Research Interests
I have a long standing interest in the role of immune receptors and their ligands in the pathogenesis of infectious diseases, autoimmunity and cancer. During an undergraduate studentship at the Novartis Institute for Biomedical Research in Vienna. I investigated novel signalling pathways triggered by Fc receptors in mast cells and the importance of such pathways in allergic disease. I continued my training during a PhD at the CRUK institute for Cancer studies in Birmingham with Steve Lee and David Adams where I focused on elucidating the molecular mechanisms of T lymphocyte recruitment to Hodgkin’s lymphoma (an EBV associated malignancy). The implications of our findings for T cell based therapies were examined by analysing the homing phenotype (chemokine receptors, selectins and integrins) and function of T cell clones prepared for a phase I clinical trial of T cell infusion therapy for advanced cancer patients.
During my post-doctoral training I continued research to develop effective T cell based therapies for human cancer. This again involved analysing the molecular mechanisms whereby T cells home to the tumour site (Nasopharyngeal carcinoma). With the renewal of our CRUK funding for a further 6 years, we began exploring the use of retroviral-mediated transfer of TCR genes to confer tumour antigen specificity to patient-derived T cells and studying the efficiency of antigen recognition.
More recently I have worked with Martin Dyer at the MRC Toxicology unit in Leicester where we investigated the role of a cytokine receptor gene, CRLF2, whose deregulated expression (through 2 novel genomic abnormalities that involve the pseudoautosomal region, PAR1, of both sex chromosomes) is involved in lymphoid transformation in B cell precursor acute lymphoblastic leukaemia and is associated with constitutive STAT5 activation. Funded by MRC technology I evaluated CRLF2 as a therapeutic target and worked with a commercial company to develop and initially characterise antibodies targeting this receptor.
Currently, I am investigating the mutation and diversity in immunity genes that are copy number variable in humans, with particular focus on the Fc gamma receptor gene family (funded by the Wellcome Trust), which is involved in inflammatory, autoimmune and infectious disease. I am developing and using novel molecular approaches to analyse the variation and mutation rate of copy number variation.
I have a long standing interest in the role of immune receptors and their ligands in the pathogenesis of infectious diseases, autoimmunity and cancer. During an undergraduate studentship at the Novartis Institute for Biomedical Research in Vienna. I investigated novel signalling pathways triggered by Fc receptors in mast cells and the importance of such pathways in allergic disease. I continued my training during a PhD at the CRUK institute for Cancer studies in Birmingham with Steve Lee and David Adams where I focused on elucidating the molecular mechanisms of T lymphocyte recruitment to Hodgkin’s lymphoma (an EBV associated malignancy). The implications of our findings for T cell based therapies were examined by analysing the homing phenotype (chemokine receptors, selectins and integrins) and function of T cell clones prepared for a phase I clinical trial of T cell infusion therapy for advanced cancer patients.
During my post-doctoral training I continued research to develop effective T cell based therapies for human cancer. This again involved analysing the molecular mechanisms whereby T cells home to the tumour site (Nasopharyngeal carcinoma). With the renewal of our CRUK funding for a further 6 years, we began exploring the use of retroviral-mediated transfer of TCR genes to confer tumour antigen specificity to patient-derived T cells and studying the efficiency of antigen recognition.
More recently I have worked with Martin Dyer at the MRC Toxicology unit in Leicester where we investigated the role of a cytokine receptor gene, CRLF2, whose deregulated expression (through 2 novel genomic abnormalities that involve the pseudoautosomal region, PAR1, of both sex chromosomes) is involved in lymphoid transformation in B cell precursor acute lymphoblastic leukaemia and is associated with constitutive STAT5 activation. Funded by MRC technology I evaluated CRLF2 as a therapeutic target and worked with a commercial company to develop and initially characterise antibodies targeting this receptor.
Currently, I am investigating the mutation and diversity in immunity genes that are copy number variable in humans, with particular focus on the Fc gamma receptor gene family (funded by the Wellcome Trust), which is involved in inflammatory, autoimmune and infectious disease. I am developing and using novel molecular approaches to analyse the variation and mutation rate of copy number variation.
