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Host Resistance in Cancer
Host resistance is popularly thought of as being due only to immunity. Rather multiple factors, both exogenous and endogenous, contribute to host resistance in a dynamic, interacting network or system with many components, including the central and autonomic nervous systems, the endocrine system, immunity, neuropeptides, growth factors, nutrition, and probably other, as yet unknown, components. Behavioral factors also play a role by acting as biologic response modifiers. Some of the lifestyle factors that provide for cancer risk interfere with these mechanisms of host resistance.
| The current paradigm for host resistance has the ungainly name of psychoneuroimmunology (PNI). In this general systems model, tumor and host cells interact within a microenvironment where cytokine/receptor interactions play a key part in mediating regulation of cellular interactions or relationships through molecular information flow by way of immune, hormonal and neural intercommunication. This is a homeostatic model of the interaction between a host and a tumor (or an infectious agent) which is based on a dynamic balance between it and the host microenvironment in which it grows. This updated version of the seed-and-soil hypothesis. |  |
Despite the genetic alterations that lead to malignant transformation the outcome of a tumor’s growth still depends on its interaction with host defenses for a net result in terms of progression, dormancy, or regression. All of the various components that go to make up host resistance share chemical mediators, which through their receptor-transmitter interactions and signaling produce complex dynamic patterns of information flow and communication, both intercellular (tumor-tumor, host-host, host-tumor) and intracellular (between the plasma membrane and the nucleus of the individual cell). Impaired host resistance in both malignant and infectious diseases seems to be a regulatory problem resulting in collapsed homeostasis and based on a breakdown of molecular communication. The locus of these events is the cell surface where transmitter-receptor interactions take place.
Behaviour is a biological response modifier. The psychosomatic basis of host resistance results from the enhancement or suppression of PNI function by attitudes and beliefs through the emotions these elicit. Thus the "tone" of host resistance may be influenced by mental and emotional states determined by the cognitive map of reality (values and belief systems) in an individual’s mind.
(See Jerry M (1996) Psychoneuroimmunology. Chapter 87, pp1731-1745 in Greger R & Windhorst U (Eds.) Comprehensive Human Physiology, Vol 2, Springer-Verlag, Berlin.)
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