个人简介
Alistair Easton graduated from The University of Glasgow having studied Medicine with an intercalated degree in Immunology. He trained in Histopathology at the Western Infirmary, the Royal Infirmary and the Southern General hospitals in Glasgow. During his training he was awarded a Pathological Society Centenary Clinical Fellowship. He completed his doctoral research in autoimmunity and pathogen ganglioside mimicry in Guillain Barre Syndrome, supervised by Prof Hugh Willison, Dr Carl Goodyear and Prof Allan Mowat. He was subsequently a Clinical Lecturer in Histopathology at the University of Glasgow.
He took up his current post as Senior Clinical Lecturer/Associate Professor of Histopathology at Southampton University in July 2014. He is currently researching novel antibody therapeutics that target ganglioside tumour associated glycolipid antigens expressed by the childhood cancer neuroblastoma and the skin cancer melanoma. He is also studying the effects of these glycolipid antigens on tumour /immune system interactions. His clinical interest is in inflammatory and malignant skin pathology.
研究领域
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Neuroblastoma is one of the most common and aggressive childhood cancers. Standard treatment involves surgery, chemotherapy, radiotherapy and maintenance therapy with retinoic acid derivatives. The poor survival rate and highly toxic nature of some of these treatments has led to a search for new, more effective, therapies.
Recent advances in immunotherapy has led to the introduction of a monoclonal antibody that targets the ganglioside GD2, which is expressed at high levels on the surface of neuroblastoma cells. Despite a 20% improvement in outcomes, more than half of patients still die of recurrent disease. Whilst this antibody is far more specific in targeting neuroblastoma than conventional therapies, it still carries risk of side-effects as GD2 is expressed at low levels on nerves. When this occurs, the subsequent nerve damage will limit the amount of therapy that can be given to patients and thus hamper the ability of doctors to eradicate any residual neuroblastoma cells.
My particular area of interest is in optomising the tumuor specificity of anti-ganglioside antibodies to minimize off-tumour binding and side-effects. Studies of anti-ganglioside antibodies in autoimmune neuropathies has led to a new understanding of how ganglioside antigens interact with each other on the surface of cells and how they are recognized and targeted by the immune system. We are using this knowledge to identify novel and unique ganglioside targets on neuroblastoma cells that will minimise side-effects and allow dose escalation to eradicate all of the malignant cells. This research is of importance in a number of cancers as aberrant ganglioside expression is a common feature of malignant cells.
Our group is also studying the mechanism of action of the anti-GD2 antibody and how it engages the cellular arm of the immune system to target and eradicate neuroblastoma cells.