Before focusing on your research on causal links between diabetes and cancer by Mendelian randomization, could you explain to us what led you to this particular area of research?
My decision to work in the field of genetics dates to the secondary school when I first learned about the mathematical beauty of Mendel’s laws. I was fascinated by the cross-disciplinary knowledge required to undertake research in human genetics.
After a BSc/MSc in Biology and Chemistry with specialisation in Human Genetics, my first junior-lead graduate research experience came from large-scale study on causes of birth defects and infertile marriages in Ukraine. Later, during an international genetic epidemiology and molecular genetics MSc and PhD in Pavia, Italy, I contributed to genetic studies for common diseases in population isolates, such as Sardinia, Italy, through extension of multi-allelic TDT test to incomplete trios using the microsatellite data from large families with Multiple Sclerosis. Subsequent employment at the GlaxoSmithKline R&D, the Psychiatry Translational Medicine & Genetics brought excitement of the first large-scale (several thousand individuals with/without depression) fine-mapping study, analyses of first Perlegen whole genome genotyping arrays, and one of the first multi-metabolite investigations on depression, relating it to blood insulin levels. As an applied statistical geneticist, on the tips of my fingers, I felt that soon all my expertise would become invaluable for novel genetic discoveries.
I then moved to a PostDoctoral position at the WTCHG/OCDEM, University of Oxford, UK to focus on large-scale studies investigating the genetic susceptibility to type 2 diabetes (T2D). During that time, within the MAGIC (Meta-Analysis of Glucose and Insulin related traits Consortium), we launched an innovative approach of performing genome-wide association studies for quantitative traits used as endophenotypes of clinical endpoints, such as T2D. My first-author Nature Genetics publication described a genome-wide significant association between a variant within the MTNR1B gene and variability of fasting glucose (FG) levels in non-diabetic individuals and related them to the pathophysiology of T2D. For the first time, we demonstrated a genetic link between circadian rhythms and T2D, underlying a range of metabolic dysfunctions. This discovery led to numerous follow-up studies.
Later, I became a Senior Lecturer followed by Reader Position in Human Genomics at the Department of Genomics of Common Diseases, Imperial College London, UK. Since 2019, I am a Professor in eOne Health at the University of Surrey, Vice-Chancellor’s Distinguished Chair and Head of Section of Statistical Multi-Omics as well as Visiting professor within PreciDIAB at the University of Lille, France. Since August 2021, I am also a Co-Director of the People-Centered AI Institute at the University of Surrey pushing forward the AI implementation for people’s health and wellbeing.