Areas of expertise

Acute myeloid leukaemia - development of novel therapeutics, cytogenetics, disease evolution

Qualifications

2011 - PhD (Cancer Research), Newcastle University

2007 - Postgraduate Certificate of Competency in Clinical Cytogenetics

2005 - BSc (1st Class with Honours) Human Genetics, Newcastle University

Previous Positions

2007 - 2011   PhD student, Molecular Carcinogenesis group, Northern Institute for Cancer Research, Newcastle University

2005 - 2007   Clinical Cytogeneticist (Grade A), Northern Genetics Service, Newcastle upon Tyne Hospitals NHS Trust

My research is focussed on chemotherapy of acute myeloid leukaemia (AML). In particular I am interested in whether DNA repair pathway defects, commonly observed in AML patients, can be exploited to both improve current therapies and facilitate development of novel agents. I also have a keen interest in determining the contribution of conventional chemotherapeutics to the development of relapsed disease via generation of DNA mutations.

Student supervision

Devi Suchitra-Devi (PhD)       2017 - date

Nurettin Ayvali (PhD)              2016 - date

Emmanouela Soura (MPhil)   2016 - 2018

Mohd Fadly (PhD)                  2014 - date

• Fordham SE, Blair HJ, Elstob CJ, Plummer R, Drew Y, Curtin NJ, Heidenreich O, Pal D, Jamieson D, Park C, Pollard J, Fields S, Milne P, Jackson GH, Marr HJ, Menne T, Jones GJ, Allan JM. Inhibition of ATR acutely sensitises acute myeloid leukemia cells to nucleoside analogs that target ribonucleotide reductase. Blood Advances 2018, 2(10), 1157-1169.
• Fordham SE, Cole M, Irving JA, Allan JM. Cytarabine preferentially induces mutation at specific sequences in the genome which are identifiable in relapsed acute myeloid leukaemia. Leukemia 2015, 29(2), 491-494.
• Fordham SE, Marr H, Allan JM. Searching for clarity in therapy-related myelodysplastic syndrome/acute myeloid leukemia prognostication. Leukemia and Lymphoma 2013, 54(3), 447-448.
• Fordham SE, Matheson EC, Scott K, Irving JAE, Allan JM. DNA mismatch repair status affects cellular response to Ara-C and other anti-leukemic nucleoside analogs. Leukemia 2011, 25(6), 1046-1049.
• Forster VJ, Nahari MH, Martinez-Soria N, Bradburn AK, Ptasinska A, Assi SA, Fordham SE, McNeil H, Bonifer C, Heidenreich O, Allan JM. The leukemia-associated RUNX1/ETO oncoprotein confers a mutator phenotype. Leukemia 2016, 30(1), 250-253.
• Middleton FK, Patterson MJ, Elstob CJ, Fordham S, Herriott A, Wade MA, McCormick A, Edmondson R, May FEB, Allan JM, Pollard JR, Curtin NJ. Common cancer-associated imbalances in the DNA damage response confer sensitivity to single agent ATR inhibition. Oncotarget 2015, 6(32), 32396-32409.
• Sunter NJ, Scott K, Hills R, Grimwade D, Taylor S, Worrillow LJ, Fordham SE, Forster VJ, Jackson G, Bomken S, Jones G, Allan JM. A functional variant in the core promoter of the CD95 cell death receptor gene predicts prognosis in acute promyelocytic leukemia. Blood 2012, 119(1), 196-205.
• Wade MA, Sunter NJ, Fordham SE, Long A, Masic D, Russell J, Harrison CJ, Rand V, Elstob C, Bown N, Rowe D, Lowe C, Cuthbert G, Bennett S, Crosier S, Bacon CM, Onel K, Scott K, Scott D, Travis LB, May FEB, Allan JM. c-MYC is a radiosensitive locus in human breast cells. Oncogene 2015, 34, 4985-4994.
• McCormick A, Earp E, Elliot K, Cuthbert G, O'Donnell R, Wilson BT, Sutton R, Leeson C, Thomas HD, Blair H, Fordham S, Lunec J, Allan J, Edmondson RJ. Functional characterisation of a novel ovarian cancer cell line, NUOC-1. Oncotarget 2017, 8(16), 26832-26844.
• Moad M, Pal D, Hepburn AC, Williamson SC, Wilson L, Lako M, Armstrong L, Hayward SW, Franco O, Cates J, Fordham SE, Przyborski S, Carr-Wilkinson J, Robson CN, Heer R. A novel model of urinary tract differentiation, tissue regeneration, and disease: Reprogramming human prostate and bladder cells into induced pluripotent stem cells. European Urology 2013, 64(5), 753-761.
• Anderson JJ, Fordham S, Overman L, Dignum H, Wood K, Proctor SJ, Crosier S, Angus B, Culpin RE, Mainou-Fowler T. Immunophenotyping of diffuse large B-cell lymphoma (DLBCL) defines multiple sub-groups of germinal centre-like tumours displaying different survival characteristics. International Journal of Oncology 2009, 35(5), 961-971.