On Jan. 8, 2026, a major advance in cell biology has revealed how our cells safeguard their genetic material during one of the most vulnerable moments in their life cycle. The study identifies a specific protein complex as a central coordinator of DNA repair during cell division.

Every time a cell divides, it must copy its entire DNA and distribute it evenly between two daughter cells. This process, called mitosis, is usually tightly regulated. However, if cells enter mitosis with unfinished or damaged DNA, chromosomes can break apart, leading to genetic instability – a hallmark of many diseases, including cancer. Until now, scientists did not fully understand how cells manage DNA damage during mitosis, when most conventional repair systems are switched off.

Now, researchers have shown that the protein complex CIP2A–TOPBP1 plays a key part in managing DNA repair processes during mitosis. This discovery provides crucial insight into how cells maintain genome stability and offers promising new directions for cancer treatment.

The research represents a highly collaborative, multidisciplinary effort. The team used a combination of innovative techniques – including advanced light microscopy, flow cytometry, proteomics, gene editing and biochemical analysis – to unravel the intricate processes that protect chromosomes during division. This integration of cutting-edge technologies was essential to observe DNA repair events in real time and map the molecular interactions that maintain genome stability.

The clinical significance of this discovery is profound. Cancer cells often endure high levels of replication stress and DNA damage, but they survive by hijacking backup repair pathways. The study reveals that tumours deficient in BRCA1 or BRCA2 – genes essential for homologous recombination repair – or exposed to drugs that induce DNA damage are particularly dependent on the CIP2A–TOPBP1 axis. Disrupting this dependency could render such cancers unable to repair their DNA, leading to cell death.

The findings challenge previous assumptions about CIP2A. Earlier studies suggested that CIP2A primarily acted as a structural tether in mitosis, holding broken chromosomes together during cell division. These new data reveal that CIP2A actively regulates MiDAS and MMEJ, underlining another critical function of this complex. This previously unknown role highlights the dynamic nature of mitotic repair and suggests opportunities for highly selective interventions that disrupt cancer-specific vulnerabilities without harming normal cells.

Building on these findings, the researchers plan to chart the mechanisms that maintain genome stability during mitosis, which remain relatively undefined. Through this, their ultimate goal is to identify novel therapeutic targets that exploit cell-cycle-specific weaknesses, improving outcomes for patients with cancers that currently lack effective treatment options. Scientists from The Institute of Cancer Research, London, led the study. The findings were published in the journal Nature Communications.