About this Research Topic
Autophagy, a fundamental cellular process responsible for the degradation and recycling of damaged organelles and proteins, plays a critical role in maintaining cellular health and homeostasis. This process is intricately linked to both cancer and inflammation, two complex and interrelated conditions that significantly impact human health. In the context of cancer, autophagy can exhibit dual roles. It can act as a tumor suppressor by removing damaged cellular components that could otherwise contribute to tumorigenesis. Conversely, in established cancers, autophagy can promote tumor survival by supporting cancer cells under metabolic stress and therapeutic assault.
Similarly, autophagy influences inflammation by regulating the secretion of inflammatory cytokines and the clearing of inflammasomes, thus potentially alleviating or exacerbating inflammatory conditions. The dynamic interactions between autophagy, cancer, and inflammation highlight a complex network where modulation of autophagy could potentially offer therapeutic benefits against cancer development and inflammatory diseases.
Understanding these connections is crucial for developing targeted treatments that can selectively enhance or inhibit autophagy to manage these conditions effectively.
Goal:
The central challenge in understanding the interplay between autophagy, adult and pediatric primary brain tumors, and inflammation lies in deciphering how autophagy's dual role can be manipulated to suppress cancer growth while simultaneously controlling inflammatory responses. Autophagy can help eliminate oncogenic stimuli and damaged cells to prevent cancer onset; however, once cancer is established, it may contribute to tumor survival. Moreover, autophagy's role in managing inflammation—by controlling immune cell function and cytokine production—adds yet another layer of complexity, as both excessive or insufficient inflammation can promote tumorigenesis.
Addressing this problem requires a multi-faceted approach. Firstly, developing precise biomarkers that can accurately measure autophagic activity in specific contexts is essential. This will enable the identification of stages at which autophagy promotes either tumorigenesis or tumor suppression. Secondly, designing drugs that can modulate autophagy with high specificity will be crucial. These drugs need to selectively enhance autophagy to remove damaged cells and suppress inflammation without supporting cancer cell survival. Integrating these strategies into clinical trials will help validate the therapeutic potential of autophagy modulation in primary brain tumors and inflammatory diseases, paving the way for new treatment paradigms.
This research topic seeks to explore the intricate relationships between autophagy, primary brain tumors, and inflammation, aiming to unravel the complex mechanisms by which autophagy and variant pathways such as ferroptosis influence cancer progression and the inflammatory response. We invite authors to contribute original research papers, comprehensive reviews, and insightful clinical studies that delve into specific themes within this scope. Key themes of interest include the role of autophagy in primary brain tumor initiation and progression, the mechanisms by which autophagy regulates inflammatory pathways, and the impact of autophagy on the tumor microenvironment of primary brain tumors. Additionally, studies that investigate the therapeutic potential of modulating autophagy in cancer and inflammatory diseases are highly encouraged. By gathering diverse contributions from these areas, this research topic aims to build a deeper understanding of how autophagy can be targeted to develop innovative therapeutic strategies in the context of brain tumors and inflammation.
Please note manuscripts consisting solely of bioinformatics or computational analysis of public genomic or transcriptomic databases that are not accompanied by validation (independent cohort or biological validation in vitro or in vivo) are out of the scope of this Research Topic.
Similarly, autophagy influences inflammation by regulating the secretion of inflammatory cytokines and the clearing of inflammasomes, thus potentially alleviating or exacerbating inflammatory conditions. The dynamic interactions between autophagy, cancer, and inflammation highlight a complex network where modulation of autophagy could potentially offer therapeutic benefits against cancer development and inflammatory diseases.
Understanding these connections is crucial for developing targeted treatments that can selectively enhance or inhibit autophagy to manage these conditions effectively.
Goal:
The central challenge in understanding the interplay between autophagy, adult and pediatric primary brain tumors, and inflammation lies in deciphering how autophagy's dual role can be manipulated to suppress cancer growth while simultaneously controlling inflammatory responses. Autophagy can help eliminate oncogenic stimuli and damaged cells to prevent cancer onset; however, once cancer is established, it may contribute to tumor survival. Moreover, autophagy's role in managing inflammation—by controlling immune cell function and cytokine production—adds yet another layer of complexity, as both excessive or insufficient inflammation can promote tumorigenesis.
Addressing this problem requires a multi-faceted approach. Firstly, developing precise biomarkers that can accurately measure autophagic activity in specific contexts is essential. This will enable the identification of stages at which autophagy promotes either tumorigenesis or tumor suppression. Secondly, designing drugs that can modulate autophagy with high specificity will be crucial. These drugs need to selectively enhance autophagy to remove damaged cells and suppress inflammation without supporting cancer cell survival. Integrating these strategies into clinical trials will help validate the therapeutic potential of autophagy modulation in primary brain tumors and inflammatory diseases, paving the way for new treatment paradigms.
This research topic seeks to explore the intricate relationships between autophagy, primary brain tumors, and inflammation, aiming to unravel the complex mechanisms by which autophagy and variant pathways such as ferroptosis influence cancer progression and the inflammatory response. We invite authors to contribute original research papers, comprehensive reviews, and insightful clinical studies that delve into specific themes within this scope. Key themes of interest include the role of autophagy in primary brain tumor initiation and progression, the mechanisms by which autophagy regulates inflammatory pathways, and the impact of autophagy on the tumor microenvironment of primary brain tumors. Additionally, studies that investigate the therapeutic potential of modulating autophagy in cancer and inflammatory diseases are highly encouraged. By gathering diverse contributions from these areas, this research topic aims to build a deeper understanding of how autophagy can be targeted to develop innovative therapeutic strategies in the context of brain tumors and inflammation.
Please note manuscripts consisting solely of bioinformatics or computational analysis of public genomic or transcriptomic databases that are not accompanied by validation (independent cohort or biological validation in vitro or in vivo) are out of the scope of this Research Topic.
Keywords: Autophagy, cancer, inflammation, homeostasis, therapeutics
Important Note: All contributions to this Research Topic must be within the scope of the section and journal to which they are submitted, as defined in their mission statements. Frontiers reserves the right to guide an out-of-scope manuscript to a more suitable section or journal at any stage of peer review.
