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Melinda Czéh

PhD


CRUK Clinical Scientist

I am a CRUK Clinical Scientist in the group of Professor Claus Nerlov in the MRC Molecular Haematology Unit at the Weatherall Institute of Molecular Medicine (WIMM). Parallel, I am working as a Paediatric Oncologist in the Department of Paediatric Haematology and Oncology (John Radcliffe Hospital) led by Dr. Kate Wheeler.

 I received my PhD from the Free University of Berlin, Germany in 2008. I performed my PhD thesis under the supervision of Professor Thomas Blankenstein by investigating the antitumor immune responses in transgenic mouse models with spontaneous tumor development. Since LoxP-TAg transgenic mice express the oncogenic SV40 TAg only at later age and spontaneously, the model allowed the characterization of antitumor immune responses, especially tolerance mechanisms in a very natural way. 

 After my PhD I trained in General Paediatrics and Paediatric Haematology and Oncology in the Children´s Hospital of Charité, Berlin and UKM, Münster, Germany from 2007 to 2016. Parallel, I was working as a Clinical/Postdoctoral Fellow by Professor Frank Rosenbauer from 2014 to 2017 in the Institute of Molecular Tumor Biology, Münster. I was investigating the role of epigenetic mechanisms during haematopoietic differentiation. Furthermore, I took part in the characterization of a mouse model with biphenotypic leukaemia and transdifferentiation mechanisms.

I moved to Oxford in November 2017 after I had awarded a CRUK Clinical Scientist Fellowship to join the group of Professor Claus Nerlov. My research activity focuses on the role of haematopoietic lineage bias in the development of different types of acute leukaemias and how this contribution changes during ageing.

Both AML and ALL are still highly aggressive malignancies that, despite advances in treatment, remain associated with significant mortality and morbidity. Whereas ALL is most commonly observed in paediatric patients, the incidence of AML increases with age, as does the number of recurrent mutations within the malignant clone. Acute leukaemias arise through the sequential acquisition of mutations that lead to pre-leukaemic clonal expansion, followed by leukaemic transformation of lineage-restricted progenitors through their acquisition of ectopic self-renewal and impaired terminal differentiation. HSCs are (with memory lymphocytes as the exception) the only long-lived cells in the haematopoietic system, a property that makes them a key target for the sequential accumulation of leukaemogenic mutations. In my project I would like to investigate the role of haematopoietic stem cells (HSCs) bias in the development of MLL-induced acute leukaemias during ageing.

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