Dr Claire Lucas
Associate Professor
Biography
Claire Lucas joined Chester Medical School as a Haematology Lecturer. Claire has over 15 years’ experience working as a NHS Scientist and Honorary lecturer. Claire’s research area of expertise is biomarkers predictive of clinical outcome in leukaemia.
Teaching and Supervision
Claire is the programme leader for MSc Haematology and MRes Medical Science, and teaches on both the undergraduate and postgraduate courses offered by Chester Medical School. She is module leader for MD6031 Haematology and Transfusion Science. MD6903 Blood Science (DL) MD7005 Blood Science MD7022 Therapeutic Advances in Treating Haematological Problems In addition to being the MSc Haematology programme lead and module lead. I also teach across the Medical School. I frequently teach across the levels and programmes including BSc Biomedical Science, BMedSci Medical Science, BSc Microbiology, BSc Pharmacology, BSc Biochemistry, MSc Biomedical Science, MSc Infection and Immunity, MSc Medical Genetics, MSc Oncology and Physician Associate programmes. I teach regularly on the following modules. MD5016 Pathophysiology MD5018 Diagnostics and Therapeutics MD5027 Professional Skills for Life Science 2 MD6029 Dissertation MD7006 Clinical Immunology MD7024 Molecular Medicine MD7058 Foundations of Clinical Medical Science MD7100 Research dissertations Claire also supervises and supports undergraduate and postgraduate students through their research dissertations and is a PhD supervisor and the Medicals Schools Postgraduate Research Tutor.
Research and Knowledge Exchange
While working in the NHS Claire developed a keen interest in research and began to study for a part-time PhD in 2006 under the supervision of Prof Richard Clark. The title of her thesis was “Biomarkers predictive of clinical outcome in chronic myeloid leukaemia (CML).” Claire's current research portfolio is a balance of translational and basic science research. Her area of expertise is biomarkers predictive of clinical outcome in both chronic myeloid leukaemia (CML) and acute myeloid leukaemia (AML). CML is a cancer of the haematopoietic stem cells. The aim of her research is to address three important questions: 1. Can we predict patients at diagnosis who will progress into blast crisis? For some patients their disease will progress to an aggressive/fatal phase known as blast crisis (BC). Patients who develop blast crisis have a very poor clinical outcome, with a long term overall-survival of <20%. The mechanisms underlying the evolution of blast crisis are poorly understood and blast crisis remains a significant challenge for clinicians and scientists. I have identified a novel protein known as Cancerous Inhibitor of PP2A (CIP2A) as a biomarker which can identify at diagnosis those patients at risk of blast crisis. (Lucas et al. 2015; Lucas CM et al. 2011). I have shown that CIP2A confers the poorest clinical outcome by creating anti-apoptotic phenotype. (Lucas et al. 2016). 2. Can we predict those patients who can successfully stop treatment? Some patients respond well to treatment but will remain on treatment indefinitely, with enduring side effects, impacting on their quality of life. My preliminary data indicates that changes in expression of an anti-apoptotic protein during treatment de-escalation may be a novel biomarker of molecular relapse. The aim here is to test this biomarker in the DESTINY clinical trial and it is hoped that this will identify patients who can successful stop treatment without relapsing. This will have both beneficial outcomes for the patient and may prove advantageous financially to Healthcare Trusts. 3. Identify novel therapeutic targets to eliminate the residual leukaemic stem cells (LSC) and potentially cure the disease. CML LSC are responsible for initiation and relapse of the disease. Treatment involves BCR-ABL tyrosine kinase inhibitors which do not kill LSC. CML will only be cured when LSC are eradicated. There is an urgent need to identify new LSC therapeutic targets. I am currently working on two potential novel targets.