What are some of the reasons you might expect human cells to have more efficient repair systems than those of a frog?

DNA damage inhibits cell division, and that is also how many forms of chemotherapeutic agents kill cancer cells. The researchers have discovered two methods or pathways used to mend DNA-protein crosslinks. At the same time, they have established how DNA replication triggers these repair processes. Associate Professor Julien Duxin compares DNA replication to a motorway and a lesion to a roadblock or a large rock in the middle of the road. For DNA replication to take place and be successful, the roadblock must first be removed.

'Cancer cells divide faster than normal cells and therefore require more DNA replication. They are therefore very sensitive to damages that disturb the replication process. However, DNA replication can also trigger damage repair. For example, you can compare DNA replication to a motorway filled with cars. If you place a rock in the middle of the road, where no one drives, no one will notice the rock. But if you are on a road that is blocked, you will realise that there is a problem that requires solving,' says Associate Professor Julien Duxin.

Cancer cells are clever and often find a way to repair themselves. For example, chemotherapy for one type of cancer cells may work for a period of six months and then stop working because the cancer cells have found a new way of removing and repairing lesions. Therefore, the next step for the researchers is to continue to study these lesions and seek to identify more pathways in which they are repaired. They focus especially on the types of DNA damages that occur during chemotherapy and how they are repaired.