In February 2025, we were shocked and deeply saddened to hear about the death of Béla Novák, Professor in Integrative Systems Biology at the University of Oxford, UK, and a beloved grandfather, father...

The Nobel Prize in Physiology or Medicine 2025 was awarded to Mary E. Brunkow, Fred Ramsdell and Shimon Sakaguchi “for their discoveries concerning peripheral immune tolerance.”

Fulcher et al. show that MDM2 times mitosis through self-catalysed ubiquitination and proteasomal destruction, triggering G1 arrest following delays in mitosis associated with chromosome instability and aneuploidy.

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Incomplete DNA replication and chromosome breakage during mitosis pose major threats to chromosome segregation. The CIP2A-TOPBP1 complex acts to mitigate this peril, but its exact role is not yet unde...

Dual cyclin A/B RxL inhibitors selectively kill small cell lung cancer cells and other cancer cells with high E2F activity.

Cell cycle checkpoints preventing the replication and inheritance of damaged DNA are crucial for maintaining genome stability and stopping the growth of damaged cells. Canonical checkpoints do this by preventing passage between cell cycle phases until damage has been repaired, or by promoting cell cycle exit. Herein we review checkpoint integration between cell cycle phases, specifically findings showing that extended spindle assembly checkpoint surveillance in mitosis is a danger signal triggering G1 cell cycle arrest. Evidence linking mitotic delays induced by activation of the spindle assembly checkpoint with positive and negative regulators of the G1 DNA damage checkpoint target p53 is discussed, with a focus on time-dependent changes to a p53-binding deubiquitinating complex USP28–53BP1 and the p53 ubiquitin-ligase mouse double minute homologue 2 (MDM2), respectively.

Maintenance of pH within membranous organelles is crucial for cellular processes such as posttranslational modifications, ligand–receptor interacti...

Momentum is building for PROTAC treatments that eliminate disease-causing proteins, including those responsible for difficult-to-treat childhood cancers.

New research unveils the important role of cell division timing mechanisms in the formation of cancer