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Journal articles on the topic 'Fibroblast growth factors'

Author: Grafiati

Published: 4 June 2021

Last updated: 25 July 2024

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1

Thomas, Kenneth A. "Fibroblast growth factors." FASEB Journal 1, no. 6 (1987): 434–40. http://dx.doi.org/10.1096/fasebj.1.6.3315806.

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2

Baird, Andrew, and Patricia A. Walicke. "Fibroblast growth factors." British Medical Bulletin 45, no. 2 (1989): 438–52. http://dx.doi.org/10.1093/oxfordjournals.bmb.a072333.

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3

Mason, Ivor. "Fibroblast growth factors." Current Biology 13, no. 9 (2003): R346. http://dx.doi.org/10.1016/s0960-9822(03)00270-7.

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4

Cheng, Maye F., Faizah S. Abdullah та Matthew B. Buechler. "Essential growth factor receptors for fibroblast homeostasis and activation: Fibroblast Growth Factor Receptor (FGFR), Platelet Derived Growth Factor Receptor (PDGFR), and Transforming Growth Factor β Receptor (TGFβR)". F1000Research 13 (21 травня 2024): 120. http://dx.doi.org/10.12688/f1000research.143514.2.

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Fibroblasts are cells of mesenchymal origin that are found throughout the body. While these cells have several functions, their integral roles include maintaining tissue architecture through the production of key extracellular matrix components, and participation in wound healing after injury. Fibroblasts are also key mediators in disease progression during fibrosis, cancer, and other inflammatory diseases. Under these perturbed states, fibroblasts can activate into inflammatory fibroblasts or contractile myofibroblasts. Fibroblasts require various growth factors and mitogenic molecules for su

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5

Cheng, Maye F., Faizah S. Abdullah, and Matthew B. Buechler. "Essential growth factor receptors for fibroblast homeostasis and activation." F1000Research 13 (February 19, 2024): 120. http://dx.doi.org/10.12688/f1000research.143514.1.

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Fibroblasts are cells of mesenchymal origin that are found throughout the body. While these cells have several functions, their integral roles include maintaining tissue architecture through the production of key extracellular matrix components, and participation in wound healing after injury. Fibroblasts are also key mediators in disease progression during fibrosis, cancer, and other inflammatory diseases. Under these perturbed states, fibroblasts can activate into inflammatory fibroblasts or contractile myofibroblasts. Fibroblasts require various growth factors and mitogenic molecules for su

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6

Chen, Gregory, and Reza Forough. "Fibroblast Growth Factors, Fibroblast Growth Factor Receptors, Diseases, and Drugs." Recent Patents on Cardiovascular Drug Discovery 1, no. 2 (2006): 211–24. http://dx.doi.org/10.2174/157489006777442478.

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7

Onoue, H., Y. Ebi, H. Nakayama, XM Ru, Y. Kitamura, and J. Fujita. "Suppressive effect of Sl/Sld mouse embryo-derived fibroblast cell lines on diffusible factor-dependent proliferation of mast cells." Blood 74, no. 5 (1989): 1557–62. http://dx.doi.org/10.1182/blood.v74.5.1557.1557.

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Abstract Two modes of mast cell growth are present, one dependent on diffusible growth factors (interleukins [IL] 3 and 4) and another dependent on contact with fibroblasts. The 3T3 fibroblast cell lines derived from WCB6F1-+/+ mouse embryos supported the proliferation of cultured mast cells (CMC), whereas the 3T3 fibroblast cell lines from WCB6F1-Sl/Sld mouse embryos did not. To investigate the relationship between growth factor-dependent and fibroblast-dependent growths of mast cells, we cocultured CMC and 3T3 fibroblasts in the presence of diffusible growth factors. WCB6F1-+/+ mouse embryo-

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8

Onoue, H., Y. Ebi, H. Nakayama, XM Ru, Y. Kitamura, and J. Fujita. "Suppressive effect of Sl/Sld mouse embryo-derived fibroblast cell lines on diffusible factor-dependent proliferation of mast cells." Blood 74, no. 5 (1989): 1557–62. http://dx.doi.org/10.1182/blood.v74.5.1557.bloodjournal7451557.

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Two modes of mast cell growth are present, one dependent on diffusible growth factors (interleukins [IL] 3 and 4) and another dependent on contact with fibroblasts. The 3T3 fibroblast cell lines derived from WCB6F1-+/+ mouse embryos supported the proliferation of cultured mast cells (CMC), whereas the 3T3 fibroblast cell lines from WCB6F1-Sl/Sld mouse embryos did not. To investigate the relationship between growth factor-dependent and fibroblast-dependent growths of mast cells, we cocultured CMC and 3T3 fibroblasts in the presence of diffusible growth factors. WCB6F1-+/+ mouse embryo-derived 3

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9

Metzler, Veronika Maria, Christian Pritz, Anna Riml, et al. "Separation of cell survival, growth, migration, and mesenchymal transdifferentiation effects of fibroblast secretome on tumor cells of head and neck squamous cell carcinoma." Tumor Biology 39, no. 11 (2017): 101042831770550. http://dx.doi.org/10.1177/1010428317705507.

