Nature. Mutated cells that divide rapidly are more prone to forming cancer

Cancer starts when cells acquire genetic mutations that prompt them to proliferate out of control until tumours are formed.  However, not all cells that carry such mutations will turn into cancer because the body has protective mechanisms to neutralise or destroy the potentially cancerous cells.  A study published in Nature in which Mariano Barbacid, Head of the Experimental Oncology Group at the Spanish National Cancer Research Centre (CNIO) participated, has identified one of these mechanisms: cell cycle length.

The authors have found that the time one cell takes to divide into two daughter cells is a critical factor when it comes to a mutation capable of developing cancer actually doing so.  In other words, in cells with the same oncogenic mutations, those cells that divide more rapidly are more likely to develop cancer.

“An average adult has millions of cells which have mutations in them, yet  cancer is not always developed”, said Rod Bremner, from the Lunefeld-Tanenbaum Research Institute (Sinai Health in Toronto, Canada) and lead author. The new study helps to understand the body’s natural defence mechanisms.

Different types of cancer

The research has been carried out on animal models with different types of cancer. To explore the influence of the cell cycle on the onset of cancer, the team introduced tumour-suppressing mutations in various animal models.  They observed that in retinoblastoma (ocular cancer in children), each of the manipulations that prevented cancer increased the cell cycle length.

They discovered that the type of mutated cell in which the retinoblastoma originated divided faster than other mutated cells that did not develop cancer.  They also tried slowing down the rate of cell division and the result was the mutated cells did not develop cancer.

None of these alterations induced by the division rate affected known resistance mechanisms, such as apoptosis – induced cell death – or the elimination of the potentially cancerous cells by the immune system. For the authors of the study, this indicates that the cell cycle length is a cancer resistance mechanism.

“Our findings explain why most cells with cancerous mutations never develop tumours. The cell cycle acts as a real “biological filter”, highlights David Santamaría, from the Cancer Research Centre (CSIC-Salamanca University), who also participated in the study.

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