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

Fifteen continuous high-grade serous ovarian carcinoma patient-derived organoids are characterized by transcriptomic, genomic, and drug sensitivity assays to reveal that they comprise communities of clonal populations and represent models of different causes of chromosomal instability and degrees of genome complexity.

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

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

SPOP mutations underlie a novel, genomically unstable subclass of prostate cancer by altering DNA repair.

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

Mutation of Glycine 34 to Arginine within the N-terminal tail of histone H3 alters post-translational modifications on Lysine 36 and is associated with a delay in replication restart, defective homologous recombination and an increase in genomic instability.

The presence of cenexin at the old centrosome imposes a functional asymmetry on the mitotic spindle that impacts chromosome alignment and segregation.

XTABLE is the first easy-to-use bioinformatic solution that has been conceived and designed solely to interrogate the transcriptomes of premalignant stages of lung squamous cell carcinoma (LUSC) and enhance the development of LUSC prevention and detection strategies.