BSc (Hons), PhD
My research focuses on understanding the epigenetic mechanisms causing tumour development in neuroendocrine tissues, and using this information to develop new diagnostic approaches and therapies. There is a key focus on pancreatic neuroendocrine tumours, particularly those caused by loss of the tumour suppressor protein menin. My work is centred into three main projects:
1) Investigating compounds that inhibit epigenetic modifying proteins to determine their efficacy at reducing tumour cell proliferation in vitro, and tumour growth in vivo, with the aim of taking successful candidates into patients. I also aim to determine the mechanisms by which these compounds elicit their effects, to refine treatments and improve understanding of epigenetic mechanisms in tumours, including the function of menin.
2) Examining microRNA (miRNA) expression and regulation in neuroendocrine tumours. This includes studying the potential use of miRNAs as tumour biomarkers. I have also been involved in a project investigating the role of the miRNAs miR-135b and miR-146b in colon cancer tumourigenesis.
3) Determining the role of the calcium sensing receptor (CaSR) in pituitary neuroendocrine tumours.
Prior to starting my postdoctoral work in Oxford I completed an undergraduate degree in Biochemistry at the University of Liverpool, before completing my PhD in 2011 at the Barts Cancer Institute in London investigating the roles of a novel protein, S100PBP, in pancreatic adenocarcinoma. Therefore throughout my career I have had an interest in studying the molecular mechanisms of cancer, and hope to continue this in my future academic career.
AMEND Research Fund Award
Society for Endocrinology Early Career Grant
UKINETs NET Patient Foundation Grant
Association of prolactin receptor (PRLR) variants with prolactinomas.
Gorvin CM. et al, (2018), Hum Mol Genet
Molecular Genetic Studies of Pancreatic Neuroendocrine Tumors: New Therapeutic Approaches.
Stevenson M. et al, (2018), 47, 525 - 548
MiR-15a/miR-16-1 expression inversely correlates with cyclin D1 levels in Men1 pituitary NETs.
Lines KE. et al, (2018), J Endocrinol
Current and emerging therapies for PNETs in patients with or without MEN1.
Frost M. et al, (2018), Nat Rev Endocrinol, 14, 216 - 227
Mice deleted for cell division cycle 73 gene develop parathyroid and uterine tumours: model for the hyperparathyroidism-jaw tumour syndrome.
Walls GV. et al, (2017), Oncogene, 36, 4025 - 4036