About this Research Topic
Autophagy, a vital cellular process for degrading and recycling damaged organelles and proteins, is crucial in maintaining cellular health and homeostasis. This process is intricately linked to cancer and inflammation, two interrelated conditions with significant implications for human health. In cancer, autophagy can act as a double-edged sword: it may suppress tumor formation by eliminating damaged cellular components, yet in established cancers, it can aid tumor survival by supporting cancer cells under metabolic stress and therapeutic challenges. Similarly, autophagy influences inflammation by regulating inflammatory cytokine secretion and clearing inflammasomes, potentially alleviating or exacerbating inflammatory conditions. The complex interplay between autophagy, cancer, and inflammation underscores a network where modulating autophagy could offer therapeutic benefits against cancer and inflammatory diseases. Despite advances, understanding these connections remains crucial for developing targeted treatments that can selectively enhance or inhibit autophagy to manage these conditions effectively.
This research topic aims to explore the intricate relationships between autophagy, primary brain tumors, and inflammation, focusing on unraveling the complex mechanisms by which autophagy and related pathways, such as ferroptosis, influence cancer progression and inflammatory responses. The central challenge lies in deciphering how autophagy's dual role can be manipulated to suppress cancer growth while controlling inflammatory responses. Addressing this requires developing precise biomarkers to measure autophagic activity and designing drugs that modulate autophagy with high specificity. These efforts aim to selectively enhance autophagy to remove damaged cells and suppress inflammation without supporting cancer cell survival, ultimately validating the therapeutic potential of autophagy modulation in primary brain tumors and inflammatory diseases.
To gather further insights into the interplay between autophagy, primary brain tumors, and inflammation, we welcome articles addressing, but not limited to, the following themes:
- The role of autophagy in primary brain tumor initiation and progression.
- Mechanisms by which autophagy regulates inflammatory pathways.
- The impact of autophagy on the tumor microenvironment of primary brain tumors.
- Therapeutic potential of modulating autophagy in cancer and inflammatory diseases.
Please note that manuscripts consisting solely of bioinformatics or computational analysis of public genomic or transcriptomic databases, without validation through independent cohorts or biological validation in vitro or in vivo, are out of the scope of this research topic.
This research topic aims to explore the intricate relationships between autophagy, primary brain tumors, and inflammation, focusing on unraveling the complex mechanisms by which autophagy and related pathways, such as ferroptosis, influence cancer progression and inflammatory responses. The central challenge lies in deciphering how autophagy's dual role can be manipulated to suppress cancer growth while controlling inflammatory responses. Addressing this requires developing precise biomarkers to measure autophagic activity and designing drugs that modulate autophagy with high specificity. These efforts aim to selectively enhance autophagy to remove damaged cells and suppress inflammation without supporting cancer cell survival, ultimately validating the therapeutic potential of autophagy modulation in primary brain tumors and inflammatory diseases.
To gather further insights into the interplay between autophagy, primary brain tumors, and inflammation, we welcome articles addressing, but not limited to, the following themes:
- The role of autophagy in primary brain tumor initiation and progression.
- Mechanisms by which autophagy regulates inflammatory pathways.
- The impact of autophagy on the tumor microenvironment of primary brain tumors.
- Therapeutic potential of modulating autophagy in cancer and inflammatory diseases.
Please note that manuscripts consisting solely of bioinformatics or computational analysis of public genomic or transcriptomic databases, without validation through independent cohorts 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.
