Haemato-oncology

I am interested in the immunology of and immunosuppression in B-CLL. I am currently looking at the involvement of the microenvironment in in B-CLL and specifically the effect of T cells and endothelial cells on the malignant clone. i am currently trying to create a basic model to study this invitro. My work involves and lots of tissue culture, flow cytometry, proliferation assays and anaysis of cytokines. I am moving onto immunofluorescence staining of Lymph nodes using multiple markers to study this in-vivo.

020 7848 5803

020 7848 5814

Leukaemia is a clonal disease initiated from a very small number of pre-leukaemic stem cells (pre-LSCs) carrying the initiating genetic events, which subsequently convert to full blown LSCs by acquiring further mutations necessary for the overt diseases such as acute myeloid leukaemia (AML). Emerging evidence indicates that pathways critical for regulation of normal stem cells are frequently hijacked or mutated in LSCs. My group is interested in understanding the molecular and cellular mechanisms underlying the oncogenic conversion of normal cells into AML stem cells.

Please visit Prof. So’s website (www.ericso.org) for further details.

78485888

78485890

Gene therapy-mediated immune rejection of cancer; cellular differentiation; molecular genetic analysis.

+44(0)2078485902

+44(0)2078485902

(Head of Division) Molecular evolution and treatment of myelodysplastic syndromes (preleukaemia); immune gene therapy for leukaemia; bone marrow transplantation for myeloid malignancies.

Tumour specific induction of apoptosis

Autologous bone marrow transplantation is an alternative therapeutic option for patients suffering from haematological malignancies lacking an HLA compatible donor. However, disease relapse remains a primary cause of death due in part to autograft contamination with clonogenic tumour cells. The multiple purging strategies developed to date have proven ineffective in eradicating the tumour cells from the autologous haemopoeitic stem cell grafts. Pharmacological and immunological approaches to eliminate the leukaemic cells from autografts are often toxic to the normal haematopoietic progenitors, limiting the clinical utility. Reduction of the tumour burden by positive/ negative selection procedures require the presence of differentially expressed membrane antigens on either the tumour cells or the normal haematopoietic progenitors and stem cells which is not generally the case in haematological malignancies. In order to improve the efficacy of cell purging we are studying a chicken anemia virus (CAV) derived protein called Apoptin. Apoptin is a protein which has been shown to induce apoptosis in a variety of human malignant and transformed cells, but not in normal cells

MicroRNA target discover

MicroRNAs(miRNAs) are a novel class of small RNA molecules that can regulate the expression of many genes.They have been shown to be involved in many fundamental processes such as differentiation, proliferation, apoptosis and play a role in cancer. Several microRNAs can act as either oncogenes or tumour suppressor genes. It is currently thought that in humans miRNAs acts mainly by mediating specific translational inhibition and to a lesser extent degradation of mRNA targets.
The role and targets of most miRNAs in humans are largely unknown. Computational identification of miRNAs targets using various algorithms provide some insight into the miRNAs targets,however the drawbacks of these predictions are that they all have a substantial false positive rate and may be biased as they are mostly based on the few known miRNA:target gene interactions.The need for a functional assay to identify the miRNA target is the need of the hour.

We have developed a novel functional assay to enable identification of functional miRNA targets. In a pilot project we used mir130a and its verified target v-maf musculoaponeurotic fibrosarcoma oncogene homolog B(MAFB)as a proof of concept,this identified a further panel of mir130a targets none of which were identified as potential targets of mir130a by the available target pridiction programmes.

020 7848 5839

Research focusses on the development of enzymes capable of delivering targeted cytosine methylation to predetermined DNA sequences. We are using these enzymes to simulate the methylation patterns observed in cancer patients, to determine the actual role of DNA methylation in disease progression. An additional and emerging basic research program seeks to address the effects of gene mutations associated with epigenetic components of the cell, that are being increasingly found in leukaemia patients, in the desease process.

0208 848 5839

My research focus is the study of immune dysfunction in leukaemia and immune reconstitution after allogeneic haematopoietic stem cell transplantation. My research group performs comprehensive phenotypic and functional studies of immunity in patients with leukaemia and allogeneic haematopoietic stem cell transplant patients with the aim of identifying signatures indicative of beneficial and detrimental clinical courses. Knowledge obtained will enable improved monitoring of patients to facilitate rapid and tailored treatment regimens and development of novel specific immunotherapeutic strategies.

020 7848 5208

020 7848 5902

• Normal Haemopoiesis and abnormalities in the myelodysplastic syndromes (MDS) and myeloid leukaemias
• Cell cycle (particular focus on G0→G1→S-phase transitions)
• Systems Biology analyses of protein interaction networks
• Epigenetics (study of specific and genome-wide DNA CpG methylation, histone code and nucleosome positioning)

(office) +44 (0)207 848 5818 (lab) +44 (0)207 848 5808 or 5830

+44 (0)207 848 5902

My research is mainly focused in multiple myeloma, a haematological malignancy characterised by accumulation of plasma cells in the bone marrow. It is becoming increasingly evident that the interaction of the tumour myeloma plasma cells with the bone marrow microenvironment is essential for the development of the disease. The pattern of expression of cell adhesion molecules and the secretion of soluble factors by both myeloma plasma cells and other bone marrow cells (fibroblasts, osteoclasts, osteoblasts, endothelial cells, etc) create a network of signals that promote malignant cells survival. These processes require the recruitment of bone marrow cells and myeloma cells to niches within the bone marrow that allow cell-cell and cell-extracellular matrix interactions that trigger these network of signals. In addition, myeloma cells can become resistant to therapeutic treatments targeting cell proliferation and survival by increasing their adhesive properties to extracellular matrix proteins. Our research is focused in increasing our understanding of the adhesion and migratory patterns of both myeloma and other bone cells and the signalling pathways involved in these processes to search for targets to develop new therapeutic agents for multiple myeloma.

+ 44 (0) 20 7848 5816