The epigenetic landscape of renal cancer

This is an accepted manuscript of an article published by Nature in Nature Reviews: Nephrology on 28/11/2016, available online: https://doi.org/10.1038/nrneph.2016.168 The accepted version of the publication may differ from the final published version.The majority of kidney cancers are associated with mutations in the von Hippel-Lindau gene and a small proportion are associated with infrequent mutations in other well characterized tumour-suppressor genes. In the past 15 years, efforts to uncover other key genes involved in renal cancer have identified many genes that are dysregulated or silenced via epigenetic mechanisms, mainly through methylation of promoter CpG islands or dysregulation of specific microRNAs. In addition, the advent of next-generation sequencing has led to the identification of several novel genes that are mutated in renal cancer, such as PBRM1, BAP1 and SETD2, which are all involved in histone modification and nucleosome and chromatin remodelling. In this Review, we discuss how altered DNA methylation, microRNA dysregulation and mutations in histone-modifying enzymes disrupt cellular pathways in renal cancers

Client-practitioner interactions within breast care services

United Kingdom (UK) breast care services are delivered within one of two models. Clients presenting with breast symptoms (symptomatic) are assessed within a ‘one stop’ (all done at one hospital attendance) out-patient setting whilst asymptomatic clients currently aged 50–70 (screening) are invited for 3 yearly breast screening by the National Health Service Breast Screening Programme (NHSBSP). A proportion of the latter are recalled for further assessment should a mammographic abnormality be suspected (assessment clients). Many other health care systems around the world also offer these three breast care approaches (symptomatic, screening and assessment services), though the timeframe between screening invitations and the age range of clients varies within the screening services (see Chap. 8)