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Books on the topic 'Vascular endothelial growth factor'

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Published: 4 June 2021
Last updated: 20 February 2023

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1

Woods, Stacy Ann. Signalling pathways regulating expression of vascular endothelial growth factor in human malignant astrocytomas. Ottawa: National Library of Canada, 2001.

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2

Perlmutter, Robin Alexandra. Differential effects of platelet-derived growth factor isoforms on large and small vessel endothelial cells and vascular smooth muscle cells. [s.l: s.n.], 1992.

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3

Liu, Bo. A study of the biological functions of vascular endothelial growth factor in tumour development. Birmingham: University of Birmingham, 1997.

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4

Dunk, Caroline Elizabeth. The role of the vascular endothelial growth factor family in trophoblast and endothelial cell function: Relating to placental development. Birmingham: University of Birmingham, 1999.

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5

International Workshop "Novel Angiogenic Mechanisms" (2002 Columbus, Ohio). Novel angiogenic mechanisms: Role of circulating progenitor endothelial cells. New York: Kluwer Academic/Plenum, 2003.

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6

I, Moldovan Nicanor, ed. Novel angiogenic mechanisms: Role of circulating progenitor endothelial cells. New York: Kluwer Academic/Plenum, 2003.

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7

Bayko, Liisa Ann. The contribution of vascular endothelial growth factor induced angiogenesis to the progression of primary human melanoma. Ottawa: National Library of Canada = Bibliothèque nationale du Canada, 1999.

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8

service), ScienceDirect (Online, ed. Tissue-specific vascular endothelial signals and vector targeting. Amsterdam: Elsevier, 2009.

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9

Sisi, Paraskevi. Investigation of the role of vascular endothelial growth factor in the process of cervical ripening during parturition. Birmingham: University of Birmingham, 1997.

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10

Fuchs, Johanna. Photodynamische - und anti - VEGF-Therapie als Kombinationstherapie bei der exsudativen altersabhängigen Makuladegeneration. Regensburg: Universitätsbibliothek Regensburg, 2017.

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11

Veillette, Christian J. H. Role of endothelin-1 in regulation of osteoblast differentiation and vascular endothelial growth factor-A in cell populations from fetal rat calvaria. Ottawa: National Library of Canada, 2002.

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12

Bandello, F. Anti-VEGF. Basel: Karger, 2010.

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13

Anti-VEGF. Basel: Karger, 2010.

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14

Harmey, Judith H. VEGF and cancer. Georgetown, Tex: Landes Bioscience/Eurekah.com, 2004.

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15

Modeling tumor vasculature: Molecular, cellular, and tissue level aspects and implications. New York: Springer, 2012.

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16

Kelleher, Siobhan. Signal transduction by endothelial cells: Investigation of early effects. Dublin: University College Dublin, 1998.

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17

Sutton, Andrew Bryan. The response of endothelial cells and pericytes to transforming growth factor beta. Manchester: University of Manchester, 1993.

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18

Wang, David I. Kuo. The effects of fibroblast growth factor 2 on the early stages on in vitro endothelial wound repair. Ottawa: National Library of Canada, 1998.

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19

Arciniegas, Enrique A. The phenotype of vascular cells in culture: Regulation by transforming growth factor Beta-1. Manchester: University of Manchester, 1995.

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20

Brozowski, Christine E. Effect of transforming growth factor-β1: Fibronectin and plasminogen activator inhibitor on migration of bovine aortic endothelial cells. [New Haven, Conn: s.n.], 1996.

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21

International Symposium on Biotechnology of Growth Factors: Vascular and Nervous Systems (1991 Milan, Italy). Growth factors of the vascular and nervous systems: Functional characterization and biotechnology. Edited by Albertini Alberto, Lenfant Claude, and Paoletti Rodolfo. Basel: Karger, 1992.

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22

Huang, Kui. Vascular Endothelial Growth Factor Receptors in Angiogenesis. Uppsala Universitet, 2001.

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23

Parker, Marcellus L. Vascular Endothelial Growth Factor: Biology, Regulation and Clinical Significance. Nova Science Publishers, Incorporated, 2013.

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24

Claesson-Welsh, Lena. Vascular Growth Factors and Angiogenesis (Current Topics in Microbiology and Immunology). Springer-Verlag Telos, 1998.

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25

Ruhrberg, Christiana. VEGF in Development. Springer, 2009.

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26

Ruhrberg, Christiana. VEGF in Development. Springer London, Limited, 2008.

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27

Christiana, Ruhrberg, ed. VEGF in development. Austin, Tex: Landes Bioscience/Eurekah.com, 2008.

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28

Rubanyi, Gabor M., and Werner Risau. Morphogenesis of Endothelium (Endothelial Cell Research Series). CRC, 2000.

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29

Michael, Simons, and Rubanyi Gabor M. 1947-, eds. Modern concepts in angiogenesis. London: Imperial College Press, 2007.

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30

Rubanyi, Gabor M., and Michael Simons. Modern Concepts in Angiogenesis. Imperial College Press, 2007.

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31

(Editor), Michael Simons, and Gabor M. Rubanyi (Editor), eds. Modern Concepts in Angiogenesis. Imperial College Press, 2007.

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32

C, Weber Peter, and Leaf Alexander 1920-, eds. Atherosclerosis: Cellular interactions, growth factors, and lipids. New York: Raven Press, 1993.

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33

Weber, Peter C. Atherosclerosis: Cellular Interactions, Growth Factors, and Lipids (Atherosclerosis Reviews). Raven Pr, 1993.

