Christian Waeber joined University College Cork (UCC) in 2013; he is Head of Department of Pharmacology and Therapeutics in University College Cork. Early in his career, Dr. Waeber worked as a Ph.D. student at Novartis Basel, where he characterized the pharmacological profile, signaling pathways and brain distribution of 5-HT1D receptors. Dr. Waeber then joined as a post-doctoral fellow the laboratory of Joel Bockaert, at the “Centre CNRS-INSERM de Pharmacologie-Endocrinologie” in Montpellier. In 1993, Dr. Waeber joined Harvard Medical School to characterize the pharmacological profile of 5-HT1-like receptors inhibiting neurogenic inflammation, a research carried out in collaboration with Michael Moskowitz.
Ten years ago, Dr Waeber switched topics, largely abandoning research on 5-HT to focus on the role of sphingosine-1-phosphate (S1P) receptors in blood vessels and brain. These blood vessel studies are significant for the treatment of cerebrovascular disorders (e.g. stroke, vasospasm), and conditions such as diabetes, atherosclerosis, pulmonary hypertension or cancer. Dr. Waeber’s team has also shown that S1P receptors have a widespread distribution both in adult and developing brain. They have characterized the CNS distribution of the S1P synthesizing enzyme, sphingosine kinase (SK), showing that it is up-regulated in neurons following ischemia. Finally, they have shown that stimulating S1P receptors with a pharmacological agent (FTY720/fingolimod) or endogenously-produced S1P (preconditioning) protects the brain from ischemia-induced damage. Finally, Dr. Waeber’s team has shown that administering fingolimod as late as 24 hours after reperfusion in a mouse model promotes long-term stroke recovery. His team has recently published that fingolimod reduces the neurological deficit and infarct volume after in situ thrombo-embolic occlusion of the middle cerebral artery, a model likely to better mimic the features of stroke in humans: combination of fingolimod and tPA improved the neurological outcome of the thrombolytic therapy and reduces the risk of hemorrhagic transformation associated to delayed administration to tPA.

Dr. Barry PhD, MA (H.Ed.) received her bachelor’s degree in Biochemistry from University College Cork, Ireland. She carried out a PhD in Pharmacology at the University of Pennsylvania, USA, investigating novel mechanisms of transcellular lipid metabolism. Subsequent post-doctoral positions in the US involved the study of isoprostanes as indices of oxidant stress. Dr. Barry returned to Ireland as a Health Research Board (HRB) fellow upon the inception of the Cork Cancer Research Centre, University College Cork, Ireland. As a HRB fellow she identified novel mitogenic signalling cascades in esophagogastric micrometastatic cancer. She later joined the Department of Pharmacology and Therapeutics, University College Cork, Ireland as a lecturer where she set up her own research group.

Dr. Barry’s area(s) of interest are how tumour signalling events drive oncogenic progression and how strategic events can be exploited to develop more effective treatment options. Her laboratory focuses on the study of different families of serine/threonine kinases that play key roles in signalling mechanisms following activation of seven-transmembrane and receptor tyrosine-kinases. In particular her group explores the role of Paks, p38 MAPKs, and PKCs which exert a variety of cellular effects including changes in proliferation, malignant transformation, cell death and differentiation. Her research has exploited the activation of p38 MAPK as well as PKC as a pro-apoptotic and anti-proliferative agent in oesophageal cancer. Re-introduction of p38 MAPK into different cancers which lack this isoform including oesophageal, renal, prostate, lung and liver has had profound effects on cancer cell proliferation and apoptosis. An important aspect of her research is to also elucidate the signalling pathways underlying the apoptotic effect of these kinases using both pharmacological and molecular experimental approaches. The identification of different kinase isoforms involved in cell proliferation and cell death in different types of cancer may have important therapeutic implications for the treatment of the disease.

In addition Dr. Barry is also exploring how epigenetic changes to the genome contribute to the progression of cancer. In particular the search for biomarkers like hyper- or hypo-methylated genes in oesophageal cancer in the context of early detection or diagnostic markers, or predicting response to treatment is an area of active research.