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**Interstitial fluid pressure (IFP)** is elevated in solid tumors due to abnormal vascular permeability, poor lymphatic drainage, and dense extracellular matrix, forming physical barriers that hinder uptake of therapeutics[1][3][4]. Strategies that lower tumor IFP—using cytotoxic drugs or anti-angiogenic agents—can improve drug penetration and efficacy and serve as early markers of therapeutic response[1]. Elevated IFP is associated with poor prognosis and increased metastasis, and the phenomenon is a major challenge for effective cancer therapy, particularly nanomedicine delivery[4]. However, “counteracting interstitial fluid pressure in tumors” is not the name of a specific molecular target; it is a concept that guides therapeutic development and biomarker evaluation[1][4][3]. The entry refers to a physiological process and therapeutic challenge, *not* a canonical target molecule like a receptor or enzyme. The correct structured target would be specific mediators of IFP (e.g., matrix-modifying enzymes, vascular permeability factors), not “counteracting interstitial fluid pressure in tumors” itself.
Reduction of interstitial fluid pressure through cytotoxic effects or targeting angiogenesis, thereby improving chemotherapy penetration
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