Skip to content
Edwin Chen

Edwin Chen

Senior Lecturer

School of Science & Technology

Staff Group(s)


Edwin Chen is a Senior Lecturer in Biomedical Sciences in the Department of Biosciences. His research group is based in the John van Geest Cancer Research Centre.

Career overview

Edwin Chen completed his BSc in Anatomy and Cell Biology at McGill University, and his PhD in Medical Science at the University of Toronto, followed by postdoctoral research posts at the University of Cambridge and Harvard University, where he investigated the molecular biology of a group of age-associated cancers called the chronic myeloproliferative neoplasms (MPN). Upon completion of his postdoctoral training, he established his independent research group at the University of Leeds in 2015, and joined the Van Geest Cancer Research Centre at Nottingham Trent University as a Senior Lecturer in Biomedical Sciences in April 2022.

Research areas

Edwin's main research interest is to understand the molecular processes that govern how blood stem cells turn into leukaemia cells and how to translate these insights into the development of new cancer therapies. To date, his work has illuminated mechanisms whereby aberrant JAK/STAT signalling and homeobox gene expression influence diverse aspects of cell function, including DNA replication and repair, lineage fate choice and immune activity.

Seminal contributions from his work include:

  • Demonstrating the existence of specific signatures associated with distinct myeloproliferative neoplasm (MPN) subtypes (Cancer Cell, 2010)
  • Revealing specific MPN subtypes lacked obligate cell cycle checkpoint activity in response to oncogene-induced replicative and DNA damage stresses (PNAS, 2014; Cell Rep, 2015; Oncogene, 2016)
  • Developing novel murine model for accelerated leukaemic progression concomitant with loss of genome integrity and chromosome instability in MPN and T-cell acute lymphoblastic leukaemias (Oncogene, 2006a; Oncogene, 2006b; Blood, 2015)
  • In understanding the mechanism of action of calreticulin mutations in leukaemogenic progression (Cancer Discov, 2016; Blood, 2018; Blood Adv, 2021).

He has 20 years of research experience in blood cancer research, has published >25 papers in leading cancer and haematology journals, and his group's work has been presented at major international conferences, including the American Society of Haematology, European Haematology Association and American Association for Cancer Research.

External activity

Edwin is a member of the British Society of Haematology, and is a Fellow of the Higher Education Academy.

Sponsors and collaborators

Edwin has received research funding as a principal investigator from the following organisations:

  • Wellcome Trust
  • Academy of Medical Sciences
  • Leukaemia UK John Goldman Fellowship
  • Lady Tata Memorial Trust


Rivera JF, Baral AJ, Nadat F, Boyd G, Smyth R, Patel H, Burman EL, Alameer G, Boxall SA, Jackson BR, Baxter EJ, Laslo P, Green AR, Kent DG, Mullally A, Chen E. (2021). Zinc-dependent multimerization of mutant calreticulin is required for MPL binding and MPN pathogenesis. Blood Advances. 5:1922-1932

Tothova Z, Valton AL, Gorelov R, Vallurupalli M, Krill-Burger JM, Holmes A, Landers CC, Haydu JE, Malolepsza E, Hartigan CR, Donahue M, Popova KD, Koochaki SHJ, Venev SV, Rivera JF, Chen E, Lage K, Schenone M, D'Andrea AD, Carr SA, Morgan EA, Dekker J, Ebert BL. (2021). Cohesin mutations alter DNA damage repair and chromatin structure and create therapeutic vulnerabilities in MDS/AML. JCI Insight. 6:e142149

Kargas V, Castro-Hartmann P, Escudero-Urquijo N, Dent K, Hilcenko C, Sailer C, Zisser G, Marques-Carvalho MJ, Pellegrino S, Wawiórka L, Freund SM, Wagstaff JL, Andreeva A, Faille A, Chen E, Stengel F, Bergler H, Warren AJ. (2019). Mechanism of completion of peptidyltransferase centre assembly in eukaryotes. eLife. 8:e44904

