Additional Documents │ Page 223 threshold while simultaneously triggering stress response pathways linked to ICD; (iii) fundamental questions remain regarding NTP’s immunomodulatory e ects, particularly on key immune checkpoints (e.g., PD-1/PD-L1, CTLA-4, and LAG-3) and the direct influence on immune cells within the TME. These opportunities are further explored in review chapter 5, with a focus on intercellular communication via gap junctions. Herein, I provided an extensive overview of their complex role in cancer, demonstrating both pro- and anti-tumoral e ects. In addition, the therapeutic potential of targeting gap junctions and their vulnerability to reactive species (ROS) is discussed, while also exploring combinatorial strategies, e.g. combining selective connexin or gap junction modulation with redox-based therapies like NTP, to enhance anti-cancer e icacy. Besides these research aspects, also technical advancement like treatment standardization and sophisticated application tools will be required to integrate NTP into clinical immunotherapy approaches. Taken together, in this thesis, I established NTP as a potent immunogenic adjuvant to standard cancer therapies, with broad implications for enhancing innate and adaptive immune responses. The ability of NTP to sensitize tumors to chemotherapy, modulate immune ligands, and improve anti-tumor immunity positions it as a promising candidate for clinical translation in an adjuvant setting for patients in high need of additional treatment options.
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