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1

Chiarotto, James Anthony. Hypoxia-induced upregulation of VEGF mRNA in cervical cancer cell lines. Ottawa: National Library of Canada, 1998.

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2

Low, Eddy Wai-Mang. Reactions toward the synthesis of minor-groove binding hypoxic cell sensitizers. Ottawa: National Library of Canada = Bibliothèque nationale du Canada, 1993.

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3

Cheng, Phillip Ming-Da. Relationship between modulation of Glomus Cell K+ current and hypoxia transduction in the rat carotid body. [New Haven, Conn: s.n.], 1997.

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4

1947-, Haddad Gabriel G., and Lister George 1947-, eds. Tissue oxygen deprivation: From molecular to integrated function. New York: M. Dekker, 1996.

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5

Jean-Marc, Pequignot, ed. Chemoreception: From cellular signaling to functional plasticity. New York: Kluwer Academic/Plenum Publishers, 2003.

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6

Cancer: Between glycolysis and physical constraint. Berlin: Springer, 2004.

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7

Koumenis, Constantinos, Amato Giaccia, and Ester Hammond. Tumor Microenvironment and Cellular Stress: Signaling, Metabolism, Imaging, and Therapeutic Targets. Springer, 2016.

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8

Koumenis, Constantinos, Amato Giaccia, and Ester Hammond. Tumor Microenvironment and Cellular Stress: Signaling, Metabolism, Imaging, and Therapeutic Targets. Springer London, Limited, 2013.

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9

Koumenis, Constantinos, Amato Giaccia, and Ester Hammond. Tumor Microenvironment and Cellular Stress: Signaling, Metabolism, Imaging, and Therapeutic Targets. Springer, 2013.

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10

Pastorekova, Silvia, and Juraj Kopacek. Tumour Hypoxia: Molecular Mechanisms and Clinical Implications. Lang GmbH, Internationaler Verlag der Wissenschaften, Peter, 2012.

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11

Cowan, David Stuart Mason. DNA targeted hypoxic cell radiosensitizers and cytotoxins. 1995.

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12

Melillo, Giovanni. Hypoxia and Cancer: Biological Implications and Therapeutic Opportunities. Springer London, Limited, 2013.

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13

Melillo, Giovanni. Hypoxia and Cancer: Biological Implications and Therapeutic Opportunities. Humana, 2016.

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14

Melillo, Giovanni. Hypoxia and Cancer: Biological Implications and Therapeutic Opportunities. Springer-Verlag New York Inc., 2013.

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15

Mechanisms by which hypoxia augments Leydig cell viability and differentiated cell function in vitro. Blacksburg, VA: Virginia Polytechnic Institute and State University, 1993.

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16

Sukhamay, Lahiri, Cherniack Neil S, Fitzgerald Robert S. 1931-, American Physiological Society (1887- ), and Federation of American Societies for Experimental Biology., eds. Response and adaptation to hypoxia: Organ to organelle. New York: Published for the American Physiological Society by Oxford University Press, 1991.

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17

Fitzgerald, Robert S., Neil S. Cherniak, and Sukhamay Lahiri. Response and Adaptation to Hypoxia: Organ to Organelle. Springer, 2013.

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18

(Editor), Sukhamay Lahiri, Gregg Semenza (Editor), and Nanduri R. Prabhakar (Editor), eds. Oxygen Sensing: Responses and Adaptation to Hypoxia (Lung Biology in Health and Disease). Informa Healthcare, 2003.

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19

Soleymanlou, Nima. Human trophoblast cell death in pathological and physiological models of hypoxia. 2006.

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20

(Editor), Sukhamay Lahiri, Neil S. Cherniak (Editor), and Robert S. Fitzgerald (Editor), eds. Response and Adaptation to Hypoxia: Organ to Organelle (Clinical Physiology Series). An American Physiological Society Book, 1991.

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21

Matejovic, Jan Francis. Structure-activity relationships of DNA-targeted hypoxic cell radiosensitizers and cytotoxins. 1995.

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22

Jamie, Goode, Chadwick Derek, Novartis Foundation, and Symposium on the Tumour Microenvironment: Causes and Consequences of Hypoxia and Acidity (2000 : London, England), eds. The tumour microenvironment: Causes and consequences of hypoxia and acidity. Chichester: Wiley, 2001.

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23

Fish, Jason Edward. Chromatin-based mechanisms control the cell-specific and hypoxia-regulated expression of endothelial nitric oxide synthase. 2006.

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24

(Editor), Jean-Marc Pequignot, Constancio Gonzalez (Editor), Colin A. Nurse (Editor), Nanduri R. Prabhakar (Editor), and Yvette Dalmaz (Editor), eds. Chemoreception: From Cellular Signalling to Functional Plasticity (Advances in Experimental Medicine and Biology). Springer, 2003.

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25

The Tumour Microenvironment - No. 240: Causes and Consequences of Hypoxia and Acidity (Novartis Foundation Symposia). Wiley, 2001.

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26

The Arterial Chemoreceptors. Springer, 2006.

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27

(Editor), Yoshiaki Hayashida, Constancio Gonzalez (Editor), and Hisatake Kondo (Editor), eds. The Arterial Chemoreceptors (Advances in Experimental Medicine and Biology). Springer, 2006.

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28

Said, Harun M., Adrian Staab, and Carsten Hagemann. Brain-Cancer Associated Tumor Marker Genes Expression Pattern in Humans. Nova Science Publishers, Incorporated, 2011.

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29

Macdougall, Iain C. Erythropoiesis-stimulating agents in chronic kidney disease. Edited by David J. Goldsmith. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0124.

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Abstract:
The advent of recombinant human erythropoietin (epoetin) in the late 1980s transformed the management of renal anaemia, liberating many dialysis patients from lifelong regular blood transfusions, in turn causing severe iron overload and human leucocyte antigen sensitization. Epoetin can be administered either intravenously or subcutaneously, but the half-life of the drug is fairly short at around 6–8 hours, necessitating frequent injections. To circumvent this problem, two manipulations to the erythropoietin molecule were engineered. The first of these was to attach an extra two carbohydrate chains to the therapeutic protein hormone (to make darbepoetin alfa), and the second was to attach a large pegylation chain to make continuous erythropoietin receptor activator. Both of these strategies prolonged the circulating half-life of the erythropoietin analogue. The next erythropoietic agent to be produced was peginesatide, a peptide-based agent which had no structural homology with native or recombinant erythropoietin, but shared the same biological and functional characteristics. Future strategies include stabilization of hypoxia-inducible factor, by orally active inhibitors of the prolyl hydroxylase enzyme, and advanced clinical trials are underway. In the meantime, several large randomized controlled trials have highlighted the potential harm in targeting a near normal haemoglobin of 13–14 g/dL (with an increased risk of cardiovascular complications), and sub-normal correction of anaemia is now advised. Some patients may show mild or severe resistance to erythropoiesis-stimulating agent (ESA) therapy, and common causes include iron insufficiency, infection, and underlying inflammation. Very rarely, patients may produce antibodies against their ESA, which neutralize not only the ESA, but also endogenous erythropoietin, causing pure red cell aplasia.
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