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Maria Santa Rocca, Andrea Di Nisio, Arianna Marchiori, Marco Ghezzi, Giuseppe Opocher, Carlo Foresta, and Alberto Ferlin

to the oncogenesis of TGCT ( Stadler et al. 2012 , Edsgärd et al. 2013 ). E2F1 (UniprotKB: Q01094) is a member of the E2F family, acting as a transcription factor with high binding affinity for the retinoblastoma tumor suppressor (RB) protein

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Takako Araki, Ning-Ai Liu, Yukiko Tone, Daniel Cuevas-Ramos, Roy Heltsley, Masahide Tone, and Shlomo Melmed

differs from pituitary regulation and report an E2F1-mediated mechanism for hPOMC transcription. We also show that E2F1 antagonists markedly suppress hPOMC expression and paraneoplastic ACTH secretion in human-derived tumor primary cultures. Our

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Michael Wagner, Melinda Wuest, Ana Lopez-Campistrous, Darryl Glubrecht, Jennifer Dufour, Hans-Soenke Jans, Frank Wuest, and Todd P W McMullen

-inducible factor 1α (HIF-1α) following downstream targets GLUT1 and hexokinase-2, similar to what we observed in our xenografts ( Parmenter et al. 2014 ). Inhibition of BRAF V600E strongly reduces tumour size and uptake of glucose derivative [ 18 F]FDG, while

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Dario Palmieri, Teresa Valentino, Ivana De Martino, Francesco Esposito, Paolo Cappabianca, Anne Wierinckx, Michela Vitiello, Gaetano Lombardi, Annamaria Colao, Jacqueline Trouillas, Giovanna Maria Pierantoni, Alfredo Fusco, and Monica Fedele

HMGA2 ( Fedele et al . 2002 , 2005 ). Our previous studies demonstrated that HMGA2 induces pituitary tumour development by enhancing E2F1 activity ( Fedele et al . 2006 ). Indeed, following the interaction with the retinoblastoma protein pRB, HMGA2

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Ann M Dorward, Kathryn L Shultz, and Wesley G Beamer

utilized our highest spontaneous frequency colony, represented by (SWR × SWXJ-9) F1 females with a population GC tumor frequency of ~25%, as a model to test two experimental strategies to mimic the chemopreventive activity of continuous E 2 . First, we

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Alexander Gorshtein, Hadara Rubinfeld, Efrat Kendler, Marily Theodoropoulou, Vesna Cerovac, Günter K Stalla, Zvi R Cohen, Moshe Hadani, and Ilan Shimon

triggered by the activation of cyclin-dependent kinase (cdk) 4 and 6, by the D-type cyclins (cyclin D1–3) ( Sherr & Roberts 1995 ). Activated cdk4 and 6 phosphorylate retinoblastoma (Rb), which becomes inactivated and releases E2F factors ( Weinberg 1995

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Laura C Hernández-Ramírez, Ryhem Gam, Nuria Valdés, Maya B Lodish, Nathan Pankratz, Aurelio Balsalobre, Yves Gauthier, Fabio R Faucz, Giampaolo Trivellin, Prashant Chittiboina, John Lane, Denise M Kay, Aggeliki Dimopoulos, Stephan Gaillard, Mario Neou, Jérôme Bertherat, Guillaume Assié, Chiara Villa, James L Mills, Jacques Drouin, and Constantine A Stratakis

WT, pLNCX2-3xFlag-ER tam -Cables1 p.E178K, pLNCX2-3xFlag-ER tam -Cables1 p.L240F, pLNCX2-3xFlag-ER tam -Cables1 p.G312D, pLNCX2-Flag-ER tam -Cables1 p.D463G or pLNCX2-3xFlag-ER tam empty vector as control. Cables1 protein levels were assessed by

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David A Pattison and Rodney J Hicks

 Non-islet cell tumour Many of these conditions are diagnosed biochemically in the appropriate clinical context (e.g. abnormal IGF-2:IGF-1 ratio, cortisol deficiency or hyperinsulinaemic hypoglycaemia with undetectable C-peptide suggesting

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Petteri Ahtiainen, Victoria Sharp, Susana B Rulli, Adolfo Rivero-Müller, Veronika Mamaeva, Matias Röyttä, and Ilpo Huhtaniemi

( Poel 1966 , Lamberts et al . 1985 ). Recent studies have elucidated the molecular pathogenesis of pituitary adenomas. Increased activation of the cyclin D1 (CCND1)/cyclin-dependent kinase 4 (CDK4)/retinoblastoma protein (RB)/transcription factor E2F1

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Ivana De Martino, Rosa Visone, Dario Palmieri, Paolo Cappabianca, Paolo Chieffi, Floriana Forzati, Antonio Barbieri, Mogens Kruhoffer, Gaetano Lombardi, Alfredo Fusco, and Monica Fedele

HMGA2 in this human neoplasia ( Finelli et al. 2002 ). The mechanism by which HMGA2 is involved in pituitary tumorigenesis is on the ability of the HMGA2 to interfere with the pRB/E2F1 pathway. In fact, we have recently shown that HMGA2 interacts with