Part of the puzzle of blood cancer may have been solved.
Daniel Tennant, Senior Lecturer in Metabolic Biochemistry at the University of Birmingham, delves into our bone marrow to find out how to treat this disease.
Dr. Daniel Tennant is a Senior Lecturer in Metabolic Biochemistry in the Institute of Metabolism and Systems Research (IMSR), situated on the second floor of the Institute of Biomedical Research. He uses stable isotope tracers to investigate changes in the use of nutrients in conditions where oxygen is limiting (hypoxia), or in the presence of genetic mutations that induce a hypoxia-like response. Dan applies the fundamental knowledge gained from these research projects to understand the pathogenesis of diseases where changes in oxygenation play a role; in particular, cancer.
Dan has recently set up the Metabolic Tracer Analysis Core (MTAC) within the IMSR in order to develop novel means to analyse cellular and tissue metabolism using stable isotope tracer molecules, and collaborates with groups worldwide who are interested in using these techniques to study the metabolism of their system, or the metabolism of labelled product.
Dr. Tennant publishes both primary research and reviews in high impact journals, including Nature Communications, Cell Metabolism, Nature Reviews Cancer and Cell, and is regularly asked to speak at international conferences.
Blood Cancer and Bone Marrow
Multiple myeloma is a blood cancer located in the bone marrow. It affects mainly elderly patients, and although treatments are successful in temporarily slowing down the disease, they are not curative. It has become clear recently that cases of myeloma are preceded by a mostly symptomless, benign disease also located in the bone marrow, called monoclonal gammopathy of undetermined significance, or MGUS. What we don’t understand at the moment is what changes in the biology of the bone marrow are needed in order for patients to develop MGUS, and then what additional changes occur that result in progression to multiple myeloma.
We focussed our research on the bone marrow, where the cancer has to stay in order to survive and divide. We investigated a cell type which forms a part of the connective tissue of the marrow and is required in healthy conditions for blood cell development and maintenance of the bone.
When we investigated the molecular profile of these connective tissue cells in patients with both MGUS and multiple myeloma, we found that both were different from healthy bone marrow, but interestingly, very similar to each other. This information tells us that when patients develop MGUS, the connective tissue cells change their molecular profile, and this change is probably sufficient to allow the disease to progress to multiple myeloma and to allow the connective tissue cells to support the cancer cells, which permit them to survive anti-cancer treatments more easily.
Our results suggest something else as well – that the signal for MGUS to become cancerous may come from another part of the bone marrow. This is the next stage for our research – to find out what this signal is, and where it comes from. However for now, our results add an important piece to the jigsaw puzzle of this cancer, which we hope will allow us to develop new treatments for multiple myeloma.
