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dc.contributor.authorGoldar, S
dc.contributor.authorKhaniani, MS
dc.contributor.authorDerakhshan, SM
dc.contributor.authorBaradaran, B
dc.date.accessioned2018-08-26T05:45:39Z
dc.date.available2018-08-26T05:45:39Z
dc.date.issued2015
dc.identifier.urihttp://dspace.tbzmed.ac.ir:8080/xmlui/handle/123456789/40956
dc.description.abstractProgrammed cell death (PCD) or apoptosis is a mechanism which is crucial for all multicellular organisms to control cell proliferation and maintain tissue homeostasis as well as eliminate harmful or unnecessary cells from an organism. Defects in the physiological mechanisms of apoptosis may contribute to different human diseases like cancer. Identification of the mechanisms of apoptosis and its effector proteins as well as the genes responsible for apoptosis has provided a new opportunity to discover and develop novel agents that can increase the sensitivity of cancer cells to undergo apoptosis or reset their apoptotic threshold. These novel targeted therapies include those targeting anti-apoptotic Bcl-2 family members, p53, the extrinsic pathway, FLICE-inhibitory protein (c-FLIP), inhibitor of apoptosis (IAP) proteins, and the caspases. In recent years a number of these novel agents have been assessed in preclinical and clinical trials. In this review, we introduce some of the key regulatory molecules that control the apoptotic pathways, extrinsic and intrinsic death receptors, discuss how defects in apoptotic pathways contribute to cancer, and list several agents being developed to target apoptosis.
dc.language.isoEnglish
dc.relation.ispartofAsian Pacific journal of cancer prevention : APJCP
dc.subjectAnimals
dc.subjectAntineoplastic Agents
dc.subjectApoptosis
dc.subjectHumans
dc.subjectInhibitor of Apoptosis Proteins
dc.subjectMolecular Targeted Therapy
dc.subjectNeoplasms
dc.subjectSignal Transduction
dc.titleMolecular mechanisms of apoptosis and roles in cancer development and treatment.
dc.typearticle
dc.citation.volume16
dc.citation.issue6
dc.citation.spage2129
dc.citation.epage44
dc.citation.indexPubmed


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