ICM Research Seminar
Speakers: Anna Lena Dittrich (Dr A Tyson-Capper, Dr H Gautrey)
Audrey Brown (Prof M Walker)
Matthew John Wood (Dr C Hilkens, Dr M Haniffa, Prof J Isaacs)
Venue: Dental Lecture Theatre F, Dental School
Date and Time: Wednesday 2nd March 2016, 13.00 pm – 14.00 pm
Anna Lena Dittrich
Tumour promoting HER2 Splice Variant Δ16HER2: Regulation and Implication in Breast Cancer
Breast cancer is one of the major types of cancer for women. The human epidermal growth factor receptor 2 (HER2) is a well-known oncogene and therapy target in 20-30% of breast tumours. Although these therapies have proven efficient, therapy resistance has been observed. The underlying mechanisms are not well understood. One possible cause are HER2 protein variants generated by alternative splicing. The aim of this project is to uncover the processes regulating the production of the highly oncogenic HER2 splice variant Δ16HER2
Decreased TCF7L2 expression enhances insulin action in primary human skeletal muscle cell cultures
Variants within transcription factor 7-like 2 (TCF7L2) are the strongest genetic predictor of type 2 diabetes risk. Expression of TCF7L2 is ubiquitous but while many studies have examined the role of TCF7L2 in beta cells, few have examined TCF7L2 function in relation to glucose metabolism in peripheral tissues. The aim of the current study is to explore if TCF7L2 has a role in glucose metabolism in primary human skeletal muscle cells.
Do Synovial Dendritic Cells Contribute to the Pathogenesis of Rheumatoid Arthritis?
Dendritic cells (DCs) are thought to play an important role in rheumatoid arthritis (RA). Found clustered with T-cells in the synovium, they may activate auto-reactive lymphocytes locally. However, the precise role they play in RA pathogenesis remains unclear. We aim to identify and compare DC subsets by phenotyping, transcriptomics and functional capacity. These subsets will be derived from the synovial tissue, fluid and peripheral blood of rheumatoid and osteoarthritis patients as well as healthy controls. These findings will be instrumental to delineating the mechanisms by which DCs contribute to the pathogenesis of RA.
Chair: Matt Barter