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Richard N. Clayton

Researcher at Keele University

Publications -  118
Citations -  8946

Richard N. Clayton is an academic researcher from Keele University. The author has contributed to research in topics: Loss of heterozygosity & Adenoma. The author has an hindex of 52, co-authored 116 publications receiving 8544 citations. Previous affiliations of Richard N. Clayton include Diabetes Australia & University Hospitals of North Midlands NHS Trust.

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Altered composition of high density lipoproteins in women with the polycystic ovary syndrome.

TL;DR: In this article, a detailed exploratory study of HDL composition in 35 obese [body mass index (BMI), > 27] and 22 nonobese subjects with polycystic ovary syndrome (PCOS) was conducted in 14 healthy obese and 18 non-obese women.
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Molecular pathogenesis of pituitary tumors.

TL;DR: In this paper, the authors describe a role for PTTG and cyclin D1 in pituitary tumorigenesis, and show that loss of pRB is evident in a proportion of somatotropinomas but is not associated with allelic loss of an RB1 intragenic marker.
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Preferential loss of Death Associated Protein kinase expression in invasive pituitary tumours is associated with either CpG island methylation or homozygous deletion.

TL;DR: It is shown that loss of the DAP kinase protein and associated genetic aberrations preferentially segregates with tumours that show an invasive phenotype, which is the first report that describes two mutually exclusive mechanisms associated with loss of D AP kinase gene expression.
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Excess Mortality Associated With Hypopituitarism in Adults: A Meta-Analysis of Observational Studies

TL;DR: Mortality benefit from GH replacement in hypopituitarism is less pronounced in women than men and there was a potential selection bias of benefit of GH replacement from a post-marketing data necessitating further evidence from long-term randomized controlled trials.
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Loss of expression of the growth inhibitory gene GADD45gamma, in human pituitary adenomas, is associated with CpG island methylation.

TL;DR: Findings show that silencing of the GADD45γ gene in pituitary tumours is primarily associated with methylation of the genes CpG island, a negative regulator of cell growth, is most likely responsible for conferring a selective growth advantage during tumour evolution and outgrowth.