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Dr Hebe Chen is a Postdoctoral Researcher in the Translational Gastroenterology Unit (Nuffield Department of Medicine). She discusses her project and benefits she has drawn from her experience as an Oxford-Celgene Fellow.

Hebe Chen smiling

What is your research background?

I received my PhD in immunology, and my interest in immunology and translational science involving patient work brought me to Professor Holm Uhlig’s lab. I am currently working as a postdoctoral researcher with Professor Holm Uhlig and Dr. Arian Laurence, in the Translational Gastroenterology Unit in Nuffield Department of Medicine.

What are you researching now?

My research currently involves 2 projects, both are related to GP130 and STAT3. The first involves studying GP130-associated Mendelian diseases. We characterise different mutations associated with GP130 and investigate its functional impact on GP130-depdenent cytokine signalling pathways and relate those to clinical phenotypes. The second project aims to investigate signalling downstream of the GP130 and IL-10 cytokine families (IL-6 and IL-10), both of which signal through STAT3, yet have contrasting effects. The goal is to generate novel anti-inflammatory therapies that would target inflammatory responses downstream of the cytokine specifically while preserving the others.

What has your experience of this Fellowship been like?

By receiving an Oxford-Celgene fellowship in July 2018 has allowed me to get a real feel of both academic and industrial environments. My experience with Celgene has been positive, with everyone being supportive and approachable. I enjoy our monthly-bimonthly conference calls with my Celgene mentor Luke Devey and other Celgene team members. For example, Joe and Veer have supported us with their expertise in computational remodelling in relation to how GP130 mutations impact at the structural level. This has allowed us to more comprehensively build on our genotype-phenotype-structure model with our spectrum of patients.

What are your aspirations for the future of this research?

STAT3 is an important molecule, yet there is no clear answer as to why STAT3 is able to generate both pro- and anti-inflammatory responses. I hope my research will answer some of the big questions in the field and contribute towards the basis of more specific therapies for a range of immune-mediated diseases. Additionally, I hope to network many scientists and clinicians from different backgrounds, both academia and industry, who I can learn from and collaborate with into the future.

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