TRAIL is a member of the Tumour Necrosis Factor (TNF) Family and a potent inducer of apoptosis in many breast carcinoma cell lines but not in normal human mammary epithelial cells. In vivo administration of soluble TRAIL causes regression of breast cancer xenografts without causing measurable toxicity. Combining it with other traditional anti-cancer therapies enhances the efficacy of TRAIL treatment. The basis for the resistance of normal breast epithelial cells to TRAIL-induced apoptosis will be investigated using filter arrays and high-density microarrays. Using a similar approach, the synergy between TRAIL and other cancer therapies will be studied.
References
Chinnaiyan, A.M., O'Rourke, K., Tewari, M. & Dixit, V.M. FADD, a novel death domain-containing protein, interacts with the death domain of Fas and initiates apoptosis. Cell 81, 505–512 (1995)
Muzio, M., Chinnaiyan et al. FLICE, a novel FADD-homologous ICE/CED-3-like protease, is recruited to the CD95 (Fas/APO-1) death-inducing signaling complex. Cell 85, 817–827 (1996)
Chinnaiyan, A.M. et al. Signal transduction by DR3, a novel death domain-containing receptor related to tumour necrosis factor receptor-1 and Fas/APO-1. Science 271, 990–992 (1996)
Pan, G. et al. The receptor for the cytotoxic ligand TRAIL. Science 276, 111–113 (1997)
Chinnaiyan, A.M. The apoptosome: heart and soul of the cell death machine. Neoplasia 1, 5–15 (1999)
Rehemtulla, A. et al. A caspase-resistant form of bcl-xL, but not wild type bcl-xL, promotes clonogenic survival after radiation. Neoplasia 1, 63–70 (1999)
Author information
Authors and Affiliations
Rights and permissions
About this article
Cite this article
Chinnaiyan, A. Using microarrays to study apoptosis. Nat Genet 23 (Suppl 3), 39 (1999). https://doi.org/10.1038/14285
Issue Date:
DOI: https://doi.org/10.1038/14285
