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K Dudley, ISTM, University of Keele, Stoke-on-Trent, United Kingdom
K Revill, ISTM, University of Keele, Stoke-on-Trent, United Kingdom
R Clayton, Dept of Medicine, University of Keele, North Staffordshire Hospital Centre, stoke, United Kingdom
W Farrell, Medical research unit, Keele University, Stoke-on-Trent, ST4 7QB, United Kingdom

Correspondence: William Farrell, Email: w.e.farrell{at}keele.ac.uk

Abstract

Investigation of the epigenome of sporadic pituitary tumours is providing a more detailed understanding of aberrations that characterise this tumour type. Early studies, in this and other tumour types adopted candidate-gene approaches to characterise CpG island methylation as a mechanism responsible for or associated-with gene silencing. However, more recently, investigators have adopted approaches that do not require <i>a priori</i> knowledge of the gene and or transcript, as example differential display techniques, and also genome-wide, array based approaches, to <i>uncover</i> or <i>unmask</i> silenced genes. Furthermore, through use of chromatin immunoprecipitation (ChIP) as a selective enrichment techniques, we are now beginning to identify modifications that target the underlying histones themselves and that have roles in gene silencing events. Collectively, these studies provided convincing evidence that change to the tumour epigenome are not simply epiphenomena but have functional consequences in the context of pituitary tumour evolution. Our ability to perform these types of studies has been and is increasingly reliant upon technological advances in the genomics and epigenomics arena. In this context, other more recent advances and developing technologies, and in particular, next generation or flow cell re-sequencing techniques offer exciting opportunities for our future studies of this tumour type.