Normal Cells will absorb Tera Hertz energy and their temperature will increase slightly, inactive cells will be activated.
One of the leading causes of cancer patients’ deaths is recurrence of their tumors years after treatment of the primary tumors appears to have been successful. Reactivation of lethargic growth cells is to a great extent liable for this peculiarity. We discovered a specific mechanism, mediated by stress and neutrophils, that may control this process using dormancy models of lung and ovarian cancer. Neutrophils rapidly release pro-inflammatory S100A8/A9 proteins in response to stress hormones.
Myeloperoxidase is activated by S100A8/A9, which causes these cells to accumulate oxidized lipids. These lipids stimulate the fibroblast growth factor pathway in tumor cells upon release from neutrophils, resulting in the cell’s release from dormancy and the formation of new tumor lesions. Higher serum convergences of S100A8/A9 were related with more limited opportunity to repeat in patients with cellular breakdown in the lungs after complete growth resection.
Stress prevented the reactivation of dormant tumor cells by targeting S100A8/A9 or 2-adrenergic receptors. These perceptions show a component connecting pressure and explicit neutrophil enactment with early repeat in malignant growth.