title: Targeting apoptosis for anticancer therapy.
abstract: Programmed cell death via apoptosis is characteristically disturbed in human cancers. This facilitates not only tumor formation and progression, but also treatment resistance. Since many currently applied anticancer treatment strategies rely on intact cell death signaling pathways for their therapeutic efficacy, a better understanding of the regulatory mechanisms that control cell death signaling pathways is critical to bypass resistance. Thus, reactivation of cell death programs in cancer cells may open new perspectives for more effective and more tumor-selective, yet less toxic anticancer therapies.
authors.affiliation: Institute for Experimental Cancer Research in Pediatrics, Goethe-University, Komturstr. 3a, 60528 Frankfurt, Germany. Electronic address: simone.fulda@kgu.de.
authors.forename: Simone
authors.initials: S
authors.lastname: Fulda
mesh_terms: D000970:Antineoplastic Agents / Q000627:therapeutic use*; D017209:Apoptosis / Q000187:drug effects*; D053148:Caspase 3 / Q000378:metabolism; D053181:Caspase 8 / Q000378:metabolism; D006801:Humans; D008954:Models, Biological; D009369:Neoplasms / Q000188:drug therapy* / Q000378:metabolism; D053220:Receptors, TNF-Related Apoptosis-Inducing Ligand / Q000378:metabolism; D015398:Signal Transduction / Q000187:drug effects*; D053221:TNF-Related Apoptosis-Inducing Ligand / Q000378:metabolism
chemical_list: D000970:Antineoplastic Agents; D053220:Receptors, TNF-Related Apoptosis-Inducing Ligand; D053221:TNF-Related Apoptosis-Inducing Ligand; C505653:TNFSF10 protein, human; D053148:Caspase 3; D053181:Caspase 8
keywords: Apoptosis; Cancer; Cell death; Death receptor; Mitochondria