Current Area of Interest

Chronic inflammation has long been understood to be a hallmark of cancer development. In the last decade some of the underlying mechanisms linking inflammation and cancer have begun to be unravelled, however, many of the processes are still poorly understood. Glycosylation is an enzymatic process whereby saccarides are added to proteins, lipids or other organic molecules, often giving rise to quite large and complex structures. The glycosylation of proteins is crucial for their correct folding but can also alter their function and stability.

As a Cancer Research Ireland (CRI) funded postdoctoral scientist in Prof Pauline Rudd’s lab, my main focus is to investigate how altered glycosylation of acute phase proteins (APPs) may play a role in breast cancer development. Acute phase proteins are mainly produced in the liver and their levels tend to increase in response to proinflammatory cytokines such as interleukin (IL) 6 and IL 1β. The work of Prof Rudd’s group to date has clearly demonstrated altered glycosylation patterns of APPs in many cancer types including breast cancer.

My current research is focused on 2 main areas: firstly, understanding the changes that occur in the liver which give rise to the altered glycosylation of APP. This includes understanding the signal transduction pathways that control the expression or activity of glycosyltransferase enzymes in the liver. Secondly, to try and understand if these secreted APPs, which contain increased sialyl lewis X structures, have any role in altering the phenotype of breast cancer cells by inducing pro-migratory, angiogenic or proliferative pathways. This research is enhancing our understanding of how inflammatory environments can augment glycan profiles on APPs and the role they play in enhancing cancer development.

Before joining Prof Rudd’s lab I worked as a senior postdoctoral fellow in the Dept of Clinical Medicine at Trinity College Dublin (2006-2010). The primary focus of my research there was investigating gene regulation events that occur in T cells after they begin to migrate when they bind to ICAM-1 through the integrin LFA-1. The aim of this research was to gain a better understanding of the molecular events that occur in a T cell as it extravasates from the blood vessel into the underlying tissue.

For my PhD thesis I worked on the expression of a T cell costimulation receptor, TNFSF14, in Coeliac disease (CD). During this research I demonstrated that CD patients with active disease had higher expression levels of TNFSF14 in circulating lymphocytes as well as increased levels of a soluble form of TNFSF14 in their serum. When we investigated changes in the small intestine, the primary site of inflammation in CD, I was also able to demonstrate increased levels of TNFSF14 during active disease. The consequence for people with CD is that TNFSF14 signalling can increase the expression of proinflammatory cytokines and thereby exacerbate the inflammation in their small intestine which gives rise to many of the clinical symptoms of the disease.

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