1. Cancer Epigenetics
My primary research interests lie within the field of cancer epigenetics.
Much of my recent work has focussed on epigenetic changes in chronic lymphocytic leukaemia (CLL). My work has examined how the epigenome alters during the progression of the disease and in response to chemotherapy, and how this can impact upon patient outcomes.
I have a keen interest in retrotransposons; mobile elements within the genome that too often are ignored in cancer research. I have demonstrated stark loss of DNA methylation at LINE_1 and Alu elements that is associated with their evolutionary origins (Barrow et al, Haematologica, in press).
Strong hypomethylation of Alu elements
Correlation of Alu methylation with IGVH status
Hypomethylation strongest among younger (AluJ) elements
Locus-specific changes highly unique to CLL
My research has also examined epigenetic changes in solid tumours. My early postdoctoral work at Brigham and Women's Hospital (Boston, USA) focussed upon epigenetic variation at imprinted loci in breast cancer (Barrow et al, Int J Cancer 137(3): 537-47).
My work at Universitätsklinikum Freiburg (Germany), in collaboration with others at the DKFZ (Heidelberg, Germany) examined smoking-associated epigenetic changes in colorectal tumours. We identified hypermethylation of the APC tumour-suppressor gene as a frequent event in the tumours of patients who were active smokers at the time of diagnosis (Barrow et al, J Pathol 243(3): 366-75).
Hypermethylation of multiple loci mapping to the APC promoter 1A in the tumours of active smokers
APC promoter hypermethylation is frequent in tumours from active smokers
APC promoter hypermethylation never observed in adjacent mucosa
2. Environmental Epigenetics
I also have a research interest in epigenetic changes in response to environmental exposures, especially with regard to how these are implicated in carcinogenesis. My collaborative work has included examining the impact of morphine exposure upon nuclear and mitochondrial DNA methylation in different regions the rat brain (Barrow et al, Epigenetics 12(12): 1038-47) and demonstrating, for the first time, that exposure to carcinogenic compounds and endocrine disruptors can modify m6A RNA methylation (Cayir et al, Environ Res 175: 228-34).
Hypomethylation of COMT in the pons in response to acute and chronic morphine exposure
Reduction in m6A RNA methylation with increasing exposure to PM2.5