Tetraploidy, aneuploidy and cancer.
By Neil J. Ganem, Z. Storchová, D. Pellman. Current Opinion in Genetics and Development, 2007
700 citations recorded by the source corpus.
Subfields: Cell Biology, Genetics, Plant Science
View Paper: https://www.semanticscholar.org/paper/07addbea6156f0790011aae9e9bc33a220ef7df6
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Citations in the corpus
- Integrated Analysis of TP53 Gene and Pathway Alterations in The Cancer Genome Atlas (2019, result): “Our genomic instability results are consistent with recent experimental data indicating that p53 is directly involved in suppression of aneuploidy by engaging a ploidy sensing checkpoint that blocks proliferation of tetraploid and aneuploid cells (Dalton et al., 2010; Ganem et al., 2007; Hanel and M”
- Aurora B-mediated abscission checkpoint protects against tetraploidization. (2009, unknown): “Failures in cytokinesis can lead to tetraploidy (Caldwell et al., 2007; Fujiwara et al., 2005; Ganem et al., 2007; Uetake and Sluder, 2004), a state that has for a long time been suspected to contribute to cancer formation (Caldwell et al.”
- Principles of Cancer Therapy: Oncogene and Non-oncogene Addiction (2009, unknown): “In addition, the CIN phenotype could result from the presence of extra centrosomes in tumor cells or from stresses placed on the mitotic apparatus due to the need to segregate supernumerary chromosomes (Ganem et al., 2007).”
- Causes and consequences of aneuploidy in cancer (2012, background): “In fact, buffering the effects of aneuploidy and facilitating a combination of whole-chromosome aneuploidies, which would otherwise be lethal in diploid cells, could be one mechanism by which genome doubling promotes transformatio”
- Mechanisms to suppress multipolar divisions in cancer cells with extra centrosomes. (2008, background): “Centrosome amplification can, in principle, arise from several types of cell division errors: centrosome overduplication, de novo synthesis of centrosomes, cell fusion, or cytokinesis failure (Boveri 1929; Nigg 2002; Ganem et al. 2007).”
- Boveri revisited: Chromosomal instability, aneuploidy and tumorigenesis (2009, background): “This might reflect an increase in DNA damage in tetraploid cells or, alternatively, a proliferative advantage of tetraploid cells that possess broken or rearranged chromosome”