Cohesin is a large ring-shaped protein complex, conserved from yeast to human, 
which participates in most DNA transactions that take place in the nucleus. It 
mediates sister chromatid cohesion, which is essential for chromosome 
segregation and homologous recombination (HR)-mediated DNA repair. Together with 
architectural proteins and transcriptional regulators, such as CTCF and 
Mediator, respectively, it contributes to genome organization at different 
scales and thereby affects transcription, DNA replication, and locus 
rearrangement. Although cohesin is essential for cell viability, partial loss of 
function can affect these processes differently in distinct cell types. 
Mutations in genes encoding cohesin subunits and regulators of the complex have 
been identified in several cancers. Understanding the functional significance of 
these alterations may have relevant implications for patient classification, 
risk prediction, and choice of treatment. Moreover, identification of 
vulnerabilities in cancer cells harboring cohesin mutations may provide new 
therapeutic opportunities and guide the design of personalized treatments.