About this Research Topic
The tumor microenvironment (TME) is a complex network encompassing several immune cell types like cancer-associated fibroblasts, endothelial cells, pericytes, and various other tissue-resident cell types. TME is crucial at all stages of cancer progression, right from tumor initiation, development, through to invasion, metastasis, and growth (de Visser KE et al.). The TME's existence bolsters tumor cell proliferation, migration, and immune evasion capabilities, thereby expediting tumor onset and progression.
The TME constitutes a meticulously organized ecosystem comprising cancer cells that are surrounded by an array of non-malignant cell types, ensconced within an altered, vascularized extracellular matrix (ECM). TME cells and their secreted molecular components are significant contributors to cancer pathogenesis and thus present attractive therapeutic targets (Chen et al). TME cells' composition and functional status hinge on factors such as the cancer-origin organ, inherent cancer cell characteristics, tumor stage, and patient-based variables. Within the TME, cells can either curb or bolster tumor growth. Tumor-associated macrophages (TAMs) and neutrophils (TANs) are often the most abundant myeloid cell types within various TMEs, demonstrating significant diversity and adaptability. This ecosystem impacts several tumorigenic processes, from directly modulating cancer cell fate and behavior (e.g., proliferation, survival, invasion) to promoting an immune-suppressive TME, stimulating tumor angiogenesis, and facilitating ECM remodeling. Besides their direct impact on cancer cells, TAMs, neutrophils, their precursors, and less studied stem cells indirectly abet tumor development by guiding supportive processes within the TME. Myeloid cells utilize diverse mechanisms to support tumor evasion, including the secretion of immune-inhibitory factors affecting T and NK cells and the production of inflammatory mediators that amplify the inflammatory response (Guc, E et al.).
Immune and stromal cells within the TME, despite being co-opted, exhibit genetic stability, making them relatively easier targets compared to genomically unstable cancer cells. We have come to appreciate the extensive complexity, interconnectedness, and variability of the TME across organs and patients. Furthermore, we acknowledge the challenges adaptive and intrinsic resistance pose to TME-targeted therapies. Recognizing this, our research domain strives to pay dedicated attention to recent advancements in understanding the interactions and mechanisms within the TME. We thereby invite submissions of original research articles and commentaries particularly addressing:
• Mechanisms employed by tumor cells facilitating autoimmune escape by modulating the status of immune cells, thereby governing tumor initiation, progression, recurrence, metastasis, and drug resistance.
• The remarkable role of the interplay amongst immune cells, leading to immune tolerance within the TME, and subsequent malignant progression.
• Target identification and validation within tumor and immune cells present within the TME.
The TME constitutes a meticulously organized ecosystem comprising cancer cells that are surrounded by an array of non-malignant cell types, ensconced within an altered, vascularized extracellular matrix (ECM). TME cells and their secreted molecular components are significant contributors to cancer pathogenesis and thus present attractive therapeutic targets (Chen et al). TME cells' composition and functional status hinge on factors such as the cancer-origin organ, inherent cancer cell characteristics, tumor stage, and patient-based variables. Within the TME, cells can either curb or bolster tumor growth. Tumor-associated macrophages (TAMs) and neutrophils (TANs) are often the most abundant myeloid cell types within various TMEs, demonstrating significant diversity and adaptability. This ecosystem impacts several tumorigenic processes, from directly modulating cancer cell fate and behavior (e.g., proliferation, survival, invasion) to promoting an immune-suppressive TME, stimulating tumor angiogenesis, and facilitating ECM remodeling. Besides their direct impact on cancer cells, TAMs, neutrophils, their precursors, and less studied stem cells indirectly abet tumor development by guiding supportive processes within the TME. Myeloid cells utilize diverse mechanisms to support tumor evasion, including the secretion of immune-inhibitory factors affecting T and NK cells and the production of inflammatory mediators that amplify the inflammatory response (Guc, E et al.).
Immune and stromal cells within the TME, despite being co-opted, exhibit genetic stability, making them relatively easier targets compared to genomically unstable cancer cells. We have come to appreciate the extensive complexity, interconnectedness, and variability of the TME across organs and patients. Furthermore, we acknowledge the challenges adaptive and intrinsic resistance pose to TME-targeted therapies. Recognizing this, our research domain strives to pay dedicated attention to recent advancements in understanding the interactions and mechanisms within the TME. We thereby invite submissions of original research articles and commentaries particularly addressing:
• Mechanisms employed by tumor cells facilitating autoimmune escape by modulating the status of immune cells, thereby governing tumor initiation, progression, recurrence, metastasis, and drug resistance.
• The remarkable role of the interplay amongst immune cells, leading to immune tolerance within the TME, and subsequent malignant progression.
• Target identification and validation within tumor and immune cells present within the TME.
Keywords: Tumor microenvironment; Cytokines; Intercellular communication; Tumor drug resistance; Tumor recurrence and metastasis; Hypoxic microenvironment; Immune escape
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.
