Why do cancer cells divide so easily?

A study by a multidisciplinary team of Weizmann Institute researchers might help develop new effective approaches to chemotherapy. The researchers tried to answer the many questions surrounding the differences between healthy and cancerous cells. While it is known that numerous …

A study by a multidisciplinary team of Weizmann Institute researchers might help develop new effective approaches to chemotherapy.

The researchers tried to answer the many questions surrounding the differences between healthy and cancerous cells.

While it is known that numerous growth factors always abound in our bodies, only cancerous cells are quickly “tempted” by these chemicals to divide again and again. On the other hand, healthy cells divide only after being exposed to growth factors for eight continuous hours.

The researchers decided to look at what happens during these eight hours in a healthy cell that resists the call to divide? And even more important, what fails to work properly in the cancerous cell during these same hours? Why do cancerous cells give in so easily to the influence of growth factors, dividing so readily?

In a study recently published in Molecular Cell, the Weizmann scientists found that when a cell first receives a signal from a growth factor, 10 groups of genes, about 8,000 in total, become activated. Of these, one group, consisting of about 10 genes governed by the tumor suppressor p53, is the most crucial: These genes prevent the cell from dividing. Only if the growth factor continues to affect the cell for eight hours does p53 release its grip on the cell’s DNA, allowing it to divide.

The researchers said that the activation of p53 at the time the cell receives a growth factor signal serves as a “brake,” preventing instant division. In this manner, the healthy cell ensures that it will not divide as a result of accidental, mistaken or otherwise superfluous growth signals, but only if the signal is continuous and necessary. In cancerous cells, this mechanism malfunctions because in most of them, p53 is defective or missing altogether, so that even a fleeting growth signal can cause them to divide, leading to cancerous growth.

This study gives a better understanding of how growth factors work and can help administer chemotherapy at intervals that will prevent the increased division of cancerous cells.

About Viva Sarah Press

Viva Sarah Press is an associate editor and writer at ISRAEL21c. She has extensive experience in reporting/editing in the print, online and broadcast fields. She has jumped out of a plane, ducked rockets and been attacked by a baboon all in the name of a good story. Her work has been published by international media outlets including Israel Television, CNN, Reuters, The Jerusalem Post and Time Out.