Matthews, HK;
Bertoli, C;
de Bruin, RAM;
(2022)
Cell cycle control in cancer.
Nature Reviews Molecular Cell Biology
, 23
pp. 74-88.
10.1038/s41580-021-00404-3.
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Abstract
Cancer is a group of diseases in which cells divide continuously and excessively. Cell division is tightly regulated by multiple evolutionarily conserved cell cycle control mechanisms, to ensure the production of two genetically identical cells. Cell cycle checkpoints operate as DNA surveillance mechanisms that prevent the accumulation and propagation of genetic errors during cell division. Checkpoints can delay cell cycle progression or, in response to irreparable DNA damage, induce cell cycle exit or cell death. Cancer-associated mutations that perturb cell cycle control allow continuous cell division chiefly by compromising the ability of cells to exit the cell cycle. Continuous rounds of division, however, create increased reliance on other cell cycle control mechanisms to prevent catastrophic levels of damage and maintain cell viability. New detailed insights into cell cycle control mechanisms and their role in cancer reveal how these dependencies can be best exploited in cancer treatment.
Type: | Article |
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Title: | Cell cycle control in cancer |
Open access status: | An open access version is available from UCL Discovery |
DOI: | 10.1038/s41580-021-00404-3 |
Publisher version: | https://doi.org/10.1038/s41580-021-00404-3 |
Language: | English |
Additional information: | This version is the author accepted manuscript. For information on re-use, please refer to the publisher’s terms and conditions. |
Keywords: | Cancer, Cell division, Checkpoints, DNA damage checkpoints, Tumour-suppressor proteins |
UCL classification: | UCL UCL > Provost and Vice Provost Offices > School of Life and Medical Sciences UCL > Provost and Vice Provost Offices > School of Life and Medical Sciences > Faculty of Life Sciences UCL > Provost and Vice Provost Offices > School of Life and Medical Sciences > Faculty of Life Sciences > Lab for Molecular Cell Bio MRC-UCL |
URI: | https://discovery.ucl.ac.uk/id/eprint/10135932 |
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