
DOI . ORG {
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Title[redir]:
Mitotic catastrophe: a mechanism for avoiding genomic instability | Nature Reviews Molecular Cell Biology
Description:
The improper distribution of chromosomes during mitosis can contribute to malignant transformation. Higher eukaryotes have developed strategies for eliminating mitosis-incompetent cells, one of which is mitotic catastrophe. From a functional perspective, mitotic catastrophe can be defined as an oncosuppressive mechanism that precedes (and is distinct from) apoptosis, necrosis or senescence. The improper distribution of chromosomes during mitosis compromises cellular functions and can reduce cellular fitness or contribute to malignant transformation. As a countermeasure, higher eukaryotes have developed strategies for eliminating mitosis-incompetent cells, one of which is mitotic catastrophe. Mitotic catastrophe is driven by a complex and poorly understood signalling cascade but, from a functional perspective, it can be defined as an oncosuppressive mechanism that precedes (and is distinct from) apoptosis, necrosis or senescence. Accordingly, the disruption of mitotic catastrophe precipitates tumorigenesis and cancer progression, and its induction constitutes a therapeutic endpoint.
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pubmed, article, google, scholar, cas, cell, mitotic, cancer, central, death, nature, cells, biol, catastrophe, checkpoint, mol, rev, information, apoptosis, kroemer, vitale, galluzzi, access, function, aneuploidy, spindle, supplementary, castedo, guido, sci, chromosome, res, phosphorylation, france, content, mitosis, tumor, cycle, paris, cookies, molecular, instability, ilio, lorenzo, cellular, differ, induces, mechanisms, therapy, caspase,
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nature portfolio permissions reprints privacy policy advertising social media radiation-induced dna damage nature rev cdk1–cyclin b1 initiates caspase-mediated specific cleavage natural ent-kaurene diterpenoid nature med selective small-molecule inhibitor nature chem author correspondence linking kinetochore-microtubule binding nature 471 nature dna damage induces supplementary information s1 cancéropôle ile-de-france personal data p53-dependent postmitotic checkpoint springerlink instant access supplementary information s2 supplementary information s3 supplementary information s4 eliminating mitosis-incompetent cells avoiding genomic instability data protection cdk1-mediated signal pathway-directed drug discovery dna damage checkpoints molecular life sciences small molecule inhibitor gene fusions induces mitotic arrest dna-binding domain article vitale pôle de biologie cancer metastasis rev differential mitotic responses privacy transcription-dependent manner cell death induced maria castedo competing financial interests homepage rights checkpoint kinase-1 targeting mitotic arrest induced hansemann-boveri hypothesis
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headline:Mitotic catastrophe: a mechanism for avoiding genomic instability
description:The improper distribution of chromosomes during mitosis can contribute to malignant transformation. Higher eukaryotes have developed strategies for eliminating mitosis-incompetent cells, one of which is mitotic catastrophe. From a functional perspective, mitotic catastrophe can be defined as an oncosuppressive mechanism that precedes (and is distinct from) apoptosis, necrosis or senescence. The improper distribution of chromosomes during mitosis compromises cellular functions and can reduce cellular fitness or contribute to malignant transformation. As a countermeasure, higher eukaryotes have developed strategies for eliminating mitosis-incompetent cells, one of which is mitotic catastrophe. Mitotic catastrophe is driven by a complex and poorly understood signalling cascade but, from a functional perspective, it can be defined as an oncosuppressive mechanism that precedes (and is distinct from) apoptosis, necrosis or senescence. Accordingly, the disruption of mitotic catastrophe precipitates tumorigenesis and cancer progression, and its induction constitutes a therapeutic endpoint.
datePublished:2011-04-29T00:00:00Z
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Cell death
Chromosomes
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Life Sciences
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Biochemistry
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name:Ilio Vitale, Lorenzo Galluzzi, Maria Castedo and Guido Kroemer are at the Institut National de la Santé et de la Recherche Médicale (INSERM), U848, Pavillon de Recherche 1, 39 rue Camille Desmoulins, F-94805 Villejuif, France.,
name:Ilio Vitale, Lorenzo Galluzzi and Maria Castedo are also at the Institut Gustave Roussy, and the Université Paris-Sud, Paris 11, F-94805 Villejuif, France.,
name:Ilio Vitale, Lorenzo Galluzzi, Maria Castedo and Guido Kroemer are at the Institut National de la Santé et de la Recherche Médicale (INSERM), U848, Pavillon de Recherche 1, 39 rue Camille Desmoulins, F-94805 Villejuif, France.,
name:Ilio Vitale, Lorenzo Galluzzi and Maria Castedo are also at the Institut Gustave Roussy, and the Université Paris-Sud, Paris 11, F-94805 Villejuif, France.,
name:Ilio Vitale, Lorenzo Galluzzi, Maria Castedo and Guido Kroemer are at the Institut National de la Santé et de la Recherche Médicale (INSERM), U848, Pavillon de Recherche 1, 39 rue Camille Desmoulins, F-94805 Villejuif, France.,
name:Ilio Vitale, Lorenzo Galluzzi and Maria Castedo are also at the Institut Gustave Roussy, and the Université Paris-Sud, Paris 11, F-94805 Villejuif, France.,
name:Ilio Vitale, Lorenzo Galluzzi, Maria Castedo and Guido Kroemer are at the Institut National de la Santé et de la Recherche Médicale (INSERM), U848, Pavillon de Recherche 1, 39 rue Camille Desmoulins, F-94805 Villejuif, France.,
name:Guido Kroemer is also at the Metabolomics Platform, Institut Gustave Roussy, F-94805 Villejuif, France; the Centre de Recherche des Cordeliers, F-75005 Paris, France; the Pôle de Biologie, Hôpital Européen Georges Pompidou, AP-HP, F-75908 Paris, France; and the Université Paris Descartes, Paris 5, F-75270 Paris, France.,
name:the Centre de Recherche des Cordeliers, F-75005 Paris, France,
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