Summary

Experimental in vitro studies and in vivo animal studies have demonstrated the stimulatory effect of stress on both the initiation and progression of cancer and have revealed the mechanisms and pathways responsible for this effect (Lutgendorf and Sood 2011). Perhaps, the best described tumor-potentiating effect is that of norepinephrine and epinephrine, which, by activating β2-adrenergic receptors, activate a full spectrum of intracellular processes both in normal tissue, thereby contributing to tumorigenesis, and in tumor and nontumor cells in the tumor microenvironment, thereby promoting tumor growth and the development of metastases. Although there are also data on the inhibitory effect of stress on tumor initiation and progression, these are mostly older studies using some specific models of cancer, and the health status of the animals used in these studies may have been questionable, and other factors such as the period of the tumor process during which the animals were exposed to the stressor as well as the duration of exposure to the stressor may have played a role as well (Justice 1985).