TY - JOUR
T1 - Dr Jekyll and Mr Hyde
T2 - Role of aneuploidy in cellular adaptation and cancer
AU - Pavelka, Norman
AU - Rancati, Giulia
AU - Li, Rong
N1 - Funding Information:
This work is supported by NIH grant RO1GM059964 to RL.
PY - 2010/12
Y1 - 2010/12
N2 - When cells in our body change their genome and develop into cancer, we blame it on genome instability. When novel species conquer inhospitable environments, we credit it to genome evolution. From a cellular perspective, however, both processes are outcomes of the same fundamental biological properties. - genome and pathway plasticity and the natural selection of cells that escape death and acquire growth advantages. Unraveling the consequences of genome plasticity at a cellular level is not only central to the understanding of species evolution but also crucial to deciphering important cell biological problems, such as how cancer cells emerge and how pathogens develop drug resistance. Aside from the well-known role of DNA sequence mutations, recent evidence suggests that changes in DNA copy numbers in the form of segmental or whole-chromosome aneuploidy can bring about large phenotypic variation. Although usually detrimental under conditions suitable for normal proliferation of euploid cells, aneuploidization may be a frequently occurring genetic change that enables pathogens or cancer cells to escape physiological or pharmacological roadblocks.
AB - When cells in our body change their genome and develop into cancer, we blame it on genome instability. When novel species conquer inhospitable environments, we credit it to genome evolution. From a cellular perspective, however, both processes are outcomes of the same fundamental biological properties. - genome and pathway plasticity and the natural selection of cells that escape death and acquire growth advantages. Unraveling the consequences of genome plasticity at a cellular level is not only central to the understanding of species evolution but also crucial to deciphering important cell biological problems, such as how cancer cells emerge and how pathogens develop drug resistance. Aside from the well-known role of DNA sequence mutations, recent evidence suggests that changes in DNA copy numbers in the form of segmental or whole-chromosome aneuploidy can bring about large phenotypic variation. Although usually detrimental under conditions suitable for normal proliferation of euploid cells, aneuploidization may be a frequently occurring genetic change that enables pathogens or cancer cells to escape physiological or pharmacological roadblocks.
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U2 - 10.1016/j.ceb.2010.06.003
DO - 10.1016/j.ceb.2010.06.003
M3 - Review article
C2 - 20655187
AN - SCOPUS:78649636162
SN - 0955-0674
VL - 22
SP - 809
EP - 815
JO - Current Opinion in Cell Biology
JF - Current Opinion in Cell Biology
IS - 6
ER -