The tumour microenvironment is a heterogenous composition of cell types that respond to local and peripheral cues and play critical roles in mediating oncogenesis. Broadly the tumour microenvironment can be grouped into stromal, vascular and immune cells. Both pre-clinical and clinical evidence has demonstrated a reciprocal relationship between the initiating tumour and the microenvironment. In part this bi-directional relationship and adaptations of the tumour microenvironment that drives tumour development is dependent on the availability of metabolites. Therefore, an emerging theme in the study of the tumour microenvironment is the identification of vulnerabilities with respect to dysfunctional metabolic pathways in the tumour microenvironment and exploiting these defects to improve primary cancer treatments, including immunotherapy.
The goal of this Research Topic will be the exploration of dysfunctional metabolism in the tumour microenvironment that consequently alters oncogenesis. These studies can include pre-clinical studies and clinical observations, however, the overall focus of this collection will seek to uncover novel mechanistic insights on specific metabolic dysfunction that occurs across a variety of solid tumour cancers. The overarching theme will be the identification of changes in the repertoire of peripheral- or tumour-derived metabolites that induce an adverse remodelling of the tumour microenvironment and drive oncogenesis.
We welcome the submission of Original Research, Review, Mini-Review, Methods, Case report, and Perspective articles that cover, but are not limited to the following topics:
• Primary tumour cell-derived metabolites and the regulation of the composition of the tumour microenvironment.
• Cellular plasticity/phenotype of tumour microenvironment cells as imparted by metabolism.
• Changes in metabolite profile in stage-specific cancer progression.
• Metabolic reprogramming of the tumour microenvironment to improve cancer therapeutic outcomes.
• Metabolic-based approaches to increase the efficacy of immunotherapy.
Manuscripts consisting solely of bioinformatics or computational analysis of public genomic or transcriptomic databases which are not accompanied by robust and relevant validation (clinical cohort or biological validation in vitro or in vivo) are out of scope for this topic.
Keywords:
Cancer-associated fibroblast, immune cell, t cell, macrophage endothelial cell, stromal cell, tumour, oncology, metabolism, Kreb/TCA cycle, oxidative phosophorylation
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.
The tumour microenvironment is a heterogenous composition of cell types that respond to local and peripheral cues and play critical roles in mediating oncogenesis. Broadly the tumour microenvironment can be grouped into stromal, vascular and immune cells. Both pre-clinical and clinical evidence has demonstrated a reciprocal relationship between the initiating tumour and the microenvironment. In part this bi-directional relationship and adaptations of the tumour microenvironment that drives tumour development is dependent on the availability of metabolites. Therefore, an emerging theme in the study of the tumour microenvironment is the identification of vulnerabilities with respect to dysfunctional metabolic pathways in the tumour microenvironment and exploiting these defects to improve primary cancer treatments, including immunotherapy.
The goal of this Research Topic will be the exploration of dysfunctional metabolism in the tumour microenvironment that consequently alters oncogenesis. These studies can include pre-clinical studies and clinical observations, however, the overall focus of this collection will seek to uncover novel mechanistic insights on specific metabolic dysfunction that occurs across a variety of solid tumour cancers. The overarching theme will be the identification of changes in the repertoire of peripheral- or tumour-derived metabolites that induce an adverse remodelling of the tumour microenvironment and drive oncogenesis.
We welcome the submission of Original Research, Review, Mini-Review, Methods, Case report, and Perspective articles that cover, but are not limited to the following topics:
• Primary tumour cell-derived metabolites and the regulation of the composition of the tumour microenvironment.
• Cellular plasticity/phenotype of tumour microenvironment cells as imparted by metabolism.
• Changes in metabolite profile in stage-specific cancer progression.
• Metabolic reprogramming of the tumour microenvironment to improve cancer therapeutic outcomes.
• Metabolic-based approaches to increase the efficacy of immunotherapy.
Manuscripts consisting solely of bioinformatics or computational analysis of public genomic or transcriptomic databases which are not accompanied by robust and relevant validation (clinical cohort or biological validation in vitro or in vivo) are out of scope for this topic.
Keywords:
Cancer-associated fibroblast, immune cell, t cell, macrophage endothelial cell, stromal cell, tumour, oncology, metabolism, Kreb/TCA cycle, oxidative phosophorylation
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.