Approximately half of all cancer patients receive radiotherapy, resulting in an overall increase in survival. FLASH radiotherapy has been demonstrated to benefit patients due to significant normal tissue sparing, thus enhancing the therapeutic window. Similarly, targeting cellular signaling pathways in conjunction with advanced radiotherapy modalities is not just beneficial for patients undergoing radiotherapy but can also be exploited to achieve radioprotection. For example, combining DNA repair inhibitors with low LET radiation has resulted in the development of several cancer drugs, whilst inhibiting radiation-induced damage to tissues. Therefore, radiobiological studies targeting cellular signaling with low and high LET radiation at FLASH or conventional dose rate will open new avenues in cancer biology. Modulation of DNA repair signaling pathways with pharmaceutical agents can further potentiate the development of radioprotectors and radiation countermeasures.
In this research topic, we aim to showcase the current research highlighting the outcomes of cellular signaling modulation alongside low and high LET radiation in normal, radioresistant or hypoxic tumor cells. We welcome Original Research and Review articles reporting the radiobiological effects of low and high LET radiation (X-rays, gamma rays, and charged particles) both at the conventional and/or FLASH dose rates with or without cell-signaling pathways inhibitors for achieving better tumor control and normal tissue sparing. We also invite the views of the scientific community on the recent achievements in the development of radiation countermeasures as a result of modulating DNA damage and repair pathways.
Multidisciplinary articles spanning the Biological, Physical and Medical fields are welcome. Articles may report the radiobiological outcomes and mechanistic insights of modulating cellular signaling pathways in pre-clinical models of cancer and radioprotection. Articles combining experimental and modelling approaches to demonstrate therapeutic benefits, normal tissue sparing and relative biological effectiveness (RBE) of low and high LET radiation with or without molecular inhibitors are also welcome. Manuscripts from the medical field should report the clinical outcomes of combining DNA repair signaling inhibitors with X-rays, proton and other charged particles. Manuscripts reporting following outcomes are especially welcome:
1. Radiobiological effects of low and high LET radiations at conventional, FLASH and ultra-high dose rates.
2. Radiobiological outcomes of inhibiting cellular signaling pathways in pre-clinical cancer models of various origin by pharmaceutics.
3. Radiation mitigation and radioprotection achieved based on the modulation of DNA damage repair and other cell-signaling pathways.
4. Relative biological effectiveness (RBE) of low and high LET charged particles with or without cellular signaling inhibitors in achieving an enhanced therapeutic window or reducing normal tissue toxicity using various quality of radiations at variable dose rates.
5. Clinical outcomes of combining cell-signaling molecules or inhibitors with radiotherapy
Please note: manuscripts consisting solely of bioinformatics or computational analysis of public genomic or transcriptomic databases which are not accompanied by validation (independent cohort or biological validation in vitro or in vivo) are out of scope for this section and will not be accepted as part of this Research Topic.
Approximately half of all cancer patients receive radiotherapy, resulting in an overall increase in survival. FLASH radiotherapy has been demonstrated to benefit patients due to significant normal tissue sparing, thus enhancing the therapeutic window. Similarly, targeting cellular signaling pathways in conjunction with advanced radiotherapy modalities is not just beneficial for patients undergoing radiotherapy but can also be exploited to achieve radioprotection. For example, combining DNA repair inhibitors with low LET radiation has resulted in the development of several cancer drugs, whilst inhibiting radiation-induced damage to tissues. Therefore, radiobiological studies targeting cellular signaling with low and high LET radiation at FLASH or conventional dose rate will open new avenues in cancer biology. Modulation of DNA repair signaling pathways with pharmaceutical agents can further potentiate the development of radioprotectors and radiation countermeasures.
In this research topic, we aim to showcase the current research highlighting the outcomes of cellular signaling modulation alongside low and high LET radiation in normal, radioresistant or hypoxic tumor cells. We welcome Original Research and Review articles reporting the radiobiological effects of low and high LET radiation (X-rays, gamma rays, and charged particles) both at the conventional and/or FLASH dose rates with or without cell-signaling pathways inhibitors for achieving better tumor control and normal tissue sparing. We also invite the views of the scientific community on the recent achievements in the development of radiation countermeasures as a result of modulating DNA damage and repair pathways.
Multidisciplinary articles spanning the Biological, Physical and Medical fields are welcome. Articles may report the radiobiological outcomes and mechanistic insights of modulating cellular signaling pathways in pre-clinical models of cancer and radioprotection. Articles combining experimental and modelling approaches to demonstrate therapeutic benefits, normal tissue sparing and relative biological effectiveness (RBE) of low and high LET radiation with or without molecular inhibitors are also welcome. Manuscripts from the medical field should report the clinical outcomes of combining DNA repair signaling inhibitors with X-rays, proton and other charged particles. Manuscripts reporting following outcomes are especially welcome:
1. Radiobiological effects of low and high LET radiations at conventional, FLASH and ultra-high dose rates.
2. Radiobiological outcomes of inhibiting cellular signaling pathways in pre-clinical cancer models of various origin by pharmaceutics.
3. Radiation mitigation and radioprotection achieved based on the modulation of DNA damage repair and other cell-signaling pathways.
4. Relative biological effectiveness (RBE) of low and high LET charged particles with or without cellular signaling inhibitors in achieving an enhanced therapeutic window or reducing normal tissue toxicity using various quality of radiations at variable dose rates.
5. Clinical outcomes of combining cell-signaling molecules or inhibitors with radiotherapy
Please note: manuscripts consisting solely of bioinformatics or computational analysis of public genomic or transcriptomic databases which are not accompanied by validation (independent cohort or biological validation in vitro or in vivo) are out of scope for this section and will not be accepted as part of this Research Topic.
