Our team is comprised of distinguished Oxford basic research scientists with expertise in drug discovery, immunology and oncology as well as clinicians with many years of expertise in providing outstanding clinical care for multiple myeloma and related plasma cell disorders.
- Chas Bountra, Structural Genomics Consortium (SGC), NDM Oxford.
- Vincenzo Cerundolo, Weatherall Institute of Molecular Medicine.
- John C. Christianson, Ludwig Institute of Cancer Research, Oxford.
- Claire Edwards, Botnar Research Centre, Oxford.
- James Edwards, Botnar Research Centre ,Oxford.
- Nicole Horwood, Kennedy Institute of Rheumatology, Oxford.
- Kilian Huber, Structural Genomics Consortium (SGC) Oxford, Target Discovery Institute, NDM, Oxford.
- M Kassim Javaid, Botnar Research Centre, Oxford.
- Benedikt Kessler, Target Discovery Institute.
- Jaimal Kothari, Oxford University Hospitals Foundation NHS Trust, Oxford.
- Anjali Kusumbe, Kennedy Institute of Rheumatology, Oxford.
- Nicholas LaThangue, Department of Oncology
- Udo Oppermann, Botnar Research Centre, Structural Genomics Consortium
- Karthik Ramasamy, Cancer and Haematology Centre, Oxford
- Paresh Vyas, Weatherall Institute of Molecular Medicine.
Chas Bountra, Structural Genomics Consortium (SGC) Oxford, NDM Oxford.
Chas Bountra is Scientific Director of the Structural Genomics Consortium at Oxford University and he is Professor of Translational Medicine in the Nuffield Department of Clinical Medicine and Associate Member of the Department of Pharmacology at the University of Oxford. He is also a Visiting Professor in Neuroscience and Mental Health at Imperial College, London. Chas is an invited expert on several government and charitable research funding bodies, and an advisor for many academic, biotech and pharma drug discovery programmes. Prior to coming back to Oxford, Chas was Vice President and Head of Biology at GlaxoSmithKline. He was involved in the identification of more than 40 clinical candidates for gastro-intestinal, inflammatory and neuro-psychiatric diseases. The SGC has become a leader in human protein structural biology and epigenetics chemical biology, and is arguably one of the most successful open innovation, public – private partnerships in the world. Furthermore, with the many recent local developments (Target Discovery Institute, Kennedy Institute, Dementia Institute, Big Data Institute), he believes Oxford is emerging as one of the major academic drug discovery centres in Europe. Chas was awarded OBE in recognition of his accomplishments in UK science and drug discovery.
- Edwards AM, Arrowsmith CH, Bountra C, Bunnage ME, Feldmann M, Knight JC, Patel DD, Prinos P, Taylor MD, Sundström M; SGC Open Source Target-Discovery Partnership. Preclinical target validation using patient-derived cells. Nat Rev Drug Discov. 2015 Mar;14(3):149-50.
- Norman TC, Bountra C, Edwards AM, Yamamoto KR, Friend SH. Leveraging crowdsourcing to facilitate the discovery of new medicines. Sci Transl Med. 2011 Jun 22;3(88):88mr1.
- Norman T, Edwards A, Bountra C, Friend S. The precompetitive space: time to move the yardsticks. Sci Transl Med. 2011 Mar 30;3(76):76cm10.
- Edwards AM, Bountra C, Kerr DJ, Willson TM. Open access chemical and clinical probes to support drug discovery. Nat Chem Biol. 2009 Jul;5(7):436-40.
Vincenzo Cerundolo, Weatherall Institute of Molecular Medicine
Vincenzo Cerundolo is Professor of Immunology and Director of the MRC Human Immunology Unit of the University of Oxford. He graduated in Medicine at the University of Padua, Italy where he completed his PhD in Immunology, and subsequently moved to the UK as an EMBO Fellow to work with Professor Alain Townsend on antigen presentation. In 1990 he described the first human antigen processing deficient cells, which led to the cloning and characterisation of TAP1 and TAP2 genes.
