Entosis: aneuploidy by invasion

A. Janssen; R.H. Medema

doi:10.1038/ncb0311-199

Entosis: aneuploidy by invasion

Research output: Contribution to journal › Article › Academic › peer-review

Abstract

Aneuploidy is one of the most prevalent phenotypes of human tumours, but the underlying cause of this phenomenon remains highly debated. Entosis, the invasion of a living cell into another cell's cytoplasm, is now shown to perturb cytokinesis and induce the formation of aneuploid cells.

Original language	English
Pages (from-to)	199-201
Number of pages	3
Journal	Nature Cell Biology
Volume	13
Issue number	3
DOIs	https://doi.org/10.1038/ncb0311-199
Publication status	Published - Mar 2011

Keywords

Aneuploidy
Animals
Cell Death
Centrosome/ultrastructure
Cytokinesis
Cytoplasm/metabolism
Female
Humans
Male
Mitosis
Models, Biological
Neoplasms/pathology
Phosphorylation
Spermatozoa/pathology
Spindle Apparatus

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10.1038/ncb0311-199

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title = "Entosis: aneuploidy by invasion",

abstract = "Aneuploidy is one of the most prevalent phenotypes of human tumours, but the underlying cause of this phenomenon remains highly debated. Entosis, the invasion of a living cell into another cell's cytoplasm, is now shown to perturb cytokinesis and induce the formation of aneuploid cells.",

keywords = "Aneuploidy, Animals, Cell Death, Centrosome/ultrastructure, Cytokinesis, Cytoplasm/metabolism, Female, Humans, Male, Mitosis, Models, Biological, Neoplasms/pathology, Phosphorylation, Spermatozoa/pathology, Spindle Apparatus",

author = "A. Janssen and R.H. Medema",

year = "2011",

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AU - Janssen, A.

AU - Medema, R.H.

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KW - Animals

KW - Cell Death

KW - Centrosome/ultrastructure

KW - Cytokinesis

KW - Cytoplasm/metabolism

KW - Female

KW - Humans

KW - Male

KW - Mitosis

KW - Models, Biological

KW - Neoplasms/pathology

KW - Phosphorylation

KW - Spermatozoa/pathology

KW - Spindle Apparatus

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DO - 10.1038/ncb0311-199

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VL - 13

SP - 199

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JO - Nature Cell Biology

JF - Nature Cell Biology

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Entosis: aneuploidy by invasion

Abstract

Keywords

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