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Abstract
Nuclear size normally scales with the size of the cell, but in cancer this 'karyoplasmic ratio' is disrupted. This is particularly so in more metastatic tumors where changes in the karyoplasmic ratio are used in both diagnosis and prognosis for several tumor types. However, the direction of nuclear size changes differs for particular tumor types: for example in breast cancer, larger nuclear size correlates with increased metastasis, while for lung cancer smaller nuclear size correlates with increased metastasis. Thus, there must be tissue-specific drivers of the nuclear size changes, but proteins thus far linked to nuclear size regulation are widely expressed. Notably, for these tumor types, ploidy changes have been excluded as the basis for nuclear size changes, and so, the increased metastasis is more likely to have a basis in the nuclear morphology change itself. We review what is known about nuclear size regulation and postulate how such nuclear size changes can increase metastasis and why the directionality can differ for particular tumor types.
Original language | English |
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Pages (from-to) | 1333-1344 |
Number of pages | 12 |
Journal | Biochemical Society Transactions |
Volume | 45 |
Issue number | 6 |
Early online date | 17 Nov 2017 |
DOIs | |
Publication status | Published - 15 Dec 2017 |
Keywords
- cancer
- karyoplasmic
- ratio
- lamin
- NET
- nuclear size
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Dive into the research topics of 'Breaking the scale: How disrupting the karyoplasmic ratio gives cancer cells an advantage for metastatic invasion'. Together they form a unique fingerprint.Projects
- 2 Finished
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Core funding renewal for the Wellcome Trust Centre for Cell Biology
1/10/11 → 30/04/17
Project: Research