Vincenzo was appointed Professor of Immunology at the University of Oxford in 2000 and became Director of the MRC Human Immunology Unit in 2010. In 2012 he was appointed Head of the Investigative Medicine Division of the newly-formed Radcliffe Department of Medicine of the University of Oxford.
Research carried out in Professor Cerundolo’s laboratory is mainly focussed on gaining a better understanding of the mechanisms that control the cell-cell interplay required for optimal expansion and activation of tumour-specific T cell populations and to apply this knowledge to the development of better treatment strategies in cancer patients.
- Howson LJ, Napolitani G, Shepherd D, Ghadbane H, Kurupati P, Preciado-Llanes L, Rei M, Dobinson HC, Gibani MM, Teng KWW, Newell EW, Veerapen N, Besra GS, Pollard AJ & Cerundolo V. MAIT cell clonal expansion and TCR repertoire shaping in human volunteers challenged with Salmonella Paratyphi. Nature Comms. In Press
- Khatamzas E, Hipp MM, Gaughan D, Pichulik T, Leslie A, Fernandes RA, Muraro D, Booth S, Zausmer K, Sun MY, Kessler B, Rowland-Jones S, Cerundolo V, Simmons A. Snapin promotes HIV-1 transmission from dendritic cells by dampening TLR8 signaling. EMBO J. 2017 Oct 16;36(20):2998-3011.
- Salio M, Gasser O, Gonzalez-Lopez C, Martens A, Veerapen N, Gileadi U, Verter JG, Napolitani G, Anderson R, Painter G, Besra GS, Hermans IF, Cerundolo V. Activation of Human Mucosal-Associated Invariant T Cells Induces CD40L-Dependent Maturation of Monocyte-Derived and Primary Dendritic Cells. J Immunol. 2017 Oct 15;199(8):2631-2638.
- Timosenko E, Ghadbane H, Silk JD, Shepherd D, Gileadi U, Howson LJ, Laynes R, Zhao Q, Strausberg RL, Olsen LR, Taylor S, Buffa FM, Boyd R, Cerundolo V. Nutritional stress induced by tryptophan-degrading enzymes results in ATF4-dependent reprogramming of the amino acid transporter profile in tumor cells. Cancer Res. 2016 Nov 1;76(21):6193-6204. Epub 2016 Sep 20.
John C. Christianson, Ludwig Institute of Cancer Research, Oxford
My lab investigates the molecular machinery and adaptive strategies used by eukaryotic cells to maintain protein and organelle homeostasis. We focus on the quality control mechanisms of the endoplasmic reticulum (ER) and specifically, the ubiquitin-proteasome dependent process of ER-associated degradation (ERAD). B-cells and derived malignancies such as multiple myeloma intrinsically depend on ER function and robust ERAD. We integrate proteomics, cell biology, functional genomics and biochemistry to identify essential ERAD factors, characterise functional complexes and determine their contribution to resolving cellular stress. As commandeered stress response pathways support cancer cell survival, our long-term goals are to identify new and susceptible targets within protein quality control mechanisms and develop pharmacological strategies to disrupt their essential activities for therapeutic intervention.
- Guna A, Volkmar N, Christianson JC and Hegde R. (2017) The endoplasmic reticulum membrane protein complex is transmembrane insertase. Science (in press). (Link)
- Schulz J, Avci D, Queisser M, Gutschmidt A, Fenech E, Lari F, Volkmar N, Hayashi Y, Hoppe T and Christianson JC. (2017) Conserved cytoplasmic domains promote Hrd1 ubiquitin ligase complex formation for ER-associated degradation (ERAD). Journal of Cell Science. 130:3322-3335. (Link)
Claire Edwards, Botnar Research Centre
My research is focused upon the role of the bone marrow microenvironment in tumour growth and cancer-induced bone disease. I have over 20 years experience in cancer and bone research, with particular expertise in the myeloma bone marrow microenvironment. I combine cellular and molecular biology, in vivo models of myeloma bone disease and analysis of patient samples to undertake detailed studies of the cellular interactions and mechanisms that drive disease pathogenesis and to evaluate new therapeutic intervention strategies. Current research is focused upon the role of adiposity, adipokines and osteoblasts in the pathogenesis of multiple myeloma.
