Tom graduated from the University of Exeter in the summer of 2019. His dissertation project involved utilizing whole genome sequencing data to search for novel recessive causes of congenital hyperinsulinism, working with Dr Thomas Laver. He subsequently began his PhD, studying the role of DNA methylation in congenital disorders of insulin secretion, supervised by Dr Sarah Flanagan and Dr Emma Dempster.
- BSc Medical Sciences (Human Genomics), University of Exeter
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During his undergraduate degree, Tom found an interest in epigenetic variation, and specifically the impact of this variation in human diseases. He also became interested in the pancreas, and the congenital disorders that can affect its function.
Investigating the role of DNA methylation in individuals with congenital disorders of insulin secretion - PhD project supervised by Dr Sarah Flanagan and Dr Emma Dempster.
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Wakeling M, Owens NDL, Hopkinson JR, Johnson MB, Houghton JAL, Dastamani A, Flaxman CS, Wyatt RC, Hewat TI, Hopkins JJ, et al
(In Press). A novel disease mechanism leading to the expression of a disallowed gene in the pancreatic beta-cell identified by non-coding, regulatory mutations controlling HK1. Nature Genetics Abstract
Hewat TI, Johnson M, Flanagan S (In Press). Congenital hyperinsulinism: current laboratory-based approaches to the genetic diagnosis of a heterogeneous disease. Frontiers in Endocrinology
Hopkins J, Childs A, Houghton J, Hewat T, Atapattu N, Johnson M, Patel K, Laver T, Flanagan S
(In Press). Hyperinsulinaemic hypoglycaemia diagnosed in childhood can be monogenic. The Journal of Clinical Endocrinology & Metabolism Abstract
Hewat TI, Laver T, Houghton J, Mannisto J, Alvi S, Brearey S, Cody D, Dastamani A, de los Santos la Torre M, Murphy N, et al (In Press). Increased referrals for congenital hyperinsulinism genetic testing in children with trisomy 21 reflects the high burden of non-genetic risk factors in this group. Pediatric Diabetes
Hewat TI, Yau D, Jerome JCS, Laver TW, Houghton JAL, Shields BM, Flanagan SE, Patel KA
(2021). Birth weight and diazoxide unresponsiveness strongly predict the likelihood of congenital hyperinsulinism due to a mutation in ABCC8 or KCNJ11. European Journal of Endocrinology
(6), 813-818. Abstract
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