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Once internalized, these agents can engage and disrupt critical oncogenic pathways for example, suppressing phosphoinositide 3-kinase (PI3K)/protein kinase B (AKT)/ mechanistic target of rapamycin (mTOR) signaling, inhibiting Wnt/-catenin activation or perturbing deoxyribonucleic acid (DNA) damage repair networks thereby inducing apoptosis or sensitizing cancer cells to subsequent therapy
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