Elf S, Abdelfattah NS, Baral AJ, Beeson D, Rivera JF, Ko A, Florescu N, Birrane G, Chen E, Mullally A. (2018). Defining the requirements for the pathogenic interaction between mutant calreticulin and MPL in MPN. Blood. 131:782-786

Elf S, Abdelfattah NS, Chen E, Perales-Patón J, Rosen EA, Ko A, Peisker F, Florescu N, Giannini S, Wolach O, Morgan EA, Tothova Z, Losman J-A, Schneider RK, Al-Shahrour F, Mullally A. (2016). Mutant calreticulin requires both its mutant C-terminus and the thrombopoietin receptor for oncogenic transformation. Cancer Discovery. 6:368-381

Ahn JS, Li J, Chen E, Kent DG, Park HJ, Green AR. (2016). JAK2V617F mediates resistance to DNA damage-induced apoptosis by modulating FOXO3A localization and Bcl-xL deamidation. Oncogene. 35:2235-2246

Schneider RK, Schenone M, Ferreira MV, Kramann R, Joyce CE, Hartigan C, Beier F, Brümmendorf TH, Germing U, Platzbecker U, Büsche G, Knüchel R, Chen MC, Waters CS, Chen E, Chu LP, Novina CD, Lindsley RC, Carr SA, Ebert BL. (2016). Rps14 haploinsufficiency causes a block in erythroid differentiation mediated by S100A8 and S100A9. Nature Medicine. 22:288-297

Godfrey AL, Chen E, Massie CE, Silber Y, Pagano F, Bellosillo B, Guglielmelli P, Harrison CN, Reilly JT, Stegelmann F, Bijou F, Lippert E, Boiron J-M, Dohner K, Vannucchi AM, Besses C, Green AR. (2016). STAT1 activation in association with JAK2 exon 12 mutations. Haematologica. 101:e15-e19

Chen E, Ahn JS, Sykes DB, Breyfogle LJ, Godfrey AL, Nangalia J, Ko A, DeAngelo DJ, Green AR, Mullaly A. (2015). RECQL5 Suppresses Oncogenic JAK2-Induced Replication Stress and Genomic Instability. Cell Reports. 13:2345-2352

Tapper W, Jones AV, Kralovics R, Harutyunyan AS, Zoi K, Leung W, Godfrey AL, Guglielmelli P, Callaway A, Ward D, Aranaz P, White HE, Waghorn K, Lin F, Chase A, Baxter EJ, Maclean C, Nangalia J, Chen E, Evans P, Short M, Jack A, Wallis L, Oscier D, Duncombe AS, Schuh A, Mead AJ, Griffiths M, Ewing J, Gale RE, Schnittger S, Haferlach T, Stegelmann F, Döhner K, Grallert H, Strauch K, Tanaka T, Bandinelli S, Giannopoulos A, Pieri L, Mannarelli C, Gisslinger H, Barosi G, Cazzola M, Reiter A, Harrison C, Campbell P, Green AR, Vannucchi A, Cross NCP. (2015). Genetic variation at MECOM, TERT, JAK2 and HBS1L-MYB predisposes to myeloproliferative neoplasms. Nature Communications. 6:6691

Chen E, Schneider RK, Breyfogle LJ, Rosen EA, Poveromo L, Elf S, Ko A, Brumme K, Levine R, Ebert BL, Mullally A. (2015). Distinct effects of concomitant Jak2V617F expression and Tet2 loss in mice promote disease progression in myeloproliferative neoplasms. Blood. 125:327-335

Chen E, Mullally A. (2014). How does JAK2V617F contribute to the pathogenesis of myeloproliferative neoplasms?. Hematology. 2014:268-276

Chen E, Ahn JS, Massie CE, Clynes D, Godfrey AL, Li J, Park HJ, Nangalia J, Silber Y, Mullally A, Gibbons RJ, Green AR. (2014). JAK2V617F promotes replication fork stalling with disease-restricted impairment of the intra-S checkpoint response.. Proceedings of the National Academy of Sciences of the United States of America. 111:15190-15195

