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Targeting DNA Damage in SCLC

2017-12Journal article Open access
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dc.contributor.authorFoy, V
dc.contributor.authorSchenk, MW
dc.contributor.authorBaker, K
dc.contributor.authorGomes, F
dc.contributor.authorLallo, A
dc.contributor.authorFrese, KK
dc.contributor.authorForster, M
dc.contributor.authorDive, C
dc.contributor.authorBlackhall, F
dc.date.accessioned2017-12-12T15:39:56Z
dc.date.available2017-12-12T15:39:56Z
dc.date.issued2017-12
dc.description.abstractSCLC accounts for 15% of lung cancer worldwide. Characterised by early dissemination and rapid development of chemo-resistant disease, less than 5% of patients survive 5 years. Despite 3 decades of clinical trials there has been no change to the standard platinum and etoposide regimen for first line treatment developed in the 1970's. The exceptionally high number of genomic aberrations observed in SCLC combined with the characteristic rapid cellular proliferation results in accumulation of DNA damage and genomic instability. To flourish in this precarious genomic context, SCLC cells are reliant on functional DNA damage repair pathways and cell cycle checkpoints. Current cytotoxic drugs and radiotherapy treatments for SCLC have long been known to act by induction of DNA damage and the response of cancer cells to such damage determines treatment efficacy. Recent years have witnessed improved understanding of strategies to exploit DNA damage and repair mechanisms in order to increase treatment efficacy. This review will summarise the rationale to target DNA damage response in SCLC, the progress made in evaluating novel DDR inhibitors and highlight various ongoing challenges for their clinical development in this disease.pt_PT
dc.description.versioninfo:eu-repo/semantics/publishedVersionpt_PT
dc.identifier.citationLung Cancer. 2017 Dec;114:12-22pt_PT
dc.identifier.doi10.1016/j.lungcan.2017.10.006pt_PT
dc.identifier.urihttp://hdl.handle.net/10400.17/2823
dc.language.isoengpt_PT
dc.peerreviewedyespt_PT
dc.publisherElsevierpt_PT
dc.subjectCHLC ONCpt_PT
dc.subjectAurora Kinases/therapeutic usept_PT
dc.subjectAzepines/therapeutic usept_PT
dc.subjectBenzimidazoles/therapeutic usept_PT
dc.subjectCarbolines/therapeutic usept_PT
dc.subjectCell Cycle Checkpoints/drug effectspt_PT
dc.subjectCell Cycle Checkpoints/genetics
dc.subjectCell Proliferation/drug effects
dc.subjectCell Proliferation/genetics
dc.subjectCytotoxins/therapeutic use
dc.subjectDNA Damage/drug effects
dc.subjectDNA Damage/genetics
dc.subjectDNA Repair
dc.subjectEtoposide/therapeutic use
dc.subjectGenomic Instability/drug effects
dc.subjectGenomic Instability/genetics
dc.subjectHeterocyclic Compounds, 4 or More Rings/therapeutic use
dc.subjectLung Neoplasms/drug therapy
dc.subjectLung Neoplasms/genetics
dc.subjectMolecular Targeted Therapy/methods
dc.subjectPhthalazines/therapeutic use
dc.subjectPiperazines/therapeutic use
dc.subjectPoly(ADP-ribose) Polymerase Inhibitors/therapeutic use
dc.subjectProtein Kinase Inhibitors/therapeutic use
dc.subjectPyrimidines/therapeutic use
dc.subjectRad51 Recombinase/antagonists & inhibitors
dc.subjectRad51 Recombinase/therapeutic use
dc.subjectSmall Cell Lung Carcinoma/drug therapy
dc.subjectSmall Cell Lung Carcinoma/genetics
dc.titleTargeting DNA Damage in SCLCpt_PT
dc.typejournal article
dspace.entity.typePublication
oaire.citation.endPage22pt_PT
oaire.citation.startPage12pt_PT
oaire.citation.titleLung Cancerpt_PT
oaire.citation.volume114pt_PT
rcaap.rightsopenAccesspt_PT
rcaap.typearticlept_PT

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