Cancer is a “wound that does not heal”, and its initiation and progression involve the crosstalk between malignant cells and their surrounding microenvironment, the tumor stroma, among which the immune components play an active and vital role in shaping the malignant transformation. For instance, in the tumor immune microenvironment (TIME) immune cells could secrete various soluble factors that may upregulate the expressions of oncogenic proteins in cancer cells, and that may also stimulate cancer cells to release chemotactic factors recruiting cancer-associated immune cells to enter the malignant niche. Function and activity of the immune cells in the tumor microenvironment are also regulated by various genetic and epigenetic mechanisms, the latter including m6A methylation, for instance. It would be helpful and interesting to further dissect the TIME.
The mechanisms underlying the crosstalk between malignant cells and the TIME remain largely unknow, despite active investigations into this field. The diversity and complexity of the TIME, which may dynamically change during different phases of cancer development, may have been underestimated. An improved insight into the cellular crosstalks in TIME upon a better understanding of the physiology of the different cell types regulating or involved in TIME may facilitate creating novel individualized anticancer strategies targeting the TIME. In order to achieve this goal, various efforts could be made, including a focus on the immune cell physiology. The interactions between cancer cells and various immune cells (e.g., neutrophils, lymphocytes, macrophages, and MDSCs) and between different immune cells in the TIME during different stages of cancer development (from initiation to metastasis) should be better clarified. The soluble signal transducing molecules with practical functions in the TIME should be further discovered with their diverse regulatory roles in different cells comprehensively revealed. Notably, the crosstalks between different cells in the TIME should be bi- or multi-directional, forming an interactive network; an isolated analysis may overlook the whole landscape. The interaction loops should be depicted rather than a unidirectional pathway. To further facilitate precisely locating promising anticancer targets in the TIME, the physiology and accurate regulatory mechanisms of immune cells need to be uncovered in depth.
This Research Topic welcomes Original Articles, Brief Communications, and Reviews aiming to further clarify the crosstalks between malignant cells and the TIME during cancer initiation and development. Specific themes to be addressed may include but are not limited to:
• Spatiotemporal dynamics of the roles of the TIME during different stages of cancer development using in vivo or in vitro models
• Physiology of immune cells involved in TIME
• Advanced methods for understanding the TIME (e.g., Hi-C and single-cell sequencing)
• Further insights into the regulatory mechanisms of immune cells in the TIME (e.g., m6A)
• Mechanistic study for the discovery of novel promising targets in the TIME for precise anticancer therapy
• Multidirectional feedback loops and networks in the TIME
• Joint actions of other components in the tumor stoma (e.g., angiogenesis, neuroendocrine factors) with the TIME
• Any other basic research themes related to cell physiology in TIME and the crosstalks between cancer cells and the TIME
Please note: studies consisting solely of bioinformatic investigation of publicly available genomic/transcriptomic/proteomic data do not fall within the scope of the section unless they are expanded and provide significant biological or mechanistic insight into the process being studied.
Keywords:
cancer, tumor immune microenvironment, crosstalk, mechanism
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.
Cancer is a “wound that does not heal”, and its initiation and progression involve the crosstalk between malignant cells and their surrounding microenvironment, the tumor stroma, among which the immune components play an active and vital role in shaping the malignant transformation. For instance, in the tumor immune microenvironment (TIME) immune cells could secrete various soluble factors that may upregulate the expressions of oncogenic proteins in cancer cells, and that may also stimulate cancer cells to release chemotactic factors recruiting cancer-associated immune cells to enter the malignant niche. Function and activity of the immune cells in the tumor microenvironment are also regulated by various genetic and epigenetic mechanisms, the latter including m6A methylation, for instance. It would be helpful and interesting to further dissect the TIME.
The mechanisms underlying the crosstalk between malignant cells and the TIME remain largely unknow, despite active investigations into this field. The diversity and complexity of the TIME, which may dynamically change during different phases of cancer development, may have been underestimated. An improved insight into the cellular crosstalks in TIME upon a better understanding of the physiology of the different cell types regulating or involved in TIME may facilitate creating novel individualized anticancer strategies targeting the TIME. In order to achieve this goal, various efforts could be made, including a focus on the immune cell physiology. The interactions between cancer cells and various immune cells (e.g., neutrophils, lymphocytes, macrophages, and MDSCs) and between different immune cells in the TIME during different stages of cancer development (from initiation to metastasis) should be better clarified. The soluble signal transducing molecules with practical functions in the TIME should be further discovered with their diverse regulatory roles in different cells comprehensively revealed. Notably, the crosstalks between different cells in the TIME should be bi- or multi-directional, forming an interactive network; an isolated analysis may overlook the whole landscape. The interaction loops should be depicted rather than a unidirectional pathway. To further facilitate precisely locating promising anticancer targets in the TIME, the physiology and accurate regulatory mechanisms of immune cells need to be uncovered in depth.
This Research Topic welcomes Original Articles, Brief Communications, and Reviews aiming to further clarify the crosstalks between malignant cells and the TIME during cancer initiation and development. Specific themes to be addressed may include but are not limited to:
• Spatiotemporal dynamics of the roles of the TIME during different stages of cancer development using in vivo or in vitro models
• Physiology of immune cells involved in TIME
• Advanced methods for understanding the TIME (e.g., Hi-C and single-cell sequencing)
• Further insights into the regulatory mechanisms of immune cells in the TIME (e.g., m6A)
• Mechanistic study for the discovery of novel promising targets in the TIME for precise anticancer therapy
• Multidirectional feedback loops and networks in the TIME
• Joint actions of other components in the tumor stoma (e.g., angiogenesis, neuroendocrine factors) with the TIME
• Any other basic research themes related to cell physiology in TIME and the crosstalks between cancer cells and the TIME
Please note: studies consisting solely of bioinformatic investigation of publicly available genomic/transcriptomic/proteomic data do not fall within the scope of the section unless they are expanded and provide significant biological or mechanistic insight into the process being studied.
Keywords:
cancer, tumor immune microenvironment, crosstalk, mechanism
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.