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Tumor microenvironment regulation refers to the wide array of biological processes and molecular mechanisms that shape the cellular, structural, and biochemical landscape surrounding tumor cells. The TME includes cancer cells, immune cells, stromal cells (such as fibroblasts), endothelial cells, the extracellular matrix, and a vast range of signaling molecules[1][2][5][7]. Interactions within the TME govern crucial aspects of tumor biology, including tumor growth, metastasis, immune escape, angiogenesis, and response to therapy[1][3][6][8]. Regulation of the TME is not mediated by a single molecule or receptor, but encompasses many pathways and cellular players, such as immune checkpoint molecules (e.g., PD-1, PD-L1), growth factors (e.g., VEGF, FGF, TGF-beta), cytokines (e.g., IL-6), metabolic regulators, and extracellular matrix proteins[1][5][6]. Drugs and experimental compounds often target specific components or regulators within the TME to modify tumor progression or sensitize cancers to therapy, but “tumor microenvironment regulation” itself is not a discrete therapeutic target.
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