
sis: adapting Boyd’s aphorism, we claim that ‘culture is as much a part of
hormonal cancer as are oncogenes’.
Our speculations are consistent with, but suggest extension of, a growing
body of research. Kiecolt-Glaser et al. [31], for example, discuss how chronic
inflammation related to chronic stress has been linked with a spectrum of con-
ditions associated with aging, including cardiovascular disease, osteoporosis,
arthritis, type II diabetes, certain cancers, and other conditions. Dalgleish
and others [15, 16, 38, 41] have argued at length that chronic immune activa-
tion and inflammation are closely related to the etiology of cancer and other
diseases. As Balkwill and Mantovani [4] put the matter, “If genetic damage
is the ‘match that lights the fire’ of cancer, some types of inflammation may
provide ‘fuel that feeds the flames’ ”.
Dalgleish [15] has suggested application of non-linear mathematics to ex-
amine the role of immune response in cancer etiology, viewing different phe-
notypic modes of the immune system - the Th1∕Th2 dichotomy - as ‘attrac-
tors’ for chaotic processes related to tumorigenesis, and suggests therapeutic
intervention to shift from Th2 to Th1. We view such a shift in phenotype as
a phase transition.
Our analysis implies a complicated and subtle biology for human can-
cer, one in which external cultural ‘messages’ become convoluted with both
pathogenic clone mutation and with an opposing, and possibly organ-specific,
variety of tumor control strategies. In the face of such a biology, anti-
inflammants [13] and other ‘magic bullet’ interventions appear inadequate,
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