Feb 2023
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.