{"@context":{"@vocab":"https://cir.nii.ac.jp/schema/1.0/","rdfs":"http://www.w3.org/2000/01/rdf-schema#","dc":"http://purl.org/dc/elements/1.1/","dcterms":"http://purl.org/dc/terms/","foaf":"http://xmlns.com/foaf/0.1/","prism":"http://prismstandard.org/namespaces/basic/2.0/","cinii":"http://ci.nii.ac.jp/ns/1.0/","datacite":"https://schema.datacite.org/meta/kernel-4/","ndl":"http://ndl.go.jp/dcndl/terms/","jpcoar":"https://github.com/JPCOAR/schema/blob/master/2.0/"},"@id":"https://cir.nii.ac.jp/crid/1362262943555334272.json","@type":"Article","productIdentifier":[{"identifier":{"@type":"DOI","@value":"10.1126/science.1140735"}},{"identifier":{"@type":"URI","@value":"https://www.science.org/doi/pdf/10.1126/science.1140735"}}],"dc:title":[{"@value":"An Oncogene-Induced DNA Damage Model for Cancer Development"}],"description":[{"type":"abstract","notation":[{"@value":"<jats:p>\n            Of all types of DNA damage, DNA double-strand breaks (DSBs) pose the greatest challenge to cells. One might have, therefore, anticipated that a sizable number of DNA DSBs would be incompatible with cell proliferation. Yet recent experimental findings suggest that, in both precancerous lesions and cancers, activated oncogenes induce stalling and collapse of DNA replication forks, which in turn leads to formation of DNA DSBs. This continuous formation of DNA DSBs may contribute to the genomic instability that characterizes the vast majority of human cancers. In addition, in precancerous lesions, these DNA DSBs activate\n            <jats:italic>p53</jats:italic>\n            , which, by inducing apoptosis or senescence, raises a barrier to tumor progression. Breach of this barrier by various mechanisms, most notably by\n            <jats:italic>p53</jats:italic>\n            mutations, that impair the DNA damage response pathway allows cancers to develop. Thus, oncogene-induced DNA damage may explain two key features of cancer: genomic instability and the high frequency of\n            <jats:italic>p53</jats:italic>\n            mutations.\n          </jats:p>"}]}],"creator":[{"@id":"https://cir.nii.ac.jp/crid/1382262943555334273","@type":"Researcher","foaf:name":[{"@value":"Thanos D. Halazonetis"}],"jpcoar:affiliationName":[{"@value":"Department of Molecular Biology and Department of Biochemistry, University of Geneva, CH-1205 Geneva, Switzerland."},{"@value":"Department of Histology and Embryology, School of Medicine, University of Athens, GR-11527 Athens, Greece."},{"@value":"Institute of Cancer Biology and Centre for Genotoxic Stress Research, Danish Cancer Society, DK-2100 Copenhagen, Denmark."}]},{"@id":"https://cir.nii.ac.jp/crid/1382262943555334272","@type":"Researcher","foaf:name":[{"@value":"Vassilis G. Gorgoulis"}],"jpcoar:affiliationName":[{"@value":"Department of Molecular Biology and Department of Biochemistry, University of Geneva, CH-1205 Geneva, Switzerland."},{"@value":"Department of Histology and Embryology, School of Medicine, University of Athens, GR-11527 Athens, Greece."},{"@value":"Institute of Cancer Biology and Centre for Genotoxic Stress Research, Danish Cancer Society, DK-2100 Copenhagen, Denmark."}]},{"@id":"https://cir.nii.ac.jp/crid/1382262943555334274","@type":"Researcher","foaf:name":[{"@value":"Jiri Bartek"}],"jpcoar:affiliationName":[{"@value":"Department of Molecular Biology and Department of Biochemistry, University of Geneva, CH-1205 Geneva, Switzerland."},{"@value":"Department of Histology and Embryology, School of Medicine, University of Athens, GR-11527 Athens, Greece."},{"@value":"Institute of Cancer Biology and Centre for Genotoxic Stress Research, Danish Cancer Society, DK-2100 Copenhagen, Denmark."}]}],"publication":{"publicationIdentifier":[{"@type":"PISSN","@value":"00368075"},{"@type":"EISSN","@value":"10959203"}],"prism:publicationName":[{"@value":"Science"}],"dc:publisher":[{"@value":"American Association for the Advancement of Science (AAAS)"}],"prism:publicationDate":"2008-03-07","prism:volume":"319","prism:number":"5868","prism:startingPage":"1352","prism:endingPage":"1355"},"reviewed":"false","url":[{"@id":"https://www.science.org/doi/pdf/10.1126/science.1140735"}],"createdAt":"2008-03-06","modifiedAt":"2024-01-10","relatedProduct":[{"@id":"https://cir.nii.ac.jp/crid/1050025031480679296","@type":"Article","resourceType":"学術雑誌論文(journal article)","relationType":["isReferencedBy"],"jpcoar:relatedTitle":[{"@language":"en","@value":"ATM-Mediated DNA Damage Signals Mediate Immune Escape through Integrin-αvβ3-Dependent Mechanisms"}]},{"@id":"https://cir.nii.ac.jp/crid/1050294960530684800","@type":"Article","resourceType":"学術雑誌論文(journal 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