In:
eLife, eLife Sciences Publications, Ltd, Vol. 6 ( 2017-03-20)
Abstract:
An estimated 350 billion of the cells in the human body are dividing at any given moment. Every cell division requires the 46 chromosomes in the cell, which store the genetic information that the cell needs to survive, to be copied and distributed evenly between the two new cells. Sometimes mistakes in cell division can result in cells that have the wrong number of chromosomes – a state called aneuploidy. Aneuploidy is rare in healthy cells but occurs in over 75% of cancers. It is the result of a process called chromosomal instability that often leads to the death of healthy cells. However, it is not well understood how aneuploidy affects how cancer cells develop or behave. Mice are commonly used to investigate cancer because they have many genetic similarities with humans. To better understand the relationship between aneuploidy and cancer, Foijer, Albacker et al. engineered mice in which they could induce aneuploidy in liver cells and immune cells called T-cells. This modification accelerated the formation of liver cancer and lymphoma – a cancer of the immune system. The number of chromosomes in the cells of these cancers varied greatly, demonstrating that these cells experience constant chromosomal instability. Overall, this suggests that aneuploidy increases the likelihood of cancer developing. The mouse cancer cells closely resemble their human counterparts, and so could potentially be used to test new cancer drugs. In the future, developing new therapies that selectively target aneuploid cells could result in cancer treatments that have fewer side effects than existing treatments.
Type of Medium:
Online Resource
ISSN:
2050-084X
DOI:
10.7554/eLife.20873.001
DOI:
10.7554/eLife.20873.002
DOI:
10.7554/eLife.20873.003
DOI:
10.7554/eLife.20873.004
DOI:
10.7554/eLife.20873.005
DOI:
10.7554/eLife.20873.006
DOI:
10.7554/eLife.20873.007
DOI:
10.7554/eLife.20873.008
DOI:
10.7554/eLife.20873.009
DOI:
10.7554/eLife.20873.010
DOI:
10.7554/eLife.20873.011
DOI:
10.7554/eLife.20873.012
DOI:
10.7554/eLife.20873.013
DOI:
10.7554/eLife.20873.014
DOI:
10.7554/eLife.20873.015
DOI:
10.7554/eLife.20873.016
DOI:
10.7554/eLife.20873.017
DOI:
10.7554/eLife.20873.018
DOI:
10.7554/eLife.20873.027
DOI:
10.7554/eLife.20873.028
Language:
English
Publisher:
eLife Sciences Publications, Ltd
Publication Date:
2017
detail.hit.zdb_id:
2687154-3
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