The duration of cell division is a key marker for cancer susceptibility

CSIC Castilla y León/DICYT For years, oncological research has focused on the so -called “hallmarks” or cancer characteristics: resistance to cell death (apoptosis), evasion of elimination by the immune system or uncontrolled proliferation, among others. However, numerous studies have shown that many human cells carry oncogenic mutations without becoming cancerous. The mystery of this “escape” has intrigued the scientific community, which tries to understand why mutated cells form tumors and others, carrying the same alterations, no. The study team “Cell Cycle Duration Determines Oncogenic Transformion Capacity”, published in Nature magazine and in which David Santamaría del Cic has actively collaborated, has analyzed various animal cancer models to address this question.

The study reveals that the key is at the time it takes for a cell to complete its division cycle. Cells with a shorter cell cycle are significantly more susceptible to transforming in cancerous, while those with longer cycles resist transformation, even in the presence of the same genetic alterations.

For example, in retinoblastoma models (a child ocular cancer), the cells of tumor origin had a cell cycle of only 26 hours, compared to the more than 77 hours of the resistant cells of the same tissue. Genetic manipulations that increased the total duration of the cell cycle managed to block the appearance of tumors, without altering other classical characteristics of cancer such as apoptosis, senescence or immune response. This pattern was repeated in other models: in lung or pituitary cancer.

A transverse finding and applicable to multiple types of cancer

The relationship between a short cell cycle and cancer propensity remained constant independently of the tumor type studied, the introduced oncogenic mutation or from the moment of the initiation of the tumor process. Thus, the duration of the cell cycle is consolidated as a universal marker of susceptibility to cancerous transformation within the same biological context.

“Our results explain why most cells with cancer mutations never form tumors. The cell cycle acts as a true” biological filter “, says David Santamaría, of the Cancer Research Center.

Implications for prevention and treatment

This discovery opens new perspectives in cancer prevention. If the total duration of the cell cycle of “initiated” cells – which with dangerous, but not yet transformed mutations is still possible to reduce the incidence of tumors in high -risk populations, such as bearers of hereditary or smokers.

In addition, the finding suggests that therapies aimed at prolonging the cell cycle could block evil transformation without affecting most healthy cells, minimizing side effects.

This research redefines the understanding of natural cancer resistance and suggests that the duration of the cell cycle is a key factor, until now little explored, in disease prevention. This advance positions CIC as an international reference in the investigation of tumor starting mechanisms and opens the door to new custom prevention and treatment strategies.