TRAIL Receptor-Induced Cell Death Regulation: An Update to Our Deadly Discussion

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TitreTRAIL Receptor-Induced Cell Death Regulation: An Update to Our Deadly Discussion
Type de publicationBook Chapter
Year of Publication2014
AuteursMicheau O, Shirley S, Morizot A
EditorAttaUrRahman, Zaman K
Book TitleTOPICS IN ANTI-CANCER RESEARCH, VOL 3
Series TitleTopics in Anti-Cancer Research
Volume3
Pagination3-36
PublisherBENTHAM SCIENCE PUBL
CityEXECUTIVE STE Y-2, P.O. BOX 7917, SAIF ZONE, SHARJAH, 1400 AG, U ARAB EMIRATES
ISBN Number978-1-60805-908-9; 978-1-60805-909-6
ISBN2468-5860
Mots-clésAPO2L, C-FLIP, Cancer, caspase, Chemotherapy, death domain, death effector domain, DISC, DR4, DR5, FADD, Glycosylation, Lexatumumab, Mapatumumab, scaffold, therapy, TRAIL, TRAIL-R1, TRAIL-R2, TRAIL-R4
Résumé

The use of TRAIL/APO2L, monoclonal antibodies or peptidomimetics targeting TRAIL receptors for cancer therapy holds great promise, due to their ability to restore cancer cell sensitivity to apoptosis in association with conventional chemotherapeutic drugs, in a large variety of tumors. TRAIL-induced cell death is tightly regulated right from the membrane and at the DISC (Death-Inducing Signaling Complex) level. The following patent and literature chapter is an update to our article ``Regulating TRAIL Receptor-Induced Cell Death at the Membrane: A Deadly Discussion'', published in the journal `Recent Patents on Anti-Cancer Drug Discovery', Volume 6, Number 3, September, 2011, Page 311 to 323, reviewing TRAIL DISC components that have been shown to regulate tumor cell fate upon TRAIL engagement.