- Gooding, S., Edwards, C.M., New approaches to targeting the bone marrow microenvironment in multiple myeloma. (2016) Current Opinions in Pharmacology 28; 43-49.
- Lwin, S.T., Olechnowicz, S.W.Z., Fowler, J.A., Edwards, C.M. Diet-induced obesity promotes a myeloma-like condition in vivo. (2015) Leukemia 29(2); 507-10.
- Fowler J.A., Mundy G.R., Lwin S.T., Edwards C.M. Bone marrow stromal cells create a permissive microenvironment for myeloma development: a new stromal role for Wnt inhibitor Dkk1. (2012) Cancer Research, 72(9): 2183-9.
James Edwards, Botnar Research Centre
James Edwards leads the Musculoskeletal Ageing research group at the University of Oxford. This work is focused upon revealing causes of ageing-related skeletal disorders including cancer development and metastases to bone, and exploring novel approaches to better treat the consequences of musculoskeletal ageing. James has worked in bone pathology and skeletal biology for over 20 years in the UK, US and Australia, revealing novel longevity links between the ageing process and skeletal changes which predispose to bone loss, cartilage wear and tumour growth, and which might be modified by interventions such as enhanced specific dietary components. This work combines advanced cellular and molecular techniques, human samples and data sets with surgical and genetically modified pre-clinical models to image and research the dynamic skeletal microenvironment to better understand how ageing impacts cancer progression and skeletal disease.
- JR. Edwards. Contribution of Osteoclasts to the Bone-Tumor Niche. Chapter 5. BONE CANCER: PRIMARY BONE CANCERS AND BONE METASTASES; FROM BASIC TO CLINICAL ASPECTS. 2nd Ed. 2014. Edited by Dominique Heymann. Elsevier. London.
- S. Roberts, P. Colombier, A. Sowman, C. Mennan, JHD. Rölfing, J. Guicheux, JR. Edwards. The Ageing Skeleton - Cellular function and dysfunction throughout life. Acta Orthopaedica. 2016 Oct 17:1-11.
- JA Sterling, JR Edwards, TJ Martin, GR Mundy. Advances in the biology of bone metastasis: How the skeleton affects tumor behavior. Bone. 2011 Jan 1;48(1):6-15.
- Zhuang J, Zhang J, Lwin ST, Edwards JR, Edwards CM, Mundy GR, Yang X. Osteoclasts in multiple myeloma are derived from Gr-1+CD11b+myeloid-derived suppressor cells. PLoS One. 2012;7(11):e48871
Nicole Horwood, Kennedy Institute of Rheumatology
Disorders of immune cell function are frequently associated with perturbation of bone homeostasis as seen in arthritis, osteoporosis and bone-associated cancers such as multiple myeloma. Over the last 20 years my research has focused upon the balance between bone formation and destruction and how this is controlled by cells of the immune system. Bone destruction is a central component to multiple myeloma, hence ways to prevent osteoclast activation or to promote controlled bone formation will not only preserve bone integrity but will have consequences for both tumour burden and the immune response. Osteoclasts also play a role in the liberation of haematopoietic stem cells from their bone marrow niches and maintenance of the niche. My current work investigates the role of glycosphingolipids in osteoclastogenesis, adipogenesis and immune cell function with a view to designing new therapeutic options for the treatment of multiple myeloma.
