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Journal of Molecular Endocrinology (2009) 42 461-468    DOI: 10.1677/JME-09-0009
© 2009 Society for Endocrinology

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Review

Pituitary tumours: all silent on the epigenetics front

K J Dudley, K Revill, R N Clayton and W E Farrell

Human Disease and Genomics Group, School of Medicine, Institute of Science and Technology in Medicine, Keele University, Stoke on Trent, Staffordshire ST4 7QB, UK

(Correspondence should be addressed to W E Farrell; Email: w.e.farrell{at}keele.ac.uk)

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 a priori knowledge of the gene and transcript, as example differential display techniques, and also genome-wide, array-based approaches, to ‘uncover’ or ‘unmask’ silenced genes. Furthermore, through use of chromatin immunoprecipitation as a selective enrichment technique; 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.







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