Chronic stress increases metastasis via neutrophil-mediated changes to the microenvironment
Stress is a known contributor to shorter survival after cancer treatment. Reasons for this have been unclear. Now, recent research using a mouse model has identified a possible mechanism by which this occurs.
All cancer patients face increased stress either through anxiety about outcomes or associated problems, such as loss of income and mobility. This stress activates the hypothalamic-pituitary-adrenal pathway with consequent increase in circulating steroid hormones.
An elevated neutrophil/lymphocyte ratio in circulating blood plasma is one of the physiological effects of stress. The neutrophils normally act to form traps for extracellular pathogens such as bacteria. A similar process will trap cancer cells, with implantation at remote sites and consequent metastasis.
Knowing the importance of stress will enable early intervention to mitigate the effect.
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