Abstract
Psychosocial stressors can modulate the different stages of neoplastic events. It is established that there is activation of 2 well-known stress axes under stress, the hypothalamic-pituitary-adrenal axis and sympatho-adrenal-medullary axis, where especially the proliferating promoting effects on the malignant tumor events are known to depend on β-adrenergic receptors. A new model focuses on the positive activating stress, which leads through the activation of the sympathetic hypothalamic-adipocyte axis to inhibition of tumor growth and reduction of obesity. This leads in mice to increased gene expression of the neurotrophin BDNF, which activates the sympathetic fibers of the white adipose tissue. Over consecutive stimulation of the β-adrenergic receptors and thus the release of leptin, its promotional effect on the tumor growth is inhibited. In the clinical context, these results support the role of complex β-adrenergic signal transduction pathways.
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