- Ersek A., Espirito Santo A.I., Vattakuzhi Y., George S., Clark A.R. and Horwood N.J. Strain dependent differences in glucocorticoid-induced bone loss between C57BL/6J and CD-1 mice. Scientific Reports. Nov 4;6:36513 (2016)
- Ersek, A., Xu, K., Antonopoulos, A., Butters, T.D., Vattakuzhi, Y., Danks, L., Freidin, A., Spanoudakis, E., Parry, S., Papaioannou, M., Hatjiharissi, E., Chaidos, A., Alonzi, D.S., Twigg, G., Hu, M., Dwek, R.A., Haslam, S.M., Roberts, I., Dell, A., Rahemtulla, A., Horwood, N.J.* and Karadimitris, A.* Glucose ceramide synthase inhibitors prevent osteoclast activation and limit myeloma-induced osteolytic lesions. Journal of Clinical Investigation, 125(6):2279-92 (2015). * Joint corresponding author, highlighted in JCI Impacts June 2015
- Nicolaidou, V., Wong, M-M., Redpath, A., Baban, D., Williams, L.M., Cope, A. and Horwood, N.J. Monocytes induce STAT3 activation in Human Mesenchymal Stem Cells to Promote Osteoblast Formation. PlosOne. 7(7):e39871 (2012)
- Lymperi, S., Ersek, A., Ferraro, F., Dazzi, F. and Horwood, N.J. Inhibition of Osteoclast Function Reduces Haematopoietic Stem Cell Numbers In Vivo. Blood. 117(5):1540-9 (2011).
Kilian Huber, Structural Genomics Consortium (SGC) Oxford, Target Discovery Institute, NDM
Our laboratory is interested in using chemical biology to identify and explore new drug targets. To this end, we use systems-level approaches such as chemical proteomics and thermal stability profiling to reveal the cellular targets and molecular mechanism of bioactive molecules and drugs and develop small molecule tool compounds, so-called chemical probes, to enable a functional assessment of new protein targets in living systems.
- Huber, K. V. M. et al., Proteome-wide drug and metabolite interaction mapping by thermal-stability profiling. Nat Meth 2015, 12 (11), 1055-1057.
- Huber, K. V. M., Superti-Furga, G., Profiling of Small Molecules by Chemical Proteomics, Proteomics in Systems Biology, Reinders, J., Ed. Springer New York: New York, NY, 2016; pp 211-218.
- Fedorov, O., Huber, K. et al., Specific CLK Inhibitors from a Novel Chemotype for Regulation of Alternative Splicing. Chemistry & Biology 2011, 18 (1), 67-76.
M Kassim Javaid, Botnar Research Centre
My group investigates the epidemiology of metabolic bone disorders focusing on osteoporosis and rare bone disorders. We focus on secondary fracture prevention and specifically the producing evidence to support the effective and effiicient introduction of fracture liaison services. In rare bone diseases we are focusing on the prevalence, natural history and health economic burden. Our methods include using routine health data as well as a prospective Rare and Undiagnosed Diseases studY (RUDY) that uses a novel online dynamic consent based model with extensive patient engagement.
- The RUDY study: using digital technologies to enable a research partnership. Teare HJA, Hogg J, Kaye J, Luqmani R, Rush E, Turner A, Watts L, Williams M, Javaid MK. Eur J Hum Genet. 2017 Jun;25(7):816-822.
- GGPS1 Mutation and Atypical Femoral Fractures with Bisphosphonates. Roca-Ayats N, Balcells S, Garcia-Giralt N, Falcó-Mascaró M, Martínez-Gil N, Abril JF, Urreizti R, Dopazo J, Quesada-Gómez JM, Nogués X, Mellibovsky L, Prieto-Alhambra D, Dunford JE, Javaid MK, Russell RG, Grinberg D, Díez-Pérez A. N Engl J Med. 2017 May 4;376(18):1794-1795.
