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My primary area of research is the pathogenesis of tumours of the pituitary. In particular, I am interested in growth hormone-secreting pituitary adenomas that can cause gigantism and acromegaly (associated with overgrowth of the soft tissues) and craniopharyngiomas, a rare tumour of the pituitary region that most commonly develops during childhood and can lead to lifelong complications.
The development of both of these tumour types is poorly understood and my work aims to investigate the genetic and molecular events that underlie their behaviour. Through collaboration with colleagues in the Oxford Centre for Diabetes, Endocrinology and Metabolism I am able to link my research findings to clinical outcomes in order to understand these tumours more thoroughly with the aim of developing better treatment strategies to improve patient welfare and outcome.
In addition to my work on pituitary tumours, I also have an interest in glioma. A mutation in the gene for isocitrate dehydrogenase (an enzyme of glucose metabolism) is frequently found in this tumour and enables the enzyme to produce a new compound: 2-hydroxyglutarate. Patients with this mutation have considerably better overall survival times than those without. We are developing a MRS scanning method to detect this compound non-invasively and thus detect the presence of the mutation without the need for a biopsy. In addition, I am using a cell-line model of this tumour to investigate what effect the mutation has on tumour cell behaviour to try to understand why it is associated with improved overall survival.
My work is funded in part by the Society for Endocrinology
Noninvasive Quantification of 2-Hydroxyglutarate in Human Gliomas with IDH1 and IDH2 Mutations.
Emir UE. et al, (2016), Cancer Res, 76, 43 - 49
The Wnt signalling cascade and the adherens junction complex in craniopharyngioma tumorigenesis.
Preda V. et al, (2015), Endocr Pathol, 26, 1 - 8
Sequence analysis of the catalytic subunit of PKA in somatotroph adenomas.
Larkin SJ. et al, (2014), Eur J Endocrinol, 171, 705 - 710
BRAF V600E mutations are characteristic for papillary craniopharyngioma and may coexist with CTNNB1-mutated adamantinomatous craniopharyngioma
Larkin SJ. et al, (2014), Acta Neuropathologica, 127, 927 - 929
BRAF V600E mutations are characteristic for papillary craniopharyngioma and may coexist with CTNNB1-mutated adamantinomatous craniopharyngioma.
Larkin SJ. et al, (2014), Acta Neuropathol, 127, 927 - 929