Abstract:

Over the last two decades my lab has focused on the mechanisms whereby blood stem cells are subverted to cause haematological malignancies, using human myeloproliferative neoplasms (MPNs) as a tractable model.

In work which transformed MPN diagnosis and catalysed development of therapeutic JAK inhibitors, we and others identified phenotypic driver mutations in JAK2 and CALR which activate the JAK/STAT pathway and are present in most MPN patients. We have subsequently employed a variety of approaches to describe the biological consequences of these mutations at molecular, cellular and organismal levels. In addition to altering clinical practice, our studies have led to unexpected insights into cancer biology as well as normal cytokine signalling, including novel roles for STAT proteins in controlling blood stem cell behaviour.

Bio:

Tony Green is Professor of Haemato-oncology at the University of Cambridge.

He studied medicine (University of Cambridge and University College Hospital, London), subsequently trained in haematology (Royal Free Hospital and Cardiff) and gained his PhD studying oncogenic retroviruses (ICRF, London 1987). Following a post-doctoral period studying haematopoiesis at the Walter and Eliza Hall Institute (Melbourne), he moved to Cambridge in 1991 as a Wellcome Trust Clinical Senior Fellow and Honorary Consultant Haematologist.  He was Head of the University of Cambridge Department of Haematology (2000-2020), President of the European Hematology Association (2015-1017) and Director of the Wellcome-MRC Cambridge Stem Cell Institute (2016-2022).

His early research explored the transcriptional control of normal blood stem cells and more recently the mechanisms by which stem cells are subverted to cause haematological malignancies, using the myeloproliferative neoplasms as a tractable model.  In work which spans basic, translational and clinical research he identified key causal mutations, described their biological consequences, led practice-changing clinical studies and discovered basic mechanisms of broad relevance for both cancer biology and cytokine signalling.