David A. Lawrence

TL;DR: Apo2L may have potent anticancer activity without significant toxicity toward normal tissues, and cooperated synergistically with the chemotherapeutic drugs 5-fluorouracil or CPT-11, causing substantial tumor regression or complete tumor ablation.

TL;DR: Apo2L/TRAIL and FasL initiate apoptosis through similar mechanisms, and FADD may be a universal adaptor for death receptors.

TL;DR: Certain tumours may escape FasL-dependent immune-cytotoxic attack by expressing a decoy receptor that blocks FasL, which was amplified in about half of 35 primary lung and colon tumours studied and DcR3 messenger RNA was expressed in malignant tissue.

TL;DR: These findings not only provide a novel insight into the pathogenesis of the transplant-related atherosclerosis, but also point to a new therapeutic strategy that involves targeting of homing, differentiation and proliferation of putative smooth-muscle progenitor cells derived from the recipient.

TL;DR: This work identifies a mechanism that positively controls apoptosis signaling by polyubiquitination and aggregation of a key initiator caspase through a previously unknown interaction of the DISC with a cullin3 (CUL3)-based E3 ligase.