Chromosomal instability through spindle assembly checkpoint alleviation facilitates malignant transformation of hepatocytes and T-cells in vivo, resulting in cancers with recurrent karyotypes.

Chromosomal instability of cancer can be quantitatively measured by phylogenetic analysis of 200 tumor cells while using evolutionary principles to account for cellular selection.

Genetic analyses reveal that purely quantitative changes in the relative copy number of chromosomes can be sufficient to disrupt the epigenetic mechanisms that define the cells' differentiated state.

Aneuploidy can cause chromosome mis-segregation and specific cellular phenotypes driven by expression of genes on the extra chromosome.

Human cell lines regress to become ‘de-sexualized’ by reconfiguring to a 2:3 X/A ratio of high fitness, thus shedding light on the evolution of mammalian sex chromosomes.

Novel segmental chromosome amplifications in Candida albicans provide rapid adaptation to the most widely used antifungal drugs.

Proximity and homology guided inter-chromosomal translocations drive karyotype evolution.

Protein kinase A (PKA) phosphorylates Raptor and inhibits mammalian target of rapamycin complex 1 (mTORC1) activity.

De novo formation of centromeres creates diverse karyotypes in flies and is accompanied by rapid turnover of centromere-associated satellite repeats.

Dosage compensation does not take place in wild yeast strains.