Dr Elise Rees is postdoctoral scientist in Professor Kwee Yong’s Multiple Myeloma Laboratory at the UCL Cancer Institute, and co-investigator on a project to investigate the role of NK cells in the development of MM
Our ability to detect, treat and even prevent cancer has made great progress over the last couple of decades but sadly, cancer remains a frequent and debilitating disease.
Whilst our treatment options are vastly improved, unresponsiveness or relapse remains a major issue. This may be in part due to the idea that frank malignancy represents the endpoint of a series of molecular steps and is therefore often difficult, or even impossible, to reverse. Understanding the complex biological systems that underlie its development is essential if we are to identify new ways of treating the disease and even more so if we hope to prevent development in the first place.
It is now well accepted that virtually all malignancies are preceded by clinically silent precursor states, where characteristic cancer molecular lesions emerge. These precursor states provide a unique opportunity to investigate the biological features that influence cancer development. The factors that drive or delay a precursor along the path to malignancy are mechanistically and clinically important, as well as potential targets for early interventions. With an understanding of the key molecular lesions that drive progression – and an understanding of how the surrounding environment is altered – treatment options could be specifically targeted and rationally based.
Our science
Our group is interested in multiple myeloma, a cancer of antibody producing plasma cells that expand in the bone marrow. More common in the elderly, the disease leads to multi-organ failure and, despite considerable therapeutic advances, remains incurable.
Myeloma is preceded by clinically defined precursor conditions called monoclonal gammopathy of uncertain significance (MGUS) and smouldering myeloma (SMM). Progression through these states is generally associated with increasing tumour burden, acquisition of secondary or additional genetic events and, ultimately, increasing risk of progression to symptomatic malignant multiple myeloma.
Importantly, whilst all patients with malignant multiple myeloma are thought to have progressed through precursor states, not all patients with MGUS or SMM will go on to develop multiple myeloma. If we hope to intervene, then it is crucial that we can select those patients that are most likely to progress to prevent the over – and possibly unnecessary – treatment of patients.
