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Books on the topic 'Fibroblast growth factors'

Author: Grafiati

Published: 4 June 2021

Last updated: 25 July 2024

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1

Baird, Andrew, 1954 July 27-, Klagsbrun Michael, and New York Academy of Sciences., eds. The Fibroblast growth factor family. New York, N.Y: New York Academy of Sciences, 1991.

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2

Pedro, Cuevas, ed. Fibroblast growth factor in the cardiovascular system. Munich: I. Holzapfel, 2002.

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3

Mullen, Elizabeth Anne. An inhibitor of angiogenesis isolated from bovine cornea. [s.l: s.n.], 1992.

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4

Drucker, Beverly Joyce. Functional and developmental studies on members of the fibroblast growth factor family. [New York]: [Columbia University], 1993.

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5

Dalton, Stephen Lewis. Cell attachment controls fibronectin and α51 integrin levels in fibroblasts: Implications for anchorage-dependent and -independent growth. [New York]: [Columbia University], 1993.

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6

Westman, Jacob. Synthesis of oligosaccharides related to heparin and heparan sulphate and their binding to fibroblast growth factors. Stockholm, Sweden: Dept. of Organic Chemistry, Arrhenius Laboratory, Stockholm University, 1995.

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7

1945-, Lippman Marc E., Ortho Pharmaceutical Corporation, and University of California, Los Angeles., eds. Growth regulation of cancer: Proceedings of an Ortho-UCLA Symposium on Growth Regulation of Cancer, held at Park City, Utah, January 17-23, 1987. New York: Liss, 1988.

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8

Kjell, Fuxe, and Wenner-Grenska samfundet, eds. Trophic regulation of the basal ganglia: Focus on dopamine neurons. Oxford, OX, UK: Pergamon, 1994.

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9

1945-, Lippman Marc E., Dickson Robert B. 1952-, and University of California, Los Angeles., eds. Growth regulation of cancer II: Proceedings of a UCLA symposium, held at Keystone, Colorado, January 21-27, 1989. New York: Wiley-Liss, 1990.

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10

Walters, Jean Elizabeth. Immunochemical studies on fibroblast growth factor-1 and fibroblast growth factor receptor 1. Oxford: Oxford Brookes University, 1998.

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11

Burgar, Helen Rachel. Fibroblast growth factor receptor signalling. Birmingham: University of Birmingham, 2002.

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12

Cocks, Helen Catherine. Fibroblast growth factor in the thyroid. Birmingham: University of Birmingham, 2003.

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13

Lyn-Cook, Richard X. Cortical development in fibroblast growth factor 2 knockout mice. [New Haven, Conn: s.n.], 1999.

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14

Smith, Conrad. Developmental changes in the injury induced expression of fibroblast growth factor-2 and fibroblast growth factor receptor 1 in the rat brain. Birmingham: University of Birmingham, 1998.

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15

Daley, Sandra J. Basic fibroblast growth factor mediates neointimal formation in porcine aortic explants. Ottawa: National Library of Canada = Bibliothèque nationale du Canada, 1997.

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16

Thompson, Stuart David. Fibroblast growth factor 2 and its receptor, FGFR 1 in the normal thyroid and multinodular goitre. Birmingham: University of Birmingham, 2000.

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17

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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18

Plowright, Elizabeth Emma. Expression of fibroblast growth factor receptor 3 in multiple myeloma causes II-6-independence and enhanced survival. Ottawa: National Library of Canada, 1999.

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19

Onwuazor, Obiageli Nneka. Mutation, SNP and isoform analysis of fibroblast growth factor receptor 3 (FGFR3) in 150 newly diagnosed multiple myeloma patients. Ottawa: National Library of Canada, 2003.

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20

Clarke, Wendy Elizabeth. Intracellular compartmentalisation of fibroblast growth factor-2 and associated high and low affinity receptors after cerebral injury to the adult rat brain. Birmingham: University of Birmingham, 1999.

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21

Spudich, Rani Karina. Effect of phenobarbital on extracellular matrix production, cell replication, transforming growth factor-B1 binding, and TGF-B receptor profile in rat dermal fibroblast cultures. [New Haven, Conn: s.n.], 1997.

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22

1948-, Goldberg I. D., and Rosen E. M, eds. Epithelial-mesenchymal interactions in cancer. Basel: Birkhäuser Verlag, 1995.

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23

Li, Xiaokun. Fibroblast Growth Factors. Elsevier Science & Technology, 2023.

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24

Fibroblast Growth Factors. Elsevier, 2018. http://dx.doi.org/10.1016/c2017-0-02803-3.

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25

Li, Xiaokun. Fibroblast Growth Factors. Elsevier Science & Technology Books, 2018.

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26

Li, Xiaokun. Fibroblast Growth Factors. Elsevier Science & Technology Books, 2023.

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27

Fibroblast Growth Factors. Elsevier Science & Technology, 2018.

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28

Endocrine Fgfs and Klothos Advances in Experimental Medicine and Biology. Springer, 2012.

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29

Seidensticker, Martin J. Fibroblast growth factors and the onset of spermatogenesis. 1997.

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30

Bates, Brian G. The biosynthesis and expression of the fibroblast growth factor-5 gene. [New York], 1993.

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31

Simons, Michael. Fibroblast Growth Factors: Biology and Clinical Application - Fgf Biology and Therapeutics. World Scientific Publishing Co Pte Ltd, 2016.

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32

Wang, Zhouguang, Xiaokun Li, Q. Adam Ye, Saverio Bellusci, and Yidong Wang, eds. Fibroblast Growth Factors and Stem Cells in Regenerative Pharmacology and Anti-Aging Intervention. Frontiers Media SA, 2022. http://dx.doi.org/10.3389/978-2-88976-288-0.