Li J, Kent DG, Godfrey AL, Manning H, Nangalia J, Aziz A, Chen E, Saeb-Parsy K, Fink J, Sneade R, Hamilton TL, Pask DC, Silber Y, Zhao X, Ghevaert C, Liu P, Green AR. (2014). JAK2V617F homozygosity drives a phenotypic switch in myeloproliferative neoplasms, but is insufficient to sustain disease. Blood. 123:3139-3151

Godfrey AL, Chen E, Pagano F, Silber Y, Campbell PJ, Green AR. (2013). Clonal analyses reveal associations of JAK2V617F homozygosity with hematologic features, age and gender in polycythemia vera and essential thrombocythemia. Haematologica. 98:718-721

Godfrey AL, Chen E, Pagano F, Ortmann CA, Silber Y, Bellosillo B, Guglielmelli P, Harrison CN, Reilly JT, Stegelmann F, Bijou F, Lippert E, McMullin MF, Boiron J-M, Döhner K, Vannucchi AM, Besses C, Campbell PJ, Green AR. (2012). JAK2V617F homozygosity arises commonly and recurrently in PV and ET, but PV is characterized by expansion of a dominant homozygous subclone. Blood. 120:2704-2707

Chen E, Staudt LM, Green AR. (2012). Janus kinase deregulation in leukemia and lymphoma. Immunity. 36:529-541

Li J, Kent DG, Chen E, Green AR. (2011). Mouse models of myeloproliferative neoplasms: JAK of all grades. Dis Model Mech. 4:311-317

Chen E, Beer PA, Godfrey AL, Ortmann CA, Li J, Costa-Pereira AP, Ingle CE, Dermitzakis ET, Campbell PJ, Green AR. (2010). Distinct clinical phenotypes associated with JAK2V617F reflect differential STAT1 signaling.. Cancer Cell. 18:524-535

Chen E, Huang X, Zheng Y, Li Y-J, Chesney A, Ben-David Y, Yang E, Hough MR.(2010) Phosphorylation of HOX11/TLX1 on Threonine-247 during mitosis modulates expression of cyclin B1. Mol Cancer. 9:246

Li J, Spensberger D, Ahn JS, Anand S, Beer PA, Ghevaert C, Chen E, Forrai A, Scott LM, Ferreira R, Campbell PJ, Watson SP, Liu P, Erber WN, Huntly BJP, Ottersbach K, Green AR. (2010). JAK2 V617F impairs hematopoietic stem cell function in a conditional knock-in mouse model of JAK2 V617F-positive essential thrombocythemia. Blood. 116:1528-1538

Beer PA, Delhommeau F, LeCouédic J-P, Dawson MA, Chen E, Bareford D, Kušec R, McMullin MF, Harrison CN, Vannucchi AM, Vainchenker W, Green AR. (2010). Two routes to leukemic transformation after a JAK2 mutation–positive myeloproliferative neoplasm. Blood. 115:2891-2900

Wood AD, Chen E, Donaldson IJ, Hattangadi S, Burke KA, Dawson MA, Miranda-Saavedra D, Lodish HF, Green AR, Göttgens B. (2009). ID1 promotes expansion and survival of primary erythroid cells and is a target of JAK2V617F-STAT5 signaling. Blood. 114:1820-1830

Chen E, Kwon YT, Lim MS, Dubé ID, Hough MR. (2006). Loss of Ubr1 promotes aneuploidy and accelerates B-cell lymphomagenesis in TLX1/HOX11-transgenic mice.. Oncogene. 25:5752-5763

Chen E, Lim MS, Rosic-Kablar S, Liu J, Jolicoeur P, Dubé ID, Hough MR. (2006). Dysregulated expression of mitotic regulators is associated with B-cell lymphomagenesis in HOX11-transgenic mice.. Oncogene. 25:2575-2587