The S-phase checkpoint has roles in all phases of the cell cycle, which has implications for the majority of cancers that lack cell cycle controls.

The localization of Rad53 cell cycle checkpoint kinase to many gene promoters and the dynamic changes in response to replication stress suggests that the kinase may coordinate genome stability and gene expression.

Retrograde signaling activates the Rad53 checkpoint kinase independently of the canonical DNA replication stress response.

Cell cycle arrest in response to a double-stranded break is initially maintained by the DNA damage checkpoint and later by the spindle assembly checkpoint.

Activation of a DNA-damage cell cycle checkpoint during aging causes genome instability and senescence in yeast mother cells.

Single-cell RNA sequencing of biopsy samples from advanced-stage lung cancer reveals tumor and immune cell features associated with response to immune checkpoint therapy.

The involvement of SETD2 in an important DNA repair pathway could explain the high frequency of SETD2 mutations in several cancers and may provide an alternative mechanism to evade the p53-mediated checkpoint.

Daughter-cell-associated factors and centrosome-based regulation is important in mitotic exit and spindle position checkpoint control.

During meiosis, budding yeast use a checkpoint involving the protein Mec1 to prevent the formation of double-strand breaks in DNA that has not completed replication.

Bariatric surgery reversed obesity-exacerbated tumor burden and increased efficacy of anti-PD-L1 immunotherapy.