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.
Keywords: APO2L, cancer, caspase, c-FLIP, chemotherapy, death domain, death
effector domain, DISC, DR4, DR5, FADD, glycosylation, Lexatumumab,
scaffold, Mapatumumab, therapy, TRAIL, TRAIL-R1, TRAIL-R2, TRAIL-R4.
