Spotlighting the Interaction Network of Hub Genes, Molecules, and Cells in the Tumor Immune Microenvironment (TIME) and their Contribution to Malignant Progression

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Background

The tumor immune microenvironment (TIME) is a complex network of interactions between cancer cells, immune cells, and other stromal cells. Dysregulation of this network can promote tumor progression and immune evasion. Several key molecules, such as cytokines, chemokines, and growth factors, play critical roles in modulating the interactions between immune cells and tumor cells within the TIME. Regulation of these key molecules is tightly controlled by multiple feedback loops and signaling pathways, both within and between immune cells and tumor cells. On the other hand, immune cells such as T cells, natural killer (NK) cells, and dendritic cells (DCs) can also produce cytokines that activate or inhibit other immune cells and recruit additional immune cells to the TIME. The crosstalk between different immune cells within the TIME is critical for the regulation of immune responses and tumor progression. However, tumor cells can also exploit these interactions to evade immune surveillance and promote their own growth and survival. Overall, the regulation of key molecules in the TIME and the crosstalk between immune cells are critical for the maintenance of immune homeostasis and the prevention of tumor progression. Dysregulation of this network can promote immune evasion and tumor growth, highlighting the importance of developing targeted therapies that can modulate the interactions between immune cells and tumor cells within the TIME.

The objective of our topic collection is to explore the network regulation of key molecules in the TIME and the crosstalk between immune cells and tumor cells in relation to tumor progression. Specifically, the scope will focus on the role of cytokines, chemokines, immune checkpoints, and antigen-presenting molecules in the regulation of the TIME and the mechanisms by which these molecules interact with immune cells to promote or inhibit tumor growth. Additionally, this topic scope aims to investigate the potential of targeting these key molecules and their regulatory pathways for cancer immunotherapy. Through this exploration, our topic collection seeks to provide a comprehensive understanding of the complex interactions between immune cells and tumor cells in the TIME, which may lead to the development of novel strategies for cancer treatment.

This Research Topic accepts Original Research, Systematic Review, Review, Mini-Review, Clinical Trial, Perspective, and Case Report. We welcome manuscripts focusing on, but not limited to, the following sub-topics:
• Preclinical research models of the tumor immune microenvironment (e.g., animal models, organoids, single-cell sequencing).
• The intricate network of molecular and cellular crosstalk between immune cells that support or inhibit tumor development and remodel tumor microenvironment.
• Preclinical and clinical trials targeting immune cells and their key molecules (e.g., cytokines, chemokines, growth factors, and immune checkpoints) to improve cancer treatment outcomes.
• Discovery of tumor immune microenvironment heterogeneity based on signature genes and protein expression profiles.
• Key molecular biomarkers and regulatory pathways involved in the TIME related to cancer diagnosis, treatment and prognosis.

Manuscripts consisting solely of bioinformatics or computational analysis of public genomic or transcriptomic databases which are not accompanied by robust and relevant validation are considered out of scope of this section.

Keywords: Tumor Immune Microenvironment (TIME), Interaction Network, Immune Activation and Evasion, Therapeutic Targets, Precision Medicine, Translational Research

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.

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