Effects on DNA Damage and/or Repair Processes as Biological Mechanisms Linking Psychological Stress to Cancer Risk

Abstract

Considerable research effort in the past several decades has focused on the impact of psychological stress, and stress hormones, on cancer progression. Numerous studies have reported that stress hormone treatment or in vivo stress exposure can enhance the growth of tumor cell lines in vitro, as well as tumors in animal models, and have begun to explore molecular mechanisms. Comparatively little research has focused on the impact of psychological stress and stress hormones on cancer initiation, in part due to inherent methodological challenges, but also because potential underlying biological mechanisms have remained obscure. In this review, we present a testable theoretical model of pathways by which stress may result in cellular transformation and tumorigenesis. This model supports our overarching hypothesis that psychological stress, acting through increased levels of catecholamines and/or cortisol, can increase DNA damage and/or reduce repair mechanisms, resulting in increased risk of DNA mutations leading to carcinogenesis. A better understanding of molecular pathways by which psychological stress can increase the risk of cancer initiation would open new avenues of translational research, bringing together psychologists, neuroscientists, and molecular biologists, potentially resulting in the development of novel approaches for cancer risk reduction at the population level.

Multi-Systemic Biological Risk and Cancer Mortality: The NHANES III Study

“…With cancer being the second leading cause of death in the U.S. and globally, having shifting underlying contributors to this burden 28-30 , a prospective analysis examining the association of an index of MSBR with cancer mortality would address a major gap in the literature. It would also allow for the ability to triangulate population-level evidence with in vivo and in vitro studies of stress and cancer outcomes 14,31,32 . Furthermore, it may also have clinical utility for cancer prediction, as the index relies upon commonly measured biomarkers to address this gap.…”

Activation of the anti‐inflammatory reflex blocks lipopolysaccharide‐induced decrease in synaptic inhibition in the temporal cortex of the rat

“…The peripheral and central nervous systems communicate with a dense, complex, and largely unknown network of biochemical interactions (Hosoi et al, ; Müller et al, ). Whereas several studies have focused on the ability of the CNS to produce peripheral ailments (Dhabhar, ; Jenkins et al, ), this study sought to determine whether the peripheral reduction of inflammation mitigates the central effects of LPS‐induced systemic stress. We have previously shown that aseptic inflammation as well as other stressors may lead to a decrease in the sI/E ratio in the TC (Garcia‐Oscos et al, ).…”

Psychoneuroimmunology of Cancer – Recent Findings and Perspectives

“…Ďalšie práce preukázali, že noradrenalín zvyšuje tvorbu kyslíkových radikálov a že noradrenalín, adrenalín a kortizol poškodzujú DNA a znižujú účinnosť reparačných procesov v bunkovom jadre [47,51,52].…”