Apoptotic Pathways as Targets for Novel Therapies in Cancer by Greet Brouckaert, Michael Kalai (auth.), Marek Los, Spencer

By Greet Brouckaert, Michael Kalai (auth.), Marek Los, Spencer B. Gibson (eds.)

As our figuring out of apoptotic pathway expands, we're coming to gain the nice strength of using this pathway to regard ailments comparable to melanoma. The publication makes an attempt to check, summarize, and speculate at the apoptotic pathways, how are they regulated and the way exact cures are getting used to regard a large choice of illnesses. exact emphasis is put on melanoma because new remedies both being built or presently within the medical surroundings are exhibiting nice promise to extend survival premiums for melanoma sufferers. Chapters will deal with the biology at the back of regulating the apoptotic pathways and what is going flawed in disorder states while different chapters will be aware of new remedies focusing on apoptotic pathways. The reader through the top of the publication must have higher perception into the certainty and usage of apoptotic pathways to struggle illnesses resembling melanoma.

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Extra resources for Apoptotic Pathways as Targets for Novel Therapies in Cancer and Other Diseases

Example text

Other than activation of DNA damage sensors, radiation can induce ceramide generation, both at the plasma membrane by activating acid sphingomyelinase and enzymatic hydrolysis of sphingomyelin, and in mitochondria by inducing de novo synthesis of ceramide (Fig. 1). Ceramide then acts as a second messenger and initiates an apoptotic response. In some cells and tissues, this occurs through activation of Bax and release of mitochondrial cytochrome c (Kolesnick & Fuks, 2003). Another DNA damageinduced pathway has been suggested for regulating apoptosis induced by various stress stimuli, including those occurring due to exposure to genotoxins or irradiation.

The induction of apoptosis by NRADD is dependent on the activation of caspase-8, but does not require the mitochondrial components of the death program. Interestingly, the Nglycosylated, NHa-terminal domain of the protein is short and unique. Deletion of this domain produces a dominant-negative form of NRADD that protects cells from ER stress-induced apoptosis, suggesting that the lumenal part of the protein is required for inducing the proapoptotic signal. , 2003a). Mobilization of ER calcium stores can sensitize mitochondria to direct proapoptotic stimuli and promote the activation of cytoplasmic death pathways.

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