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34

Remesal, Ana. Effects of Oxidative Stress and Antenatal Corticosteroids on the Pulmonary Expression of Vascular Endothelial Growth Factor (VEGF) and Alveolarization. INTECH Open Access Publisher, 2012.

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35

Maes, Christa. Angiogenesis & Bone: The Role Of The Vascular Endothelial Growth Factor Family In Bone Development And Repair (Acta Biomedica Lovaniensia). Leuven Univ Pr, 2004.

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36

Beverungen, Mirjam. Überprüfung der Wirkung von gefäßinduzierenden Wachstumsfaktoren (VEGF=Vascular Endothelial Growth Factor) auf die Vaskularisierung und Osteogenese in festen Knochenersatzstoffen. 2010.

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37

Weber, Peter C. Atherosclerosis: Its Pathogenesis and the Role of Cholesterol (Atherosclerosis Reviews). Raven Pr, 1991.

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38

Processing Of Vegfc And Vegfd By The Pcs And Tumorigenesis. Biota Publishing, 2013.

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39

H, Harmey Judith, ed. VEGF and cancer. Georgetown, Tex: Landes Bioscience/Eurekah.com ; New York, N.Y. : Kluwer Academic/Plenum Publishers, 2004.

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40

Harmey, Judith H. VEGF and Cancer. Springer, 2012.

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41

Harmey, Judith H. VEGF and Cancer. Springer, 2004.

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42

Cimpean, Anca Maria, Andreea Adriana Jitariu, and Marius Raica. Growth Factors and Their Corresponding Receptors as Targets for Ovarian Cancer Therapy. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190248208.003.0011.

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Ovarian cancer remains one of the most aggressive and difficult to manage malignancies regarding evaluation and therapeutic options. The high mortality persists despite extensive research in the field. Current conventional chemotherapy does not improve disease-free survival and does not decrease recurrences amongst patients. This calls for a stringent reconsideration of the drugs selection, focused on the most targeted strategies and personalization of the therapy. Targeted agents against growth factors and their corresponding receptors are already approved as first- or second-line neoadjuvant therapy with controversial results. This chapter critically discusses the role of growth factors as vascular endothelial growth factor, fibroblast growth factors, or platelet-derived growth factors and their corresponding receptors in the pathogenesis, progression, and selection of therapeutic strategies. Other growth factors, such as nerve growth factor or endocrine gland derived growth factor, seem to have a strong involvement in ovarian carcinogenesis but their actual impact is not fully understood.
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43

The Textbook Of Angiogenesis And Lymphangiogenesis Methods And Applications. Springer, 2012.

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44

Levi, Marcel, and Tom van der Poll. Coagulation and the endothelium in acute injury in the critically ill. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0307.

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Vascular endothelial cells play a pivotal mediatory role in many responses to systemic inflammation, including the cross-talk between coagulation and inflammation in sepsis. Endothelial cells respond to the cytokines expressed and released by activated leukocytes, but can also release cytokines themselves. Furthermore, endothelial cells are able to express adhesion molecules and growth factors that may not only promote the inflammatory response further, but also affect a myriad of downstream responses. It has recently become clear that, in addition to these mostly indirect effects of the endothelium, injured endothelial cells directly interfere with platelet-vessel wall interactions, neutrophil entrapment through formation of extracellular nets, and activation of inflammation and coagulation mediated by microparticles. The role of the glycocalyx as an important interface between the endothelium and regulation of coagulation in inflammatory states has also gained a lot of recent attention.
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45

G, Mikos Antonios, and Johnson Peter C, eds. Angiogenesis. New Rochelle, NY: Mary Ann Liebert, 2010.

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46

Angiogenesis. New Rochelle, NY: Mary Ann Liebert, 2010.

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47

G, Mikos Antonios, and Johnson Peter C, eds. Advances in tissue engineering angiogenesis. New Rochelle, NY: Mary Ann Liebert, Inc., 2010.

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48

Eremina, Vera. Role of vascular endothelial growth factor A in the glomerulus: Analysis of phenotypes with glomerular-specific alterations of VEGF-A expression in murine transgenic lines. 2006.

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49

Woywodt, Alexander, and Diana Chiu. Drug-induced and toxic glomerulopathies. Edited by Neil Turner. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0082.

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Glomerulopathies induced by particular exogenous compounds or molecules include those attributable to toxicity, and those caused by inducing an immune or autoimmune response. Tubules are more commonly the target of toxicity as they absorb and concentrate components of filtrate. Damage to endothelial cells may account for thrombotic microangiopathy in response to calcineurin inhibitors. Endothelial cells are also likely to be the target in drug-induced small vessel vasculitis. Toxicity to podocytes accounts for focal segmental glomerulosclerosis caused by pamidronate and other agents. Chloroquine can cause a remarkable pseudo-storage disorder with inclusions in podocytes that resemble those seen in Fabry disease. The mechanism by which drugs cause minimal change disease, another podocyte disorder, is not known. Membranous nephropathy may be caused by exposure to gold, mercury, and some other drugs; this is antibody mediated and presumably the targets are altered podocyte surface molecules. Inhibitors of the mammalian target of rapamycin (mTOR) cause proteinuria, possibly through effects on vascular endothelial growth factor, inhibitors of which are associated with not only proteinuria (an expected podocyte effect) but also thrombotic microangiopathy (endothelial cell effect). This latter may be through disturbing podocyte-endothelium cross-signaling.
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50

Maragoudakis, Michael E. Angiogenesis: Models, Modulators, and Clinical Applications. Springer, 2014.

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