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STRESS-INDUCED MODULATION OF THE TUMOR MICROENVIRONMENT: MECHANISMS AND IMPLICATIONS FOR CANCER PROGRESSION.

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Area of Science:

  • Oncology
  • Neuroendocrinology
  • Immunology

Background:

  • Chronic stress significantly impacts tumor cell biology and the tumor microenvironment (TME).
  • Stress activates the hypothalamic-pituitary-adrenal axis and sympathetic nervous system, releasing glucocorticoids and catecholamines.
  • These neuroendocrine mediators disrupt TME components, influencing malignant neoplasm aggressiveness.

Purpose of the Study:

  • To review the impact of stress-induced signals on the TME's immune, stromal, vascular, and metabolic aspects.
  • To analyze how these TME alterations contribute to an aggressive tumor phenotype.
  • To explore the interplay between neurohumoral stress, the gut, and the intratumoral microbiome in tumor progression.

Main Methods:

  • Systematic review of current scientific literature.
  • Analysis of molecular interactions between stress mediators and TME cellular elements.
  • Investigation of the neuroendocrine-gut-microbiome axis in cancer.

Main Results:

  • Stress mediators significantly alter immune surveillance, stromal remodeling, vascularization, and metabolism within the TME.
  • The gut microbiome and neurohumoral stress pathways form a complex network that supports tumor growth and aggressiveness.
  • Deregulation of TME components by stress hormones is a key factor in promoting malignant processes.

Conclusions:

  • Stress significantly influences the TME, driving tumor progression and aggressiveness.
  • Targeting stress-induced pathways and their effects on the TME offers novel therapeutic opportunities.
  • Further understanding of molecular interactions is crucial for developing innovative cancer treatments that mitigate stress-related adverse effects.