Simon Boulton

He currently occupies the position of Senior Scientist and group leader of the DSB Repair Metabolism Laboratory at the Francis Crick Institute, London.

Fortunately, cells have evolved specialised repair processes that are remarkably efficient in correcting specific types of DNA damage.

Indeed, defects in genes that repair DNA damage are the underlying cause of a number of hereditary ageing/cancer predisposition syndromes such as Fanconi anemia and Blooms.

"[12] According to the Royal Society, Boulton's research has resulted in several major breakthroughs in understanding; these are viewed as highly promising with regard to the potential development of new cancer treatments.

[14] To fulfil these tasks, Boulton studies the DNA damage repair inside a specific worm called C. elegans, then extends these findings to human cells.

[14][22] After receiving his Ph.D. from Cambridge, Boulton completed postdoctoral fellowships funded by the European Molecular Biology Organization and the Human Frontier Science Program at Harvard Medical School.

[3] He has also demonstrated that a newly identified helicase, RTEL1, plays a crucial role in repairing double-stranded DNA breaks by means of homologous recombination (HR) – a discovery that has great therapeutic significance and that has already led to the development of treatments, with a drug currently undergoing clinical tests.

[3] Boulton won the Colworth Medal[2] from the Biochemical Society in 2006,[3] and was selected to give the EACR Young Cancer Researcher of the Year award lecture in 2008.

The election committee said that it was "particularly impressed by his pioneering role in establishing the nematode worm, C. elegans, as a model system to study genome instability.