Bill Farrell

Biography

My early career was spent as a chemical analyst in the petrochemical industry and subsequently followed with studied toward a BSc degree in Biochemistry and Medical Cell Biology at the University of Liverpool (First call Honours). After a period at Astra Zeneca (formerly ICI Diagnostics) as research scientist I went on to complete a PhD in Molecular Biology at the University of Manchester. A lectureship at Liverpool John Moores was then followed by appointment to the University of Keele where most of my academic career and research has been performed. I am Professor of Human Genomics In addition I have completed sabbatical research and extended visits to US institutions that include the Thomas Jefferson, Philadelphia, NIH (Bethesda Washington DC) and Cedars Sinai, Los Angeles. I am also on the editorial boards, as Senior Associate Editor for Endocrine Diabetes and Metabolism Case Reports and Scientific Editor for the journals Endocrine Related Cancer, Neuroendocrinology and Endocrine Pathology.

Research and scholarship

ISTM Research themes: 

1.  
2. Diagnostic Engineering and Proteomics

My PhD training was carried out at the University of Manchester examining the expression and molecular biology of the POMC gene and glucocorticoid receptor regulation. As a PI at the University of Keele my research has focused primarily on the molecular biology of pituitary tumours and more recently on epigenetic changes in bladder tumours and rheumatoid arthritis. In a multi-institution collaboration we have also investigate genome-wide changes to the fetal epigenome and in particular in the context of folic acid supplementation and folate metabolism. Our first study of methylation mediated silencing in pituitary tumours described epigenetic silencing of the CDKN2A gene and numerous other laboratories have since replicated these findings. Many of our published studies are regarded as novel and “first past the post”. While early studies adopted candidate gene approaches more recent studies have employed whole genome analysis. As example, we were the first to employ whole genome amplification to perform a high-density allelotyping of pituitary adenomas and in a subsequent study to employ this new-found knowledge to a retrospective cohort of recurrent pituitary tumours. In 2004 we identified, from the pituitary, a novel pro-apoptotic gene of previous unknown function on the basis of its differential methylation. More recently our laboratory (Dudley et al., 2008), used a siRNA approach to reverse epigenetic change in a murine pituitary cell line model and thereby identify, in an expression array-based (genome-wide) approach, numerous novel silenced genes in these cells and many of these gene were also found to be subject to epigenetic silencing in primary human pituitary tumours. Our laboratory is also the first to described genome-wide DNA BeadArray analysis of each of the major pituitary adenoma subtype (Duong et al., 2012) and to show the effects of the so name epidrugs on gene and pituitary receptor expression (Al-Azzawi et al., Yacqub-Usman et al., 2012a, 2012b, 2013).These findings and reports over the past several years have led to numerous invitations to speak and also to chair symposia both nationally and internationally.

Fetal Epigenetics

A highly productive and rewarding area of research has also been possible through our Fetal Epigenetic Group

Membership of this multidisciplinary group has capitalised on our expertise in epigenetics, and in particular unbiased whole-genome analyses in relation to cancer related and cancer predisposition genes. Our focus, as a group has been centred around nutrition and in particular the role of folic acid and its metabolites on the fetal epigenome. Our success, built on an enthusiastic team approach has resulted in our research attracting funding from several sources including the WCRF. Our publications have generated considerable interest within both the scientific community and the media. We were particularly heartened that a review published by us in the BJOG, (Nafee TM et al, 2008) was the second most frequently cited paper of 2008. More recently, and attracting world-wide attention we identified from more than 27,000 genome-wide site a panel of genes associated with fetal birth weight. In these cases changes were associated with methylation changes (Fryer AA, et al., [2010 and 2011]) Epigenetics.