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dc.contributor.authorTaylor, Kathryn
dc.contributor.authorMicha, Dimitra
dc.contributor.authorRanson, Malcolm R
dc.contributor.authorDive, Caroline
dc.date.accessioned2009-07-07T12:04:12Z
dc.date.available2009-07-07T12:04:12Z
dc.date.issued2006-06
dc.identifier.citationRecent advances in targeting regulators of apoptosis in cancer cells for therapeutic gain. 2006, 15 (6):669-90 Expert Opin Investig Drugsen
dc.identifier.issn1744-7658
dc.identifier.pmid16732718
dc.identifier.doi10.1517/13543784.15.6.669
dc.identifier.urihttp://hdl.handle.net/10541/72750
dc.description.abstractApoptosis is a fundamental cellular death process that is essential for normal tissue homeostasis, whose deregulation is associated with several human disease states, including cancer. Increased understanding of cancer biology has led to the hypothesis that although cancer cells are inherently resistant to the engagement of apoptosis due to the deregulation of molecular components of core apoptotic machinery or of survival signalling cascades, they are primed to die as a result of microenvironmental and oncogenic proapoptotic stress. Recently, deeper insight into the molecular regulation of apoptosis and, specifically, into its deregulation in cancer has led to the development of promising therapies to restore apoptosis and enable selective tumour cell kill. It is hoped that these mechanism-based therapies will exhibit less problematic toxicity profiles than those of conventional agents. Moreover, the development of tailored therapies directed at malignancies bearing specific alterations in apoptotic or survival signalling components may be used in combination approaches to overcome the resistance to other forms of treatment.
dc.language.isoenen
dc.subjectCanceren
dc.subjectTumour Necrosisen
dc.subject.mesh1-Phosphatidylinositol 3-Kinase
dc.subject.meshAlkaloids
dc.subject.meshAnimals
dc.subject.meshAntineoplastic Agents
dc.subject.meshApoptosis
dc.subject.meshBenzophenanthridines
dc.subject.meshCaspases
dc.subject.meshClinical Trials as Topic
dc.subject.meshDrug Evaluation, Preclinical
dc.subject.meshHumans
dc.subject.meshNeoplasms
dc.subject.meshOligonucleotides, Antisense
dc.subject.meshProtein Kinase Inhibitors
dc.subject.meshProto-Oncogene Proteins c-bcl-2
dc.subject.meshReceptors, Tumor Necrosis Factor
dc.subject.meshRecombinant Proteins
dc.subject.meshSignal Transduction
dc.subject.meshTNF-Related Apoptosis-Inducing Ligand
dc.subject.meshThionucleotides
dc.subject.meshX-Linked Inhibitor of Apoptosis Protein
dc.subject.meshbcl-X Protein
dc.titleRecent advances in targeting regulators of apoptosis in cancer cells for therapeutic gain.en
dc.typeArticleen
dc.contributor.departmentPaterson Institute for Cancer Research, Clinical and Experimental Pharmacology Group, University of Manchester, Wilmslow Road, Withington, Manchester, M20 4BX, UK.en
dc.identifier.journalExpert Opinion on Investigational Drugsen
html.description.abstractApoptosis is a fundamental cellular death process that is essential for normal tissue homeostasis, whose deregulation is associated with several human disease states, including cancer. Increased understanding of cancer biology has led to the hypothesis that although cancer cells are inherently resistant to the engagement of apoptosis due to the deregulation of molecular components of core apoptotic machinery or of survival signalling cascades, they are primed to die as a result of microenvironmental and oncogenic proapoptotic stress. Recently, deeper insight into the molecular regulation of apoptosis and, specifically, into its deregulation in cancer has led to the development of promising therapies to restore apoptosis and enable selective tumour cell kill. It is hoped that these mechanism-based therapies will exhibit less problematic toxicity profiles than those of conventional agents. Moreover, the development of tailored therapies directed at malignancies bearing specific alterations in apoptotic or survival signalling components may be used in combination approaches to overcome the resistance to other forms of treatment.


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