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- W2062496875 abstract "Tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL) is a member of the TNF superfamily and has been shown to induce apoptosis in cancer cells but not normal cells. TRAIL triggers apoptosis through binding to its receptors DR4 and KILLER/DR5. Chemo or radiotherapy induces apoptosis through activation of p53 in response to cellular damage, whereas TRAIL induces apoptosis independent of p53. Mutations or deletions of p53 occurred in more than half of human tumors confer resistance to chemo-radiotherapy. Treatment of TRAIL-resistant tumors with agents targeting death receptors, intrinsic Bcl-2 family members, inhibitor of apoptosis proteins or PI3K/Akt pathway restores the sensitivity to TRAIL-induced apoptosis. Combination of rhTRAIL or the agonist antibody for TRAIL receptor with conventional chemotherapeutic agents results in enhanced efficacy in preventing tumor progression and metastasis. Therefore, the rational design of TRAIL-based therapy combining with other modality that either synergizes to apoptosis induction or overcomes the resistance represents a challenging strategy to achieve the systemic tumor targeting and augment the antitumor activity of cancer therapeutics." @default.
- W2062496875 created "2016-06-24" @default.
- W2062496875 creator A5031949493 @default.
- W2062496875 date "2008-10-20" @default.
- W2062496875 modified "2023-10-11" @default.
- W2062496875 title "The promise of cancer therapeutics targeting the TNF-related apoptosis-inducing ligand and TRAIL receptor pathway" @default.
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- W2062496875 doi "https://doi.org/10.1038/onc.2008.298" @default.
- W2062496875 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/18931688" @default.
- W2062496875 hasPublicationYear "2008" @default.
- W2062496875 type Work @default.