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December 22, 2009
Physiological Stress Response: Molecular Basis and Clinical Implications
Raghavendra Rao
Senior Scientist Clinical Research and Head CAM Program,
HCG Bangalore Institute of Oncology, Bengaluru, India
raghav.hcgrf@gmail.com
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Abstract
Stress that seems to affect us is not just limited to the Brain and Behaviour but has its influence deep down to our genes. The increasing incidence of ageing related diseases such as diabetes, ischemic heart disease, autoimmune diseases, cancers etc point to the alterations in our gene expressions and consequent cellular metabolism and homeostasis that causes disease.
Studies have shown that both acute and chronic stressors that activate the HPA and SAM axis also influence genes that regulate cell cycle, maintain cell integrity, modulate immune senescence, maintain immune memory, cause angiogenesis, promote progression of cancers and metastases etc. Be it diabetes or cancers inflammation remains a critical pathway by which cell destruction and repair homeostasis can go haywire leading to the above said conditions.
The physiologic stress response (PSR) can have heterogeneous effects in a variety of cancers. It is therefore important to understand which, i) endocrine and neurobiological molecules mediate effects of stressors on tumor biology, ii) characterize specific aspects of tumor biology that are affected by the PSR, iii) Understand the biological influence of the PSR on the cancer continuum, iv) assess the effects of ageing on immune senescence and physiological homeostasis and finally v) identify molecular pathways by which behavioral or pharmacological interventions can protect against the deleterious effects of the PSR on tumor biology.
Understanding these mechanisms will provide new insights into treatment of these chronic inflammatory conditions.