Cancer will affect half the population in the UK in the coming years, with many of those still dying of the disease because of late presentation and lack of therapeutic options. Hence, Medical School researchers are actively studying this disease to better understand mechanisms, develop better diagnostic markers and develop novel therapeutic avenues to improve patient outcomes.
We are continuing to follow multi-disciplinary approaches to solve the problems associated with cancer. We work with clinicians (oncologists, gastroenterologists, surgeons, pathologists and endocrinologists), physicists, data-scientists, engineers and mathematicians. We also work closely with industry (large and small) to drive forward novel innovations in the cancer field.
We take a translational approach to our research into cancers, simultaneously we work to ensure that our research broadens scientific understanding of Cancer, how to treat it and identify routes to early diagnosis. Our research teams are working to use blood-based biomarkers to identify the presence of oesophageal cancer, manipulate bacteria to target and treat cancer and studying signalling irregularities in tumour cells. Our research focus areas is focussed on how to improve patient health and wellbeing.
Germline defects in the genes APC and MUTYH cause the familial polyposis syndromes FAP and MAP. Patients with these syndromes are at very high risk of developing intestinal cancers. This patient focused research, brings together international academic expertise, industry and NHS genetics, gastroenterology and surgical services. A combination of long term prospective analysis of endoscopic data, genomic analyses and 3D organoid models, will lead to better understanding of the natural history and genetic causes of familial polyposis syndromes. This work will identify those at high risk of cancer development and lead to improvements in clinical management and to the development of novel genetically targeted personalised therapies.
Certain bacteria will only grow in a tumour, not in healthy tissue. This is because a tumour cell’s metabolism is different to that of healthy cells. The bacteria use the nutrients provided by the tumour to grow. In addition, the tumour evades the host immune system by supressing it. So the bacteria not only hijack a tumour’s nutrients, but they also use the tumour to hide from the immune system. We use these tumour-targeting cell-invasive bacteria to deliver therapeutic payloads directly into tumour cells. Consequently, only tumour cells stop multiplying, not healthy cells.
