The nuclear envelope environment and its cancer connections.
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TLDR
The progress that has been made in understanding of the nuclear envelope and the implications of changes in this environment for cancer biology are summarized.Abstract:
Aberrant nuclear morphology is already used as a diagnostic criterion for cancer, but why is the nucleus deformed in cancer cells? This Review discusses how components of the nuclear envelope and the adjoining lamina are deregulated in cancer cells and the consequences of this change in cell morphology.read more
Citations
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ERK1/2 MAP kinases: structure, function, and regulation.
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Physical limits of cell migration: Control by ECM space and nuclear deformation and tuning by proteolysis and traction force
Katarina Wolf,Mariska te Lindert,Marina Krause,Stephanie Alexander,Joost te Riet,Amanda L. Willis,Robert M. Hoffman,Carl G. Figdor,Stephen J. Weiss,Peter Friedl +9 more
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The ErbB/HER family of protein-tyrosine kinases and cancer.
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Segmentation of Nuclei in Histopathology Images by Deep Regression of the Distance Map
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References
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TL;DR: Telomere length is a biomarker of somatic cell aging in humans and is consistent with a causal role for telomere loss in this process, and fibroblasts from Hutchinson-Gilford progeria donors had short telomeres, consistent with their reduced division potential in vitro.
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A Tense Situation: Forcing Tumour Progression
TL;DR: The changing force that cells experience needs to be considered when trying to understand the complex nature of tumorigenesis.
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Loss of a-Type Lamin Expression Compromises Nuclear Envelope Integrity Leading to Muscular Dystrophy
Teresa Sullivan,Diana Escalante-Alcalde,Harshida Bhatt,Miriam R. Anver,Narayan K. Bhat,Kunio Nagashima,Colin L. Stewart,Brian Burke +7 more
TL;DR: It is shown that mice lacking A-type lamins develop to term with no overt abnormalities, however, their postnatal growth is severely retarded and is characterized by the appearance of muscular dystrophy.
Journal ArticleDOI
Lamin A-Dependent Nuclear Defects in Human Aging
Paola Scaffidi,Tom Misteli +1 more
TL;DR: It is shown that the same molecular mechanism responsible for HGPS is active in healthy cells, and inhibition of this splice site reverses the nuclear defects associated with aging.