Dr Claire Lucas
Head of Division
Biography
Dr Claire Lucas is Head of Medical Sciences at UoC Medical School. An expert in chronic myeloid leukaemia biomarkers, she is passionate about education, innovation, and leadership. Claire has over 15 years’ experience working as a NHS Scientist. Claire’s research area of expertise is biomarkers predictive of clinical outcome in leukaemia.
Teaching and Supervision
Dr Claire Lucas is Head of Division for Medical Science at UoC Medical School, overseeing all programmes within the Medical Sciences Division. An expert in chronic myeloid leukaemia biomarkers, she actively teaches across undergraduate and postgraduate modules. Claire previously led the MSc Haematology and MRes Medical Science programmes and supervises research dissertations.
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.