Dr Benjamin Fairfax
Currently (October 2022) Associate Professor and Principal Investigator at the Department of Oncology, Medical Science Division, University of Oxford, UK.
Clinical Research Fellow
I am supported by a Wellcome for MB PhD postdoctoral Fellowship. I am a clinical trainee in Medical Oncology and a Senior Research Fellow at Worcester College. I studied the molecular interactions and determinants of GABAB receptor activity for my PhD in Steve Moss's laboratory at the MRC-LMCB at UCL.
Cellular specific eQTL
My work focuses upon understanding the genetics of gene expression in subsets of highly purified primary blood cells. It is increasingly apparent that the functional properties of a genetic polymorphism (usually a SNP) depend upon the cell type analysed. Many SNPs have opposing effects on gene expression in different cellular environments and only through interrogation of specific cell subsets can this divergence in the functional properties of polymorphisms be revealed. We aim to characterise the functional consequences of monocyte expression quantitative trait loci with reference to chronic inflammatory states and intrinsic responsiveness to Toll-like receptor (TLR) agonists.
Induced Quantitative Trait Loci - iQTL
In a similar manner to cellular specificity, we propose that SNPs may only demonstrate association with a trait, and hence reveal a functional property, under certain biological conditions. These may be developmental stages or pathological states such as hypoxic stress and infection. To investigate this hypothesis we are currently researching context specific eQTL in primary monocytes - these are expression quantitative traits that are revealed after specific biological stimuli - 'iQTL'.
Genomics guided cancer treatment
Chronic inflammation is a feature of many malignant tumours. Not only does this chronic inflammation act to promote tumourigenesis, but it is intricately linked with dysregulated angiogenesis imperative for tumour survival and the promotion of metastasis. One of the chief driving forces behind this are tumour associated activated macrophages which secrete large amount of cytokines that sustain further immune activation and additionally act as tumour growth factors. Improved understanding of the genetics of inflammation may help shed further light onto these processes. In addition, there are few areas of medicine that stand to benefit more from the 'genomics revolution' than Oncology. I am interested in the application of genetic techniques to improve individual cancer treatment and identify those who will benefit most from specific medications.
Keywords: Inflammation, Cancer, Endotoxin Tolerance, Innate, Immunity, Chromatin