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Caroline Wilson, Hannah Brown, and Ingunn Holen

Introduction The process of metastatic spread of the primary breast tumour to bone is undoubtedly inefficient, with less than 0.01% of tumour cells released into the circulation able to form bone metastases ( Cameron et al . 2000 ). Multiple

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Kjell Öberg and Steven W J Lamberts

at any age ( Katznelson et al . 2011 ). In most cases, acromegaly is caused by the presence of a benign tumour in the pituitary gland ( Sanno et al . 2003 ), which secretes excess growth hormone (GH) with a concomitant increase in insulin

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R Formosa, A Xuereb-Anastasi, and J Vassallo

Introduction Pituitary tumours represent the most common neoplasms of the brain. Screening of familial cases of pituitary tumours identified germ-line mutations in the aryl hydrocarbon receptor-interacting protein ( Aip ), which occur almost

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H K Gleeson and S M Shalet

afflict brain tumour survivors; in one survey 43% had a self-reported endocrine condition ( Gurney et al. 2003 b ). These may impact negatively on growth, body composition, fertility, quality of life, morbidity and mortality. Hypothalamic–pituitary

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Anna Angelousi, Eva Kassi, Narjes Ansari-Nasiri, Harpal Randeva, Gregory Kaltsas, and George Chrousos

’, ‘circadian rhythms’, ‘adrenal tumours’, ‘thyroid cancer’, ‘pituitary adenomas’, ‘parathyroid adenomas’, ‘ovarian tumours’, ‘testicular tumours’. The above keywords were also combined with the Boolean operators AND and OR. Two of the authors (AA and EK

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Cuong V Duong, Richard D Emes, Frank Wessely, Kiren Yacqub-Usman, Richard N Clayton, and William E Farrell

Introduction The genesis and outgrowth of sporadic pituitary adenomas are, in common with most other tumour types, characterised by inappropriate expression of hormone and growth factor receptors, mediators in their associated signal transduction

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Kreepa G Kooblall, Victoria J Stokes, Omair A Shariq, Katherine A English, Mark Stevenson, John Broxholme, Benjamin Wright, Helen E Lockstone, David Buck, Simona Grozinsky-Glasberg, Christopher J Yates, Rajesh V Thakker, and Kate E Lines

Introduction Multiple endocrine neoplasia type 1 (MEN1) is an autosomal dominant disorder characterised by the combined occurrence of parathyroid tumours and neuroendocrine tumours (NETs) of the pancreas and pituitary. Over 90% of patients

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W Imruetaicharoenchoke, A Fletcher, W Lu, R J Watkins, B Modasia, V L Poole, H R Nieto, R J Thompson, K Boelaert, M L Read, V E Smith, and C J McCabe

may represent new or refined diagnostic, prognostic or therapeutic markers for particular types of cancer, and to more fully understand the mechanisms responsible for tumour formation and progression. We previously characterised PBF (pituitary

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Marie-Lise Jaffrain-Rea, Mariolina Angelini, Donatella Gargano, Maria A Tichomirowa, Adrian F Daly, Jean-François Vanbellinghen, Emanuela D'Innocenzo, Anne Barlier, Felice Giangaspero, Vincenzo Esposito, Luca Ventura, Antonietta Arcella, Marily Theodoropoulou, Luciana A Naves, Carmen Fajardo, Sabina Zacharieva, Vincent Rohmer, Thierry Brue, Alberto Gulino, Giampaolo Cantore, Edoardo Alesse, and Albert Beckers

. 2006 , 2007 , Beckers & Daly 2007 ). Because mutations are likely to be inactivating and associated with tumour loss of heterozygosity (LOH), AIP is viewed as a new pituitary tumour suppressor gene in 11q13 ( Vierimaa et al . 2006 ). Most PA

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Catherine Goudie, Fady Hannah-Shmouni, Mahmure Kavak, Constantine A Stratakis, and William D Foulkes

Hyperinsulinism Wilms tumour, hepatoblastoma, lateralised overgrowth, macrosomia, macroglossia, omphalocele/umbilical hernia, neonatal hypoglycaemia 130650 Carney complex (AD) PRKAR1A , other 17q24.2 PPNAD Thyroid carcinoma Pituitary adenoma