Professor Tony Green
Haematopoiesis and haematological malignancies
Emeritus Professor of Haemato-oncology
Biography
Tony Green 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 appointed Professor of Haemato-oncology in the University of Cambridge in 1999, served as Head of the University Department of Haematology from 2000-2020, and served as Director of the (Wellcome-MRC) Cambridge Stem Cell Institute from 2016 until 2022. He stepped down as a Group Leader in October 2025.
He has held multiple academic, clinical and educational leadership roles, both nationally and internationally, has been appointed to visiting professorships at multiple universities, was elected Fellow of the Academy of Medical Sciences (2001) and President of the European Haematology Association (2015-2017). Recent awards include the Jean Bernard Award by the European Haematology Association (2020) and the Donald Metcalf award by the International Society for Experimental Hematology (2021).
Research
Following early research which explored the transcriptional control of normal blood stem cells, the Tony Green focussed for over 3 decades on the mechanisms by which haematopoietic stem cells are subverted to cause haematological malignancies. In particular he explored the molecular and cellular pathogenesis of a group of pre-leukaemic disorders, the myeloproliferative neoplasms (MPNs), recognising that these disorders provide a paradigm for the earliest stages of tumorigenesis, inaccessible in other cancers.
In studies which spanned basic, translational and clinical research he led practice-changing clinical studies, described the MPN “mutational landscape” and identified causal mutations in JAK2 and CALR which activate the JAK/STAT pathway. These findings revolutionised MPN diagnosis (which had previously been challenging) and catalysed development of therapeutic JAK-family tyrosine kinase inhibitors and antibodies to mutant CALR. The Green lab’s more basic research illuminated 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. Particular highlights include: the first demonstration in any cancer that mutation order affects stem and progenitor behaviour, thus influencing clinical presentation, disease outcome and response to therapy; the description of paradigm-shifting non-canonical mechanisms of JAK/STAT signalling; a new biological classification of the MPNs together with personalised predictions based on a knowledge bank; the use of somatic mutations to reveal human cellular ancestry, stem cell dynamics and life-long clonal evolution; and the discovery that JAK signalling through HNRNPA1 represses retrotransposon activity and protects the genome of haematopoietic stem cells.
Key Publications
- Li J, Williams MJ, Park HJ, Bastos HP, Wang X, Prins D, Wilson NK, Johnson C, Sham K, Wantoch M, Watcham S, Kinston SJ, Pask DC, Hamilton TL, Sneade R, Waller AK, Ghevaert C, Vassiliou GS, Laurenti E, Kent DG, Göttgens B, Green AR. STAT1 is essential for HSC function and maintains MHCIIhi stem cells that resist myeloablation and neoplastic expansion. Blood. 2022 Oct 6;140(14):1592-1606. doi: 10.1182/blood.2021014009. PMID: 35767701.
- Williams N, Lee J, Mitchell E, Moore L, Baxter EJ, Hewinson J, Dawson KJ, Menzies A, Godfrey AL, Green AR*, Campbell PJ*, Nangalia J*. (* Joint senior authors). Life histories of myeloproliferative neoplasms inferred from phylogenies. Nature. 602, 162-168 (2022).
- Prins D, Park HJ, Watcham S, Li J, Vacca M, Bastos HP, Gerbaulet A, Vidal-Puig A, Gottgens B, Green AR. The stem/progenitor landscape is reshaped in a mouse model of essential thrombocythaemia and causes excess megakaryocyte production. Science Advances. 6(48):eabd3139, 2020 (PMID 33239297). PMCID: PMC7688335
- Grinfeld, J+, Nanglia, J+, Baxter EJ, Wedge DC, Angelopoulos N, Cantrill R, Godfrey AL, Papaemmanuil E, Gundem G, MacLean C, Cook J, Mudie L, O’Meara S, Teague JW, Butler AP, Massie CE, Williams N, Nice FL, Anderson CL, Hasselbach HC, Guglielmelli P, McMullin MF, Vannucchi AM, Harrison CN, Gerstung M, Green AR*, Campbell PJ*. (+joint first authors, *joint senior authors). Disease heterogeneity and personalized prognosis in myeloproliferative neoplasms. N Engl J Med. 379: 1416-1430, 2018. (PMID 30304655).PMCID: PMC7030948
- Lee-Six H, Øbro NF, Shepherd MS, Grossmann S, Dawson K, Belmonte M, Osborne RJ, Huntly BJP, Martincorena I, Anderson E, O’Neill L, Stratton MR, Laurenti E, Green AR*, Kent DG*, Campbell PJ* (*joint senior authors). Population dynamics of normal human blood inferred from spontaneous somatic mutations. Nature. 561: 473-478, 2018. (PMID 30185910). PMCID: PMC6163040
- 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
- Nangalia J*, Massie CE*, Baxter EJ, Nice FL, Gunes G, Wedge DC…….Papaemmanuil E, Campbell PJ and Green AR. Somatic CALR mutations in myeloproliferative neoplasms with nonmutated JAK2. N Engl J Med, 369(25): 2391-2405, 2013. (*joint first authors). (PMID 24325359)
- 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