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Coordinated regulation of co-complex members compensates for aneuploidy-induced stoichiometric imbalances in human cancer.

The wtf meiotic drivers change the fitness landscape of meiosis in outcrossed Schizosaccharomyces pombe demonstrating that genetic parasites can favor the evolution of variants that disrupt meiotic fidelity.

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

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

Strengthening of spindle assembly checkpoint activity and attachment error correction through BubR1 manipulation preserves genomic integrity and protects against tumor formation.

Rapid acquisition of chromosome rearrangements, together with independently acting transmission distorter alleles on each chromosome, drive near complete sterility in fission yeast hybrids.

Complex chromosomal rearrangements similar to those described in cancer and developmental syndromes occur in plants during postzygotic genome elimination, a centromeric-derived incompatibility.

Multiple age-related changes in chromosome architecture could explain why human oocyte aneuploidy increases with advanced maternal age.

The creation of a non-invasive assay for detecting urothelial cancer could have a profound impact on how we find and treat the disease.

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