How can a cell become cancerous?

How can a cell become cancerous? The ability of mutations to cause cancer depends on how fast they force cells to divide,  researchers have found.

The researchers have identified cell cycle length—the time it takes one cell to divide into two daughter cells—as a critical factor in determining whether a mutation actually drives cancer or is completely harmless.

So fast-dividing cells shown to be more vulnerable to cancer-causing mutations.

The research findings, published in Nature, have implications for developing new treatments that enhance the body's natural defenses against cancer.

Cancer starts when cells acquire genetic mutations that prompt them to proliferate out of control, forming tumors. Not all cells that carry such mutations will turn into cancer, however. This is because the body has evolved ways to prevent cancer from forming by neutralizing or destroying the suspect cancerous cells. The protective mechanisms include apoptosis, or programmed cell death and clearance by the immune system, among others.

An average adult has millions and millions of cells which have mutations in them, yet, thankfully, we don't develop cancer all the time.

Now, scientists have identified the speed at which mutated cells divide as another mechanism of cancer resistance.

The study shows that mutated cells that divide rapidly and have shorter cell cycles are more prone to turning cancerous. In comparison, those with longer cycles exhibit resistance. The finding was consistent across various tissues and types of cancer, including retinoblastoma, pituitary cancer, and lung cancer.

The researchers also found that most mutation-carrying cells eventually exit the cell cycle and stop dividing.

The most common way that mutated cells escape cancer is just by becoming normal cells. They divide abnormally a little bit and then they stop and look like any other normal cell.

To explore the relationship between cell cycle length and cancer, the team examined the effect of suppressing cancer by introducing known tumor-suppressing mutations in several preclinical models.

They began by targeting retinoblastoma, a cancer of the retina, and observed that every manipulation that blocked cancer increased cell cycle length. Most importantly, they then discovered that the mutated cell type from which retinoblastoma originates divides faster than mutated cell types that never form cancer.

Other experiments showed that slowing down the rate of cell division suppressed cancer independently of other known resistance mechanisms, such as apoptosis and immune clearance, indicating that cell cycle length is a distinct mechanism of cancer resistance.

The team also demonstrated that in other tissues, such as the lung and pituitary gland, cancer consistently develops in the mutated cell type that divides the fastest, while those with slower division rates are protected from cancer.

 The researchers also showed that the cell cycle length consistently predicts the cancer cell of origin, regardless of when the tumor-suppressing mutation was introduced.

Combined, the findings suggest that interventions targeting cell cycle length could be a strategy for cancer prevention. By targeting the cell cycle length, it may be possible to develop therapies that prevent the initiation of cancer in high-risk individuals.

The work suggests that we might be able to intervene in cancer-prone cells to slow them down a little bit with the right therapeutic agents. That can happen only after a thorough understanding of the mechanisms governing cell cycle rate in different cell types. The scientists are now moving in that direction. 

Rod Bremner, Cell cycle duration determines oncogenic transformation capacity, Nature (2025). DOI: 10.1038/s41586-025-08935-x. www.nature.com/articles/s41586-025-08935-x