Lesley Stark is a Reader/principle investigator in the Edinburgh Cancer Research Centre at the University of Edinburgh. She received a B.Sc in cell biology from the University of Aberdeen (1990) and a PhD in cancer research from the University of Edinburgh (1994). She undertook post-doctoral training with Professor R. Hay at the University of St Andrews where her work focussed on the interaction between the HIV protein, vpr, and the NF-kB pathway. She then moved to the University of Edinburgh where she began her work on the role of NF-kB in the anti-tumour mechanisms of aspirin and similar agents. In 2002 she was awarded a Caledonian Research Foundation fellowship, was appointed as a lecturer at the University of Edinburgh in 2005, promoted to Senior lecturer in 2008 and to  reader in 2012. She has an active research group studying NF-kB nucleolar stress response and precision cancer prevention. Her more recent studies are focussed on nucleolar stress, senescence and ageing.

1990 BSc Cell Biology and Immunology, 1st class honours, University of Aberdeen.

1995 PhD, University of Edinburgh. Supervisor: Professor C Bird

2002. Caledonian Research Foundation Fellowship.

2014. Fellow of the Royal Society of Biology (FRSB)

2020. Post Graduate Certificate in Academic Practice (PgCAP)

2020. Fellow of the Higher Education Authority (FHEA)

1. Identification of mechanisms that disrupt nucleolar function in response to aspirin and similar stresses, and those that link disrupted nucleolar function to changes in cell phenotype, with emphasis on the NF-kB signalling pathway.

2. Identification of biomarkers of aspirin response in colorectal cancer

In addition to its role in ribosome biogenesis, the nucleolus acts as a critical stress sensor and coordinates downstream responses to stress such as differentiation, cell cycle arrest, autophagy, senescence and apoptosis. In keeping with its central role, perturbations in nucleolar function contribute to the aetiology of many common diseases including ischaemic heart disease, neurodegenerative disorders and cancer. Hence, the organelle is emerging as an attractive therapeutic target. Our research is focussed on understanding  how nucleolar function is altered in response to stress, and how specific changes lead to altered cell growth, death and disease, so that the organelle can be effectively targeted for therapeutic purpose.   We are particularly interested in signalling between nucleoli and the NF-kB pathway as we have shown this is important in regulating cellular homeostasis. Our current research aims to delineate a novel TIF-IA-NF-kB nucleolar stress pathway and determine the role of this signalling axis in aging and senescence.

Another area of interest in the lab is  the mechanisms underlying the anti-tumour activity of aspirin. We have used this agent extensively as a tool to delineate nucleoli-NFkB signalling pathways. We have then used a combination of animal models, organoid culture and ex vivo treatment of tumour explants to demonstrate that pathways identified in in vitro studies have pharmacological and physiological relevance. Our recent finding that aspirin alters nucleolar function is extremely exciting and reveals new potential biomarkers of aspirin response.

A structure in the cell called the nucleolus is dysfunctional in many common disease, including Alzheimer's, Parkinsons disease and cancer. It is also known to play a role in aging. If the environment of a cell changes, for example if nutrients are decreased or the cell is exposed to toxic agents, nucleoli respond and send signals to other parts of the cell to change the rate of growth/death and many other cellular processes. However, how nucleoli sense changes in the environment, and the signals they send to the other parts of the cell, remain poorly understood. Our research is focussed on understanding the role of nucleoli in stress response and cancer progression. We are particularly interested in a factor in the cell called NF-kB. This factor has an important role in keeping cells healthy and we have shown that it is controlled by nucleoli in stress conditions. Further understanding of how nucleoli and NF-kB signal to each other will allow us to design new therapeutic agents that target the pathways involved.

We are also interested in how aspirin prevents colon cancer and have recently demonstrated that this acts through altering signalling between nucleoli and NF-kB. We are currently determining whether the molecules we have identified in our cell models can be used as biomarkers of aspirin response.  

Undergraduate- Cancer Biology and Medicine [MSBM10019] (2015-present)

MSc- Course coordinator for the Cancer Cell Biology elective of the Biomedical Sciences MScR [BIME11126] 2014-present

IGMM Director of Masters Teaching. 2019-present

Member of the Biomedical Sciences Board of Studies   2018-present