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33

Bothwell, M. Neuronal Growth Factors (Current Topics in Microbiology & Immunology). Edited by M. Bothwell. Springer, 1991.

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34

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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35

Carroll, Camilla Ma. The effects of the angiogenic growth factors, platelet derived growth factor and basic fibroblast growth factor, on the survival,perfusion and function of the latissmus dorsi muscle flap. 1997.

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36

Growth regulation of cancer: Proceedings of an Ortho-UCLA Symposium on Growth Regulation of Cancer, held at Park City, Utah, January 17-23, 1987 (UCLA symposia on molecular and cellular biology). Liss, 1988.

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37

Growth Regulation of Cancer (UCLA Symposia on Molecular and Cellular Biology). John Wiley & Sons Inc, 1990.

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38

(Editor), K. Chapman, S. P. Jackson (Editor), D. G. Wilkinson (Editor), and George G. Lunt (Editor), eds. Extracellular Regulators of Differentiation and Development (Biochemical Society Symposia). Ashgate Publishing, 1996.

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39

Fibroblast Growth Factor 23. Elsevier, 2021. http://dx.doi.org/10.1016/c2018-0-03274-0.

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40

White, Kenneth, Christian Faul, and Orlando Gutierrez. Fibroblast Growth Factor 23. Elsevier, 2021.

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41

White, Kenneth, Christian Faul, and Orlando Gutierrez. Fibroblast Growth Factor 23. Elsevier, 2021.

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42

Duman, Ronald S. Neurotrophic Mechanisms of Depression. Edited by Dennis S. Charney, Eric J. Nestler, Pamela Sklar, and Joseph D. Buxbaum. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190681425.003.0027.

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Early theories of depression and treatment response were centered on the monoamine neurotransmitters, but more recent work has focused on functional and structural synaptic plasticity and the role of neurotrophic factors, particularly brain derived neurotrophic factor (BDNF). Neurotrophic factors regulate all aspects of neuronal function, including adaptive plasticity, synapse formation, and neuronal survival. Chronic stress and depression cause reductions in levels of BDNF and other key factors, including vascular endothelial growth factor (VEGF) and fibroblast growth factor 2 (FGF2), in cortical regions that contribute to atrophy and loss of neurons observed in depressed patients and rodent stress models. In contrast, these neurotrophic factors are upregulated by chronic administration of typical antidepressants and are required for antidepressant responses. Moreover, fast acting, highly efficacious antidepressant agents such as ketamine rapidly increase BDNF release and synapse formation, paving the way for a new generation of medications for the treatment of depression.

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43

Steinfeld, R. Modulation of the Interaction Between Fibroblast Growth Factor-2 and Fibroblast Growth Factor Receptor-1 by Cell Surface Heparan Sulfate Proteoglycans. Leuven University Press, 1996.

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44

Fibroblast Growth Factor Receptor (FGFR) Signaling Pathway in Tumor. MDPI, 2020. http://dx.doi.org/10.3390/books978-3-03936-785-6.

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45

Padela, Sanna. Hepatocyte growth factor and fibroblast growth factor-7 in neonatal lung development and injury. 2006.

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46

Ashton, Anthony. Fibroblast Growth Factor: Methods and Protocols (Methods in Molecular Medicine). Humana Press, 2001.

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47

Baumgarten, Leora B. The role of Ca²⁺ channels and Ca²⁺ pools in Bradykinin stimulated changes in intracellular Ca²⁺ in human fibroblasts. 1992.

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48

Gutiérrez, Orlando M. Fibroblast growth factor 23, Klotho, and phosphorus metabolism in chronic kidney disease. Edited by David J. Goldsmith. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0119.

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Fibroblast growth factor 23 (FGF23) and Klotho have emerged as major hormonal regulators of phosphorus (P) and vitamin D metabolism. FGF23 is secreted by bone cells and acts in the kidneys to increase urinary P excretion and inhibit the synthesis of 1,25 dihydroxyvitamin D (1,25(OH)2D) and in the parathyroid glands to inhibit the synthesis and secretion of parathyroid hormone. Phosphorus excess stimulates FGF23 secretion, likely as an appropriate physiological adaptation to maintain normal P homeostasis by enhancing urinary P excretion and diminishing intestinal P absorption via lower 1,25(OH)2D. The FGF23 concentrations are elevated early in the course of chronic kidney disease (CKD) and may be a primary initiating factor for the development of secondary hyperparathyroidism in this setting. Klotho exists in two forms: a transmembrane form and a secreted form, each with distinct functions. The transmembrane form acts as the key co-factor needed for FGF23 to bind to and activate its cognate receptor in the kidneys and the parathyroid glands. The secreted form of Klotho has FGF23-independent effects on renal P and calcium handling, insulin sensitivity, and endothelial function. Disturbances in the expression of Klotho may play a role in the development of altered bone and mineral metabolism in early CKD. In addition, abnormal circulating concentrations of both FGF23 and Klotho have been linked to excess cardiovascular disease, suggesting that both play an important role in maintaining cardiovascular health.

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49

Zhang, Zhe. Cell Surface Heparan Sulfate Proteoglycans As Co-Receptors for Fibroblast Growth Factor. Leuven Univ Pr, 2002.

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50

Wang, Zhouguang, Xiaokun Li, Li Lin, Saverio Bellusci, and Jin-San Zhang, eds. The Fibroblast Growth Factor Signaling Pathway in Metabolic Regulation, Development, Disease and Repair After Injury. Frontiers Media SA, 2020. http://dx.doi.org/10.3389/978-2-88966-128-2.

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