A cure for cancer is another step closer...
Our DNA is constantly being damaged by factors such as sunlight, pollution and carcinogens in food. Repairing this damage is essential to protect against cancer.
In most people the cells can repair themselves. However, for some with hereditary diseases, this damage cannot be repaired, which can make them 1,000 times more likely to suffer from cancer.
At the Genome Damage and Stability Centre, we are focusing on hereditary disorders. Discovering the nature of DNA repair defects not only helps us to diagnose and find cures for these conditions, but also gives us insight into potential cancer treatments, as well as promoting our understanding of the development of the immune and neurological systems and the ageing process.
Our research is vital in the fight against disease. Understanding what happens inside our cells will accelerate progress towards developing a cure for cancer.
Vital research into DNA repair, genome stability, cancer and genetic disorders
The strands of DNA that make up our genomes are damaged continually, by factors such as sunlight, carcinogens in food, cigarette smoke and pollution. Repairing this damage is essential to protect against cancer, but some people with hereditary diseases cannot repair this damage, and are up to 1,000 times more susceptible to cancer than normal individuals. In many cases these people may also have problems with their immune and neurological systems, and some may show premature ageing. Research into DNA repair is vital in the fight against disease.
At the Genome Damage and Stability Centre we are focusing on several of these hereditary disorders. One area of research studies xeroderma pigmentosum, Cockayne Syndrome and trichothiodystrophy. Patients with xeroderma pigmentosum cannot remove sunlight-induced damage from their DNA, resulting in permanent genetic changes in the skin, which can lead to skin cancer. Cockayne Syndrome and trichothiodystrophy patients have very similar DNA repair defects to xeroderma pigmentosum patients yet, curiously, they show no increase in skin cancer. However, they do have a variety of other symptoms and in the case of Cockayne Syndrome, show dramatic premature ageing. This is an enigma that we are trying to solve.
Another aspect of our research focuses on how cells repair a particular type of damage called the double-strand break, in which both strands of DNA are broken at the same place. We have shown that the strands are stitched back together by a process known as non-homologous end-joining (NHEJ). This process is also used during development of the immune response. Taking these observations as a clue, we have identified molecular defects in NHEJ in three disorders associated with severe immunodeficiency.
We are also studying the way in which cells deal with single-strand DNA breaks. These occur more frequently than double-strand breaks, both during normal development, as a result of cell metabolism, and following exposure to certain types of chemicals. We are investigating links between defects in repair of single-strand breaks and neurological disease in three hereditary genetic disorders.
Although these disorders are rare, discovering the nature of the defects not only helps diagnosis and work towards a cure for these conditions, but also gives important insights into carcinogenesis, immunodeficiency, neurodegeneration and ageing. This will accelerate progress towards developing cures for cancer and other disorders.
Find out more about research in the School of Life Sciences.