- Improving patient outcomes in fibrous dysplasia/McCune-Albright syndrome: an international multidisciplinary workshop to inform an international partnership. Boyce AM, Turner A, Watts L, Forestier-Zhang L, Underhill A, Pinedo-Villanueva R, Monsell F, Tessaris D, Burren C, Masi L, Hamdy N, Brandi ML, Chapurlat R, Collins MT, Javaid MK. Arch Osteoporos. 2017 Dec;12(1):21.
Benedikt Kessler, Target Discovery Institute
My research interests have been focused on understanding molecular processes underlying disease with a particular emphasis on the ubiquitin proteasome system and antigen presentation. Our laboratory is using proteomics based techniques as an integrative tool in biomedical research for many years. The research focus has been concentrated on the biology of the ubiquitin-proteasome pathway, in particular deubiquitylating enzymes.
- Turnbull AP, Ioannidis S, Krajewski WW, Pinto-Fernandez A, Heride C, Martin ACL, Tonkin LM, Townsend EC, Buker SM, Lancia DR, Caravella JA, Toms AV, Charlton TM, Lahdenranta J, Wilker E, Follows BC, Evans NJ, Stead L, Alli C, Zarayskiy V, Talbot AC, Buckmelter AJ, Wang M, McKinnon CL, Saab M, McGouran AF, Century H, Gersch M, Pittman MS, Marshall CG, Raynham TM, Simcox M, Stewart LMD, McLoughlin SB, Escobedo JA, Bair KW, Dinsmore CJ, Hammonds TR, Kim S, Urbe S, Clague MJ, Kessler BM, Komander D. Molecular basis of USP7 inhibition by selective small molecule inhibitors. Nature 2017 Oct 26;550(7677):481-486.
- Chauhan D, Tian Z, Nicholson B, Kumar KG, Zhou B, Carrasco R, McDermott JL, Leach CA, Fulcinniti M, Kodrasov MP, Weinstock J, Kingsbury WD, Hideshima T, Shah PK, Minvielle S, Altun M, Kessler BM, Orlowski R, Richardson P, Munshi N, Anderson KC. A small molecule inhibitor of ubiquitin-specific protease-7 induces apoptosis in multiple myeloma cells and overcomes bortezomib resistance. Cancer Cell. 2012 Sep 11;22(3):345-58.
- Altun M, Kramer HB, Willems LI, McDermott JL, Leach CA, Goldenberg SJ, Kumar KG, Konietzny R, Fischer R, Kogan E, Mackeen MM, McGouran J, Khoronenkova SV, Parsons JL, Dianov GL, Nicholson B, Kessler BM. Activity-based chemical proteomics accelerates inhibitor development for deubiquitylating enzymes. Chem Biol. 2011 Nov 23;18(11):1401-12.
Jaimal Kothari, Oxford University Hospitals
I am a clinical Haematologist based at the Churchill Hospital, with a special interest in the clinical management of myeloma and associated plasma cell dyscrasias . I am co-chair of the Thames Valley Regional Myeloma multi-disciplinary team meeting as well as the clinical lead for late phase clinical trials for Haematology. In my trial capacity, I am involved in driving forward myeloma clinical trial strategy and delivery in Oxford and I also am a primary investigator for Phase II/III trials in myeloma and Waldenstroms Macroglobulinaemia.
- Panitsas F, Kothari J, Vallance G, et al. Treat or palliate: outcomes of very elderly myeloma patients. Haematologica. 2018 Jan;103(1):e32-e34
- Blombery P, Kothari J, Yong K, et al. Plasma cell neoplasm associated chronic neutrophilic leukemia (CNL) with membrane proximal and truncating CSF3R mutations Leuk Lymphoma. 2014 Jul;55(7):1661-2
- Hira-Kazal R, Sayar Z, Kothari J et al. Cryoglobulinaemia identified by repeated analytical failure of laboratory tests Lancet. 2014 Jan 25; 383(9914):382
Anjali Kusumbe, Kennedy Institute of Rheumatology
We are interested in exploring the contributions of the vasculature in defining the tissue microenvironments and unravelling the changes occurring in the vascular microenvironments during tumour growth. Our group seeks to elucidate the blood vessel-derived signals underlying the regional specialization of tissue microenvironments, and how these specialized vascular niches instruct cell fate and behavior in normal and tumour tissue.
