Lindsay Spender

Biography

Lindsay graduated from The University of Birmingham, U.K. before working in the pharmaceutical industry for four years helping to identify novel anti-viral therapeutic agents. She was then accepted on the Welcome Prize Studentship programme to study for a PhD in immunology at Imperial College, London, where she carried out research into the pathological effects of a common childhood respiratory virus. Lindsay then joined Professor Paul Farrell’s laboratory in the Ludwig Institute for Cancer Research, London as a postdoctoral scientist working on Epstein-Barr virus. There she developed a long term interest in B-cell biology, lymphomas and cancer. Lindsay joined Gareth’s laboratory at The Beatson Institute for Cancer Research in Glasgow in 2004 to study the mechanisms of TGF-beta induced tumour suppressor activity in human B cells and B cell lymphomas. She has continued as senior postdoctoral scientist in Gareth’s following the move to Dundee. Lindsay’s work is supported by the AICR.

Research Interest

TGF-beta has a vital role in protection against developing cancer through its tumour suppressor activity. This can be attributed to its potent ability to arrest cell proliferation and through its induction of programmed cell death (apoptosis). I have been interested in studying the mechanisms of TGFβ tumour suppressor activity. One of the best model systems in which to study this aspect of TGF-beta biology is in normal primary human B cells and Burkitt’s Lymphoma (BL) cell lines. Our detailed molecular analyses of this model system has revealed that TGF beta signalling acts as a central regulator of centroblastic B cell apoptosis via co-ordinated regulation of the BCL2 family of cell death and survival proteins (Spender et al., CDD 2009, Spender et al JBC 2013). Based upon these studies and those of others we have investigated the potential of targeting survival pathway signalling as a therapeutic target in B cell malignancies (Spender and Inman, Expert Opinion Ther. Targets 2009a) and have discovered that dual targeting of the pro-survival BCL2 family and the PI3K/mTOR pathway may be a valuable approach for lymphoma management (Spender and Inman, Mol. Cancer Res, 2012). We have also revealed novel pathways of cytostasis in B cells (Spender and Inman, JBC 2009). Our current studies have expanded to investigate how TGF beta signalling may regulate melanoma cell survival.