Dying cancer cells are thought to be a rich source of tumour antigens and danger signals into the tumour microenvironment. Work from the Olcina lab has found that targeting complement can increase tumour cell death following radiotherapy which may in turn modulate anti-tumour immune responses. However, how to productively harness these responses to maximise productive inflammation while limiting normal tissue toxicity is still unclear. To uncover these mechanisms, we will explore modes of cell death following complement inhibition.
Our group works in a collaborative and multidisciplinary manner. We are interested in a basic to translational approach to science, so we collaborate with clinicians and use patient samples or clinical data whenever possible. We also have experience working with in a range of model systems ranging from cell lines to in vivo mouse models. Students can also expect to receive training in bioinformatics and cell and molecular biology techniques.
Group Leader - Immune Radiation Biology
- Associate Research Fellow - St Hilda’s College
- Course Director for the MSc in Radiation Biology
Understanding how tumours exploit our first line of immune defence to their advantage
Monica Olcina studied Pharmacy at the University of Manchester. After completing the required training to become a registered pharmacist she moved to Oxford to undertake her Masters and DPhil studies in Radiation Biology. In 2014, she joined Stanford University where she worked as a Cancer Research Institute Irvington Postdoctoral Fellow to identify novel pathways that could be targeted to improve radiotherapy. In 2019 she moved to the University of Zurich to continue these studies. In December 2020 she joined the Department as a Junior Group Leader.
The Olcina group is particularly interested in
1. Understanding the causes and consequences of complement system dysregulation in the tumour microenvironment.
- The complement system is one of our first lines of defence. We have found that components of this system are dysregulated in cancer and such dysregulation is usually associated with poor patient survival outcome. We work to understand how and why this dysregulation occurs.
2. Targeting the innate immune stress response to improve tumour control and reduce normal tissue toxicity to cancer treatments.
- We have found that targeting certain key members of the complement system can improve tumour control following radiation therapy while reducing radiation-induced toxicity in the bowel. We are working to uncover the mechanisms underlying these enticing effects.
Callum Beach - DPhil (joint student with Prof Tim Maughan and Prof Simon Leedham)
Dominika Majorova - Research Assistant
Kelly Lee - MRes Student (joint student with Prof Hammond)
Dr Tatsuya Suwa - Sponsored Researcher - Takeda Medical Foundation, British Council Japan Association Scholarship Scheme
Qingyang Zhang - DPhil Student