Dr Quentin M. Anstee is an Academic Hepatologist in the Institute of Cellular Medicine. A practising clinician, he is also an Honorary Consultant Hepatologist in the Liver Unit at the Freeman Hospital, Newcastle.
Dr Anstee's primary research interest is the study of genetic modifiers of progressive liver disease. His translational research has extended from the bench to the bedside with particular focus on the pathogenesis and management of Non-Alcoholic Fatty Liver Disease & Steatohepatitis (NAFLD/NASH), including the identification of genetic and epigenetic modifiers of Hepatic Fibrosis progression. He co-ordinates the European Union Horizon 2020 funded EPoS: Elucidating Pathways of Steatohepatitis consortium (EPoS) and is actively involved in biomarker discovery projects and ongoing clinical trials of new therapies for NAFLD.
Dr Anstee's clinical practice is based in the Regional Liver Unit at the Freeman Hospital. His particular specialist interest is the diagnosis and treatment of Non-Alcoholic Fatty Liver Disease (NAFLD), an increasingly common, progressive liver disease that is strongly associated with features of the 'metabolic syndrome' (including obesity, type 2 diabetes mellitus and dyslipidaemia). Working closely with Professor Chris Day, he leads the regional NAFLD specialist clinical service based at the Freeman Hospital, Newcastle.
Dr Anstee trained in medicine at University College London where he was awarded First Prize in Medicine in the final MB BS examination (The Philip Seth Belasco & Douglas Cree Prize, 1997).
His post-graduate specialist clinical training in Hepatology/Gastroenterology & General Medicine was undertaken at hospitals in North-West London. Prior to joining ICM, he worked as Clinical Lecturer in Medicine & Hepatology at Imperial College London and St Mary's Hospital from 2007-2010.
He has expertise in the management of patients with a range of acute and chronic liver conditions including:
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Dr Anstee's primary research interest is the study of genetic modifiers of progressive liver disease. His translational research has extended from the bench to the bedside with particular focus on the pathogenesis and treatment of Non-Alcoholic Fatty Liver Disease (NAFLD/NASH), gentic and epigenetic modifiers of Hepatic Fibrosis progression and identification of genetic factors that promote Alcohol Addiction. He co-ordinates the €6 million European Union Horizon 2020 funded EPoS: Elucidating Pathways of Steatohepatitis consortium (EPoS) and was a member of the preceeding European Union FP7 funded Fatty Liver: Inhibition of Progression (FLIP) consortium. Through these and other projects he has established ongoing fruitful collaborations with scientific partners based at several UK and international liver units.
Dr Anstee's scientific research has employed gene-driven and phenotype‐driven ethyl-nitrosourea (ENU) mutagenesis screens and more traditional targeted genetic modification techniques to generate and study models of complex genetic disease traits including alcohol addiction, non-alcoholic steatohepatitis, drug induced liver injury (paracetamol toxicity and antibiotic related idiosyncratic drug reactions) and liver fibrosis. He has a long-standing research collaboration with investigators at the MRC Mammalian Genetics Unit, MRC Harwell and leads the Genetics of Liver Disease (UK-GoLD) network.
He is a principal investigator in ongoing clinical trials of new therapies for fatty liver disease and hepatic fibrosis.
Dr Anstee has previously received a HEFCE Clinical Senior Lecturer Award and an MRC Clinical Research Fellowship to study genetic modifiers of Non-Alcoholic Steatohepatitis (NASH) & Liver Fibrosis.
He has received research grant funding from sources including the European Union, MRC, Wellcome Trust, Academy of Medical Sciences and the NIHR.
This research is funded by the European Commission Framework 7 Programme.
Lecture topics include: 'Non-Alcoholic Fatty Liver Disease (NAFLD)', 'Alcoholic Liver Disease', 'Viral Hepatitis (hepatitis C)', 'Cirrhosis & its Complications', 'Genetics of NAFLD'.