In a recent PLoS One study, perhaps the first in the area of hematological tumors, and specifically leukemia, Shelly Inbar and colleagues from the Neuroimmunology Research Unit, Department of Psychology, Tel Aviv University, Israel, demonstrate marked adverse effects of stress hormones and prostaglandin E2 (PGE2) on survival rates of leukemic animals.
An increasing body of evidence indicates that psychological stress might be linked to the onset, expression or progression of several human malignancies such as tumors of the breast, skin, reproductive system and the gastrointestinal tract.
It appears that the activation of the sympathetic nervous system (SNS) and the hypothalamic–pituitary–adrenal (HPA) axis play a central role in cancer progression, through suppression of cell-mediated immunity and/or through direct effects of catecholamines and prostaglandins (PGs) on tumor growth.
To date, these issues have not been directly addressed in the context of leukemia.
In the PLoS One study the authors report that in rats already bearing leukemia (for two or six days) exposure to a combination of epinephrine and corticosterone significantly decreased survival rates. When these stress hormones were administered simultaneously with leukemia cells, an approximate 3-fold decrease in survival rates was evident. PGE2 and epinephrine by themselves caused similar effects, while corticosterone alone had smaller and non-significant effects.
Furthermore, a short paradigm of swim stress markedly reduced survival rates of the CRNK-16 challenged rats, whereas a prolonged administration of the beta-blocker nadolol or the COX inhibitor indomethacin significantly improved survival rates.
Previous research indicates that patients undergoing treatment for hematological malignancies experience high levels of anxiety and depression, and that these two psychological factors are strongly linked to profound cellular immunity suppression through the release of stress hormones.
Thus, as discussed by the authors, this study provides further insights into stress-tumor interactions, and underlines the importance of considering stress responses in the clinical setting of leukemia treatment, specifically addressing the potential beneficial effects of beta-blockers and COX inhibitors.