I am a Cancer Research UK Career Development Fellow in the Department of Oncology, based at the MRC Weatherall Institute of Molecular Medicine.
I came to Oxford to start my own lab after a postdoctoral position at the Gurdon Institute in Cambridge.
My lab’s research focuses on understanding how our cells repair damaged DNA, because mutations caused by DNA damage enable a normal cell to become cancerous. This is highlighted by the fact that people with mutations in many genes involved in DNA repair are predisposed to cancer, and that somatically acquired defects in such genes can drive tumour formation. Furthermore, some of the most effective cancer treatments work in tumour cells by inducing DNA damage, particularly DNA double-strand breaks, which are especially toxic and difficult to repair accurately without introducing mutations. Exploiting knowledge of DNA double-strand break repair is therefore likely to lead to more effective and personalised cancer therapies and treatments for patients with DNA repair disorders in future.
My research fellowship at Oriel College is funded by the Against Breast Cancer charity, as the two major breast cancer susceptibly genes (BRCA1 and BRCA2) are important for DNA repair. However, we still do not understand exactly how they work at the molecular level, so this is a major research focus for us.
Blackford AN & Jackson SP (2017) ATM, ATR, and DNA-PK: the trinity at the heart of the DNA damage response. Mol. Cell 66, 801-817.
Balmus G et al. (2016) Synthetic lethality between PAXX and XLF in mammalian development. Genes Dev. 30, 2152-2157.
Ochi T et al. (2015) PAXX, a paralog of XRCC4 and XLF, interacts with Ku to promote DNA double-strand break repair. Science 347, 185–188.