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Samuel M O’Toole, David S Watson, Tatiana V Novoselova, Lisa E L Romano, Peter J King, Teisha Y Bradshaw, Clare L Thompson, Martin M Knight, Tyson V Sharp, Michael R Barnes, Umasuthan Srirangalingam, William M Drake, and J Paul Chapple

and somatic mutations have classified PCC/PGL into four molecularly defined groups, including a pseudohypoxia-linked subtype ( Fishbein et al. 2017 ). These pseudohypoxic tumors occur due to mutations that impact regulation of the hypoxia

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Robert C Fowkes and George Vlotides

of pituitary homeostasis and angiogenesis, may help elucidate unknown aspects of pituitary tumorigenesis. Angiogenesis and hypoxia in pituitary tumors Pathological angiogenesis is a key mechanism involved in tumor growth as well as other disorders

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M J Grimshaw

apoptosis: endothelins can protect several cell types – including tumour cells, macrophages and endothelial cells – from apoptosis induced by cellular stresses including hypoxia and serum starvation and v) immune modulation: trafficking, differentiation and

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Yvonne Arvidsson, Anders Bergström, Linda Arvidsson, Erik Kristiansson, Håkan Ahlman, and Ola Nilsson

-random and organ-specific ( Chambers et al . 2002 ). Tumour hypoxia (O 2 deprivation) initiates the metastatic cascade by changing the microenvironment of the tumour, resulting in prolonged tumour cell survival and resistance to chemotherapy. As solid

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N Burrows, J Resch, R L Cowen, R von Wasielewski, C Hoang-Vu, C M West, K J Williams, and G Brabant

carcinomas, changes in the PI3K pathway occur later and are associated with aggressive transition ( Paes & Ringel 2008 ). To date, there has been no comprehensive analysis of the potential role of signalling mediated via hypoxia-induced transcription

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K S Kimbro and J W Simons

Introduction Lethal clones of human cancer have the ability to adapt to hypoxic environments in primary or metastatic sites. Epigenetic and genetic mechanisms of adaptation to hypoxia, such as genetic instability, aerobic glycolysis

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Shalini Patiar and Adrian L Harris

Introduction Hypoxia is a reduction in the normal level of tissue oxygen tension and occurs in many disease processes including cancer. It results in the death of both cancer cells and normal cells if it is severe or prolonged but

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Annika Blank, Anja M Schmitt, Esther Korpershoek, Francien van Nederveen, Thomas Rudolph, Nicole Weber, Räto Thomas Strebel, Ronald de Krijger, Paul Komminoth, and Aurel Perren

neoplasia type 2 (MEN2) and succinate dehydrogenase (SDH) syndromes. The underlying molecular mechanisms leading to PCCs/sympathetic PGLs are not fully understood. Several studies suggest that classic hypoxia signalling involving hypoxia inducible factor-1α

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Rodrigo A Toledo, Yuejuan Qin, Subramanya Srikantan, Nicole Paes Morales, Qun Li, Yilun Deng, Sang-Woo Kim, Maria Adelaide A Pereira, Sergio P A Toledo, Xiaoping Su, Ricardo C T Aguiar, and Patricia L M Dahia

pheochromocytomas have been limited to mutations of some of these susceptibility genes ( Burnichon et al . 2011 ). A majority of hereditary pheochromocytomas and paragangliomas are related to the hypoxia pathway through mutations of the VHL gene or those encoding

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Ales Vicha, David Taieb, and Karel Pacak

dehydrogenase 1 ( IDH1 ; Gaal et al . 2010 ), and most recently hypoxia-inducible transcription factor 2α ( HIF2A ; Zhuang et al . 2012 , Toledo et al . 2013 ), fumarate hydratase ( FH ; Castro-Vega et al . 2013 ), and H-RAS protein ( H-RAS ; Crona et