Andrew Teschendorff is a Principal Investigator at the Shanghai Institute of Nutrition and Health (Chinese Academy of Sciences). His main research goal is to elucidate the role of epigenetic changes in aging and cancer-risk. He trained as a Mathematical Physicist (BSc, University of Edinburgh 1995 and PhD, Cambridge University 2000). From 2003 to 2008 he held Cambridge-MIT and Isaac Newton Fellowships, working in Statistical Cancer Genomics at the CRUK Cambridge Research Institute and University of Cambridge. From 2008 to 2013 he held the Heller Research Fellowship at the UCL Cancer Institute in London. In 2013 he moved to Shanghai to lead a lab in Computational Systems Epigenomics. From 2015 to 2019 he held an International Newton Fellowship from the Royal Society in association with UCL London. He is the recipient of a Highly Cited Researcher award from Clarivate in recognition of how his work published in premier journals has influenced the epigenomics, aging and cancer systems biology fields. He is an associate editor for Genome Biology and Genome Medicine and holds patents on algorithms for cancer risk prediction and cell-type deconvolution.
My lab is interested in elucidating the role of epigenetic changes, notably DNA methylation (DNAm), in aging and cancer-risk, and to do so at a systems-level. To this end, we have been developing computational methods that address some of the key emerging challenges, such as how to infer biological aging at cell-type resolution, or how to quantify cellular plasticity, epigenetic reprogramming and cancer-risk in preneoplastic lesions at single-cell resolution. I will describe computational methods and resources we have developed to tackle these challenges and how application of these methods have led to novel biological insights in aging and cancer risk. I will present data linking cellular plasticity and reprogramming to cancer-risk in a pan-tissue setting, that is supportive of an epigenetic stem-cell model of oncogenesis, whilst also highlighting the value and importance of DNAm as a sensitive, and potentially causal, marker for quantifying cancer-risk.