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Cancer cells with albumin-binding properties" refer to tumor cells that have increased capacity to internalize and metabolize serum albumin, typically through the overexpression of specific albumin-binding receptors such as SPARC (secreted protein acidic and rich in cysteine), GP60 (albondin), and proteins involved in caveolae-mediated endocytosis such as caveolin-1. This property enables these cells to scavenge nutrients from albumin and has been therapeutically exploited by designing albumin-bound chemotherapeutic agents that take advantage of the enhanced permeability and retention (EPR) effect and active receptor-mediated uptake. Notable clinical advances include albumin-bound paclitaxel (nab-paclitaxel, Abraxane), leveraging this pathway to increase drug delivery to tumors. The best predictive molecular biomarkers for the efficacy of albumin-bound therapies are the expression levels of SPARC and caveolin-1[1][3][5][6][7][9]. This is not a single molecular target and should be redefined in terms of the specific protein or pathway of interest.
Enhanced Permeability and Retention (EPR) effect for passive uptake; Receptor-mediated endocytosis (via SPARC, GP60, Cav-1); Intratumoral drug delivery via albumin carrier systems
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