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In this circuitry, TGF-β/SMAD3 operates as a principal switch: tumor-derived TGF-β1 activates SMAD3, repressing mature adipocyte identity while inducing fibroblast-like programs (for example, FN1, collagens, ACTA2) that facilitate CAA emergence and premetastatic niche formation
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The peptide incorporates specific amino acid substitutions at key positions to enhance stability against enzymatic degradation while preserving high affinity for the GHRH receptor
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