BSc (Hons), MRes
Novel approaches to targeting ATM deficient tumours
ATM is a central protein involved in maintaining genome stability and coordinating the DNA damage response (DDR) to ionising radiation and DNA damaging chemotherapies. A proportion of tumours are ATM deficient due to somatic mutations that arise during tumour development, and this identifies a potential molecular subgroup for targeted therapies. In addition, a number of ATM kinase inhibitors have recently entered clinical development. Both somatic loss of ATM function and inhibition of ATM kinase present opportunities to identify molecular targets that are synthetically lethal to tumours with loss or inhibition of ATM.
I graduated with a BSc in Medical Sciences from the University of Leeds. During the third year of my undergraduate degree, I trained in the Cell, Developmental and Cancer Biology department at Oregon Health and Science University (OHSU). Here, I worked on the regulation of invadopodia in breast cancer. Prior to starting the DPhil programme in Oxford, I studied the MRes in Translational Cancer Medicine at King's College London which focused on tumour immunology.