Introduction Pituitary tumours represent approximately 10–15% of intracranial tumours. Most of them are non-invasive, showing slow growth and remaining within the sella and/or displacing the surrounding tissues; however, up to 25–55% of
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Dorota Dworakowska and Ashley B Grossman
G Carreno, J K R Boult, J Apps, J M Gonzalez-Meljem, S Haston, R Guiho, C Stache, L S Danielson, A Koers, L M Smith, A Virasami, L Panousopoulos, M Buchfelder, T S Jacques, L Chesler, S P Robinson, and J P Martinez-Barbera
formation of tumours resembling human ACP ( Gaston-Massuet et al. 2011 , Andoniadou et al. 2013 ). In both models, tumoural pituitaries show the presence of β-catenin-accumulating cells forming clusters, which share a common molecular signature with
W E Farrell
Pathogenesis of pituitary tumours Pituitary adenomas Pituitary adenomas are common intracranial neoplasms, comprising 10–15% of diagnosed brain tumours ( Kovacs & Hovarth 1987 ). Tumours may arise from any of the
Pedro Marques, Sayka Barry, Eivind Carlsen, David Collier, Amy Ronaldson, Sherine Awad, Neil Dorward, Joan Grieve, Nigel Mendoza, Samiul Muquit, Ashley B Grossman, Frances Balkwill, and Márta Korbonits
Introduction The great majority of pituitary neuroendocrine tumours (PitNETs) are benign, although they can cause significant burden to patients due to mass effects, invasion and/or due to excessive or low hormone secretion ( Di Ieva et al
M Muşat, M Korbonits, B Kola, N Borboli, M R Hanson, A M Nanzer, J Grigson, S Jordan, D G Morris, M Gueorguiev, M Coculescu, S Basuand, and A B Grossman
Introduction Pituitary tumours account for 10–15% of all intracranial neoplasms. Despite extensive research, the pathogenesis of the majority of pituitary adenomas remains to be clarified. Deregulation of various cell-cycle pathways
Gregory A Kaltsas, Jane Evanson, Alexandra Chrisoulidou, and Ashley B Grossman
extending to the parasellar region ( Freda & Post 1999 ). However, in ∼9% of cases, an aetiology other than a pituitary adenoma is encountered, parasellar tumours being the second commonest cause after non-tumorous cystic lesions ( Freda et al . 1996 ). The
Paraskevi Xekouki, Emily J Lodge, Jakob Matschke, Alice Santambrogio, John R Apps, Ariane Sharif, Thomas S Jacques, Simon Aylwin, Vincent Prevot, Ran Li, Jörg Flitsch, Stefan R Bornstein, Marily Theodoropoulou, and Cynthia L Andoniadou
, clear cell renal cell carcinoma (ccRCC), pancreatic carcinoma, oesophageal squamous cell carcinoma, urothelial carcinoma of the bladder and skin basal cell carcinoma ( Zanconato et al. 2016 ). Pituitary tumours account for 10–15% of intracranial
B Shan, J Gerez, M Haedo, M Fuertes, M Theodoropoulou, M Buchfelder, M Losa, G K Stalla, E Arzt, and U Renner
Introduction RSUME is a small RWD-domain containing protein that was recently cloned from lactosomatotroph GH3 rat pituitary tumour cells overexpressing the cytokine signal transducing protein gp130 ( Carbia-Nagashima et al . 2007 ). These cells
Ben C Whitelaw
How and when to use temozolomide to treat aggressive pituitary tumours Temozolomide is an oral chemotherapy which has an established role in treating glioblastoma multiforme (GBM) and has since 2006 been used to treat aggressive and malignant
Antônio Ribeiro-Oliveira Jr, Giulia Franchi, Blerina Kola, Paolo Dalino, Sérgio Veloso Brant Pinheiro, Nabila Salahuddin, Madalina Musat, Miklós I Góth, Sándor Czirják, Zoltán Hanzély, Deivid Augusto da Silva, Eduardo Paulino Jr, Ashley B Grossman, and Márta Korbonits
Introduction Pituitary tumours are very common neoplasms, with a reported prevalence of 17% in the general population, and they constitute 10% of intracranial neoplasms ( Asa & Ezzat 2002 , Ezzat et al . 2004 ). Although these tumours cause