- Kusumbe AP# (2016) Vascular niches for disseminated tumor cells in bone. Journal of Bone Oncology; 5 (3); 112–116. Special Issue on ‘The Microenvironment in Bone Metastasis’
- Paresh Vyas, Weatherall Institute of Molecular Medicineli>Kusumbe AP, Ramasamy SK, Itkin T, Mae M, Langen U, Betsholtz C, Lapidot T, Adams RH# (2016). Age-dependent modulation of vascular niches for haematopoetic stem cells. Nature 532: 380-384.
- Kusumbe AP, Ramasamy SK, Adams RH (2014) Coupling of angiogenesis and osteogenesis by a specific vessel subtype in bone. Nature 507: 323-328.
Nicholas LaThangue, Department of Oncology (link to CV and homepage)
Udo Oppermann, Botnar Research Centre, Structural Genomics Consortium
Our research interests are focused on identification of molecular disease mechanisms and on validation of novel drug targets. We have contributed systematic mechanistic studies on several metabolic protein families of medical interest, using structural, biochemical and cell biological methods. Current research centers around epigenetics and metabolism in areas of medical importance, such as inflammation, oncology and mesenchymal biology in general. By using systems-based approaches including next-generation sequencing and other single cell technologies such as mass cytometry we aim to understand benign and malignant mesenchymal and haematological diseases, in which the inflammatory and ageing environment is an initiator of metabolic alterations that are key drivers of disease.
- Carbonneau M, M et al The oncometabolite 2-hydroxyglutarate activates the mTOR signalling pathway. Nature Commun. 2016 Sep 14;7:12700. doi: 10.1038/ncomms12700.
- Johansson C, et al Structural analysis of human KDM5B guides histone demethylase inhibitor development. Nature Chem Biol. 2016 Jul;12(7):539-45. doi: 10.1038/nchembio.2087.
- Nowak RP, et al Advances and challenges in understanding histone demethylase biology. Curr Opin Chem Biol. 2016 Aug;33:151-9. doi: 10.1016/j.cbpa.2016.06.021.
Karthik Ramasamy, Cancer and Haematology Centre, Oxford
As a lead clinician for myeloma within the Thames Valley network (circa 2.5 million population) we have developed a robust clinical service for myeloma patients and patients with other plasma cell dyscrasias. We treat over 1500 patients in our region and make available both experimental therapies and transplantation in addition to conventional therapies. Our interests lie in developing clinical studies, which address key clinical concerns for myeloma patients. This includes renal impairment, bone disease and refractory relapse. We have prospective studies in these areas to investigate and manage these myeloma related end organ damages. We work closely with basic science groups and pharmaceutical industry to deliver experimental therapies for patients who fail conventional treatments for myeloma. We are also interested in understanding and optimising real world clinical outcomes with currently licensed therapies for myeloma.
- Augmenting Autologous Stem Cell Transplantation to Improve Outcomes in Myeloma. Maybury B, Cook G, Pratt G, Yong K, Ramasamy K. Biol Blood Marrow Transplant. 2016 Jun 8. pii: S1083-8791(16)30135-5.
