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Jenny Welander, Adam Andreasson, Michael Brauckhoff, Martin Bäckdahl, Catharina Larsson, Oliver Gimm, and Peter Söderkvist

two groups: VHL - and SDHx -mutated tumors form one cluster (Cluster 1) with a hypoxia-related transcription signature, whereas RET / NF1 / TMEM127 / MAX -mutated tumors form another cluster (Cluster 2) and display transcription profiles

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Roland Därr, Joan Nambuba, Jaydira Del Rivero, Ingo Janssen, Maria Merino, Milena Todorovic, Bela Balint, Ivana Jochmanova, Josef T Prchal, Ronald M Lechan, Arthur S Tischler, Vera Popovic, Dragana Miljic, Karen T Adams, F Ryan Prall, Alexander Ling, Meredith R Golomb, Michael Ferguson, Naris Nilubol, Clara C Chen, Emily Chew, David Taïeb, Constantine A Stratakis, Tito Fojo, Chunzhang Yang, Electron Kebebew, Zhengping Zhuang, and Karel Pacak

affecting hypoxia-signaling pathways because many of the associated tumors express a so-called ‘pseudohypoxic signature’ and most of them converge on the hypoxia-signaling pathway ( Jochmanova et al . 2013 ). Germline mutations in the von Hippel

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Stefan J Barfeld, Harri M Itkonen, Alfonso Urbanucci, and Ian G Mills

, including c-Myc, which is overexpressed and predictive of poor prognosis in a subset of cases ( Hawksworth et al . 2010 ). Other examples include hypoxia-inducible factor 1α (HIF1A), which is associated with PCa metastasis ( Ranasinghe et al . 2013 ). In

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Kathrin A Schmohl, Peter J Nelson, and Christine Spitzweg

. 2011 , Bronckaers et al. 2014 ). In response to specific stimuli, including hypoxia and inflammation, the angiogenic switch occurs in the quiescent endothelium, initiating coordinated endothelial cell proliferation, invasion, migration and ultimately

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J Riedemann and V M Macaulay

human prostate cancer cells that express low levels of IGF1R and lack IRS-1 ( Reiss et al. 2000 , Valentinis et al. 2000 ). IGF1R activation protects cells from a variety of apoptosis-inducing agents, including osmotic stress, hypoxia and

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Dermot O'Toole, Anne Couvelard, Vinciane Rebours, Magali Zappa, Olivia Hentic, Pascal Hammel, Philippe Levy, Pierre Bedossa, Eric Raymond, and Philippe Ruszniewski

disease progression and survival in patients with melanoma ( Dhawan et al . 2002 ). Chemotherapy-induced Akt has been found to confer acquired resistance in many cellular systems ( Huang & Hung 2009 ). Hypoxia-regulating proteins have also been implicated

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S W Lowe

p53 is activated by a variety of cellular stresses, including DNA damage, hypoxia, and mitogenic oncogenes, but the extent to which each signal engages p53 as a tumour suppressor remains unknown. In non-immortal cells, the adenovirus E1A oncogene activates p53 to promote apoptosis, whereas oncogenic ras activates p53 to promote cellular senescence. Inactivation of p53 prevents E1A-induced apoptosis or Ras-induced senescence, allowing proliferation to continue unabated. In each instance, the ability of the oncogene to activate p53 involves the same functions as are required for their transforming potential, implying that p53 activation acts as a fail-safe mechanism to counter hyperproliferative signals. Furthermore, p19(ARF) is strictly required for oncogene signalling to p53. The fact that ARF--itself a tumour suppressor--acts as an intermediary in this response argues that the tumour suppressor activity of p53 can arise from its ability to eliminate oncogene-expressing cells.

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Daniele Generali, Stephen B Fox, Alfredo Berruti, Maria P Brizzi, Leticia Campo, Simone Bonardi, Simon M Wigfield, Paolo Bruzzi, Alessandra Bersiga, Giovanni Allevi, Manuela Milani, Sergio Aguggini, Luigi Dogliotti, Alberto Bottini, and Adrian L Harris

Introduction Hypoxia is a common feature in solid tumors. It is a pathophysiologic consequence of a structurally and functionally disturbed microcirculation and the deterioration of oxygen diffusion conditions ( Hockel & Vaupel 2001

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Trisha Dwight, Edward Kim, Karine Bastard, Diana E Benn, Graeme Eisenhofer, Susan Richter, Massimo Mannelli, Elena Rapizzi, Aleksander Prejbisz, Mariola Pęczkowska, Karel Pacak, and Roderick Clifton-Bligh

Introduction Cells sense and respond to low oxygen conditions in large part via hypoxia-inducible factor (HIF)-mediated transcription ( Kaelin et al. 2016 ). In normoxia, HIF-α is hydroxylated by oxygen-dependent prolyl hydroxylases (PHDs

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Eamonn R Maher

The heterodimeric HIF transcription factors regulate cellular responses to hypoxia. Each heterodimer consists of a specific α-subunit (HIF1α, HIF2α and HIF3α) which, in hypoxic conditions, complexes with the HIFβ (ARNT) subunit ( Kaelin & Ratcliffe