A single gene allele underlies differences in aneuploidy tolerance in yeast.

Dosage-compensated gene expression facilitates chromosomal aneuploidy, which presents a rapid route to phenotypic evolution in natural yeast isolates.

Aneuploidy produces a protein expression signature characteristic of altered metabolism and redox homeostasis, and the loss of UBP6 ameliorates several aneuploidy-associated phenotypes.

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.

Aneuploid human embryonic cells are eliminated by p53-mediated apoptosis in a gene dosage dependent manner.

Cell competition is an important mechanism selecting against aneuploid cells.

Many natural isolates of budding yeast carry extra chromosome copies and show lower-than-expected expression at a subset of amplified genes, which show unique evolutionary signatures.

Global analyses using aneuploid Drosophila revealed the dynamic roles of RNA m⁶A modification in regulating gene expression and development under genomic imbalance, highlighting its potential relationships with dosage-related effects.

Detection of aneuploidy and/or mutations in ctDNA may represent a promising approach to detecting patients with MPNST.

RNA-level regulation of gene expression is negatively associated with protein-level regulation across cellular pathways in normal tissues and cancer.