- Safety of treatment (Tx) with Pomalidomide (POM) and low-dose dexamethasone (LoDEX) in patients with relapsed or refractory multiple myeloma (RRMM) and renal Impairment (RI), including those on dialysis. Ramasamy K, Meletios A. Dimopoulos, et al . Blood 126 (23) 347 Dec 2015
- Double Relapsed and/or Refractory Multiple Myeloma: Clinical Outcomes and Real World Healthcare Costs. Gooding S, Lau IJ, Sheikh M, Roberts P, Wong J, Dickens E, Bullement A, Elvidge J, Lee D, Ramasamy K. PLoS One. 2015 Sep 14;10(9):e0136207. doi: 10.1371/journal.pone.0136207
- Real-world use of pomalidomide and dexamethasone in double refractory multiple myeloma suggests benefit in renal impairment and adverse genetics: a multi-centre UK experience. Maciocia N Melville A, Maciocia P Cheesman S, Sharpley F, Ramasamy K et al Br J Haematol. 2017 Mar;176(6):908-917. doi: 10.1111/bjh.14547. Epub 2017 Feb 17
- Optimizing the management of patients with spinal myeloma disease. Molloy S, Lai M, Pratt G, Ramasamy K, et al; UK Spinal Myeloma Working Group. Br J Haematol. 2015 Jul 17. doi: 10.1111/bjh.13577.
Paresh Vyas, Weatherall Institute of Molecular Medicine
I lead academic clinical haematology in Oxford. Oxford has one of the largest haematology science programs in Europe and one of UK’s largest haematology clinical trial portfolios. My main research focus is on normal human haemopoiesis and Acute Myeloid Leukaemia (AML), the most common, aggressive leukaemia and a related preleukaemic condition called Myelodysplasia (MDS) (~5000 AML and MDS cases/year/UK). More recently, in collaboration with Professor Oppermann and Dr Ramasamy we have begun to study myeloma biology focussing on mechanisms of therapy resistance.
- Karamitros D, Stoilova B, Aboukhalil Z, Hamey F, Reinisch A, Samitsch M, Quek L, Otoo G, Repapi E, Donndeea J, Usukhbayar B, Calvo J, Taylor S, Goardon N, Six E, Pflumio F, Porcher C, Majet R, Gottgens B, Vyas P. Functional and transcriptional heterogeneity of human hemopoietic lympho-myeloid progenitors at the single cell level. Nature Immunology. 19, 85–97 (2017)
- Amatangelo MD, Quek L, Shih A, Stein EM, Roshal M, David MD, Marteyn B, Rahnamay Farnoud N, de Botton S, Bernard OA, Wu B, Yen KE, Tallman MS, Papaemmanuil E, Penard-Lacronique V, Thakurta A, Vyas P, Levine RL. Enasidenib induces acute myeloid leukemia cell differentiation to promote clinical response. Blood 130. 732-741 2017.
- Goardon N, Marchi E, Atzberger A, Quek L, Schuh A, Woll P, Mead A, Alford KA, Rout R, Chaudhury S, Gilkes A, Knapper S, Soneji S, Beldjord K, Begum S, Rose S, Geddes N, Griffiths M, Standen G, Sternberg A, Cavenagh J, Hunter H, Bowen D, Killick S, Robinson L, Price A, Macintyre E, Virgo P, Burnett A, Craddock C, Enver T, Jacobsen SEW, Porcher C and Vyas P. Co-existence of LMPP-like and GMP-like Leukemia Stem Cells in Acute Myeloid Leukemia. Cancer Cell 19 p138-52 (2011).
- Quek L, Otto GW, Garnett C, Lhermitte L, Lau I, Karamitros D, Doondeea J, Usukhbayar B, Goardon N, Ivey A, Gu Y, Gale R, Davies B, Sternberg A, Killick S, Hunter H, Cahalin P, Price A, Carr A, Griffiths M, Virgo P, Mackinnon S, Hills R, Grimwade D, Freeman S, Burnett A, Russell N, Craddock C, Mead AJ, Peniket A, Porcher C & Vyas P. Functional and genetic heterogeneity of distinctive leukemic stem cell populations in CD34- human acute myeloid leukaemia. Journal of Experimental Medicine 213:1513-1535 (2016).