Death Receptors in Cancer Therapy [Hardcover]

An in depth review of our latest understanding of the molecular events that regulate cell death and those molecules that provide targets for developing agonists or antagonists to modulate death signaling for therapeutic purposes. The authors focus on the extrinsic system of death receptors, their regulation and function, and their abnormalities in cancer. Topics of particular interest include resistance to apoptosis, TRAIL signaling, death receptors in embryonic development, mechanisms of caspase activation, and death receptor mutations in cancer. Additional chapters address death signaling in melanoma, synthetic retinoids and death receptors, the role of p53 in death receptor regulation, immune suppression of cancer, and combination therapy with death ligands.An in depth review of our latest understanding of the molecular events that regulate cell death and those molecules that provide targets for developing agonists or antagonists to modulate death signaling for therapeutic purposes. The authors focus on the extrinsic system of death receptors, their regulation and function, and their abnormalities in cancer. Topics of particular interest include resistance to apoptosis, TRAIL signaling, death receptors in embryonic development, mechanisms of caspase activation, and death receptor mutations in cancer. Additional chapters address death signaling in melanoma, synthetic retinoids and death receptors, the role of p53 in death receptor regulation, immune suppression of cancer, and combination therapy with death ligands.Mammalian Cell Death Pathways: Intrinsic and ExtrinsicE. Robert McDonald III and Wafik S. El-DeiryResistance to Apoptosis in Cancer TherapyDavid J. McConkeyStructures of TNF Receptors and Their Interactions With LigandsSarah G. Hymowitz and Abraham M. de VosDeath Receptor Signaling in Embryonic Ectodermal DevelopmentPreet M. ChaudharyAdaptor Proteins in Death Receptor SignalingNien-Jung Chen and Wen-Chen YehCaspase Activation by the Extrinsic PathwayXiaolãg