Professor Tony Green
Cambridge Institute for Medical Research, Cambridge Biomedical Campus
Tony Green is Professor of Haemato-oncology at the University of Cambridge, Head of the University Department of Haematology and Chair of the Haematology senior staff committee in Addenbrooke's Hospital.
He trained in medicine at the University of Cambridge and University College Hospital London, subsequently completing his haematology training at the Royal Free Hospital and the University Hospital of Wales, Cardiff. He gained his PhD in molecular biology at the Imperial Cancer Research Fund in London and subsequently spent a post-doctoral period at the Walter and Eliza Hall Institute in Melbourne as a Hamilton-Fairley Travelling Fellow.
Tony moved to Cambridge in 1991 as a Welcome Trust Senior Fellow and honorary Consultant, was appointed as Head of Department in 2000. He was elected Fellow of the Academy of Medical Sciences in 2001 and Newton Abraham Visiting Professor at the University of Oxford in 2011.
Tony Green runs the specialist myeloproliferative disorder clinic at Addenbrooke's Hospital and since 1997 has been chief investigator for the PT-1 suite of international clinical trials in essential thrombocythaemia. His research interests focus on the management and molecular pathogenesis of the myeloproliferative disorders, with a particular focus on JAK/STAT signalling. He has published widely (over 160 peer-reviewed papers) with senior-author papers in both clinical and more basic journals including NEJM, Lancet, Blood, Nature, EMBO J, PNAS and Development. In addition he has organized numerous national and international scientific meetings and has given plenary talks at ASH, EHA and multiple national hematology societies.
Professor Green has been a member of the ESH executive committee since 2003, was recently elected to the American Association of Physicians and was chair of the ASH Scientific Committee on Hematopoietic Cytokines and Factors for 2010. He was chair of the EHA Education Committee 2005-09, and in this role he particularly worked to establish the Molecular Haemopoiesis workshop, to introduce webcasting, and to further strengthen the Education Program of the EHA Annual Congress. He was a member of the scientific program committee for the EHA Annual Congress in 2006, 2007 and 2008. He is currently a member of the EHA board, chair of the EHA scientific program committee for the 2012 Annual Congress and chair of the Fellowships and Grants committee.
Bloodwise, Wellcome Trust, Cancer Research UK, The Leukaemia and Lyphoma Society
The Green Lab focuses on the mechanisms whereby blood stem cells are subverted during the genesis of haematological malignancies. Over the past decade we have increasingly concentrated on JAK/STAT signalling which is dysregulated in many cancers and plays a key role in multiple stem cell systems. In particular we have explored the molecular and cellular pathogenesis of a group of pre-leukaemic disorders, the myeloproliferative neoplasms (MPNs), in studies which have spanned basic, translational and clinical research. The myeloproliferative neoplasms harbour mutations that activate the JAK/STAT pathway, are experimentally tractable and provide a paradigm for the earliest stages of tumorigenesis, inaccessible in other cancers. We described the MPN “mutational landscape” and identified causal mutations which revolutionised their diagnosis and catalysed development of therapeutically valuable JAK-family tyrosine kinase inhibitors. Our more basic research is illuminating the mechanisms whereby the JAK/STAT pathway regulates diverse aspects of cellular function including chromatin biology, DNA replication, genome-wide transcriptional programs and stem cell fate. Recent highlights include: identification of calreticulin mutations in most patients with a JAK2-unmutated MPN, thus establishing an unexpected link with endoplasmic reticulum biology; the first demonstration in any cancer that mutation order affects stem and progenitor behaviour, thus influencing clinical presentation, disease outcome and response to therapy; and the description of paradigm-shifting non-canonical mechanisms of JAK/STAT signalling.
Potential post-docs, clinical fellows and students:
We are always keen to hear from good people. Please email (email@example.com) with a copy of your CV including the details of two referees.
Blood stem cells produce a large number of cell types and are the best studied adult stem cell system. We are interested in the molecular mechanisms that control the formation and behavior of normal blood stem cells and how these processes are perturbed during the development of haematological malignancies. In particular we have focussed on a group of human pre-leukaemic disorders, called the myeloproliferative neoplasms, in studies which span basic, translational and clinical research. Our basic studies are illuminating the fundamental mechanisms by which these disorders arise, and have a broad relevance for other cancers and for the normal process of blood cell formation. Moreover, our results have already had major clinical impact, with new diagnostic approaches embedded in international guidelines and multiple JAK inhibitors in clinical trials.
- Park HJ, Li J, Hnnah R, Biddie S, Leal-Cervantes A, Kirschner K, Flores Santa Cruz D, Sexl V, Gottgens B, Green AR. Cytokine-induced megakaryocytic differentiation is regulated by genome-wide loss of a uSTAT transcriptional program. EMBOJ, doi: 10.15252/embj.201592383. PMID:26702099
- *Ortmann CA, *Kent DG, Nangalia J, Silber Y, Wedge DC, Grinfeld J, .... Harrison CN, Vassiliou G, Vannucchi A, Campbell PJ, Green AR. Effect of mutation order on myeloproliferative neoplasms. *Co-first author. N Engl J Med, 372(7):601-12, 2015. PMCID:PMC4660033
- Chen E, Beer PA, Godfrey AL, Ortmann CA, Li J, Costa-Pereira AP, Ingle CE, Dermitzakis ET, Campbell PJ, Green AR. Distinct clinical phenotypes associated with JAK2V617F reflect differential STAT1 signaling. Cancer Cell, 18(5): 524-535, 2010. PMCID:PMC2996868
- Dawson MA†, Bannister AJ†, Gottgens B, Foster SD, Bartke T, Green AR*, Kouzarides T* (*joint senior authors; †joint first author). JAK2 phosphorylates histone H3Y41 and excludes HP1alpha from chromatin. Nature, 461(7265): 819-822, 2009. PMCID:PMC3785147
- Baxter EJ, Scott LM, Campbell PJ, East C, Fourouclas N, Swanton S, Vassiliou GS, Bench AJ, Boyd EM, Curtin N, Scott M, Erber WN, Cancer Genome Project, Green AR. Acquired mutation of the tyrosine kinase JAK2 in human myeloproliferative disorders. Lancet 365: 1054-61, 2005. PMID:15781101