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Fibroblasts play a central role in tumor invasion, recurrence, and metastasis in head and neck squamous cell carcinoma. The aim of this study was to investigate the influence of tumor cell self-produced factors and paracrine fibroblast–secreted factors in comparison to indirect co-culture on cancer cell survival, growth, migration, and epithelial–mesenchymal transition using the cell lines SCC-25 and human gingival fibroblasts. Thereby, we particularly focused on the participation of the fibroblast-secreted transforming growth factor beta-1.Tumor cell self-produced factors were sufficient to e

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10

COUTTS, JACQUELINE C., and JOHN T. GALLAGHER. "Receptors for fibroblast growth factors." Immunology and Cell Biology 73, no. 6 (1995): 584–89. http://dx.doi.org/10.1038/icb.1995.92.

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11

Pablo, Juan L., and Geoffrey S. Pitt. "Fibroblast Growth Factor Homologous Factors." Neuroscientist 22, no. 1 (2014): 19–25. http://dx.doi.org/10.1177/1073858414562217.

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12

van Scheltinga, A. F. T., S. C. Bakker, and R. S. Kahn. "Fibroblast Growth Factors in Schizophrenia." Schizophrenia Bulletin 36, no. 6 (2009): 1157–66. http://dx.doi.org/10.1093/schbul/sbp033.

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13

Wellstein, Anton, and Frank Czubayko. "Inhibition of fibroblast growth factors." Breast Cancer Research and Treatment 38, no. 1 (1996): 109–19. http://dx.doi.org/10.1007/bf01803789.

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14

PARIS, SONIA, and JACQUES POUYSSÉGUR. "Mitogenic Effects of Fibroblast Growth Factors in Cultured Fibroblastsa." Annals of the New York Academy of Sciences 638, no. 1 The Fibroblas (1991): 139–48. http://dx.doi.org/10.1111/j.1749-6632.1991.tb49024.x.

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15

SASADA, REIKO, MASAHARU SENO, TATSUYA WATANABE, and KOICHI IGARASHI. "Mitogenic Effects of Fibroblast Growth Factors in Cultured Fibroblastsa." Annals of the New York Academy of Sciences 638, no. 1 The Fibroblas (1991): 149–60. http://dx.doi.org/10.1111/j.1749-6632.1991.tb49025.x.

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16

DIONNE, CRAIG A., MICHAEL JAYE, and JOSEPH SCHLESSINGER. "Mitogenic Effects of Fibroblast Growth Factors in Cultured Fibroblastsa." Annals of the New York Academy of Sciences 638, no. 1 The Fibroblas (1991): 161–66. http://dx.doi.org/10.1111/j.1749-6632.1991.tb49026.x.

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17

IMOKAWA, Genji, Yukihiro YADA, Naoko MORISAKI, and Mitsutoshi KIMURA. "Biological characterization of human fibroblast-derived mitogenic factors for human melanocytes." Biochemical Journal 330, no. 3 (1998): 1235–39. http://dx.doi.org/10.1042/bj3301235.

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To clarify the paracrine linkage between human fibroblasts and melanocytes in cutaneous pigmentation, we studied the effects of human fibroblast-derived factors on the proliferation of human melanocytes. In medium conditioned for 4 days with human fibroblast culture, factors were produced that markedly stimulated DNA synthesis of human melanocytes. The stimulatory effect was higher in medium conditioned with fibroblasts from aged skin than in medium conditioned with fibroblasts from young skin, and was interrupted by inhibitors of tyrosine kinase, such as tyrphostin, genistein and herbimycin,

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18

Rettig, W. J., H. P. Erickson, A. P. Albino, and P. Garin-Chesa. "Induction of human tenascin (neuronectin) by growth factors and cytokines: cell type-specific signals and signalling pathways." Journal of Cell Science 107, no. 2 (1994): 487–97. http://dx.doi.org/10.1242/jcs.107.2.487.

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The extracellular matrix protein tenascin (TN) is expressed with precise temporo-spatial patterns during embryonic and fetal development and is induced in healing wounds, inflammatory lesions and solid tumors. These tissue patterns suggest that TN synthesis may be modulated by soluble factors present in developing tissues or released from injured, inflammatory or neoplastic cells. To characterize the extrinsic control of human TN we examined the effects of several signalling molecules on cultured neural, melanocytic and fibroblastic cells. Results obtained with alpha TN antibodies in enzyme-li

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19

Gray, A. J., J. T. Reeves, N. K. Harrison, P. Winlove, and G. J. Laurent. "Growth factors for human fibroblasts in the solute remaining after clot formation." Journal of Cell Science 96, no. 2 (1990): 271–74. http://dx.doi.org/10.1242/jcs.96.2.271.

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Fibroblasts adhere to, and readily grow into, fibrin clots that form as a result of the cleavage of fibrinogen by thrombin. Subsequent fibroblast replication is believed to be stimulated by mitogens released by entrapped platelets, such as platelet-derived growth factor. We suggest that the supernatant remaining after the fibrinogen-thrombin reaction could stimulate fibroblast replication, even in the absence of other blood components. To examine this hypothesis we expressed liquid from a fibrin clot and measured its mitogenic activity on human lung fibroblasts, in serum-free conditions, using

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20

Goldsmith, K. T., R. B. Gammon, and R. I. Garver. "Modulation of bFGF in lung fibroblasts by TGF-beta and PDGF." American Journal of Physiology-Lung Cellular and Molecular Physiology 261, no. 6 (1991): L378—L385. http://dx.doi.org/10.1152/ajplung.1991.261.6.l378.

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Growth factors produced by alveolar macrophages are thought to promote the fibroblast proliferation within interstitial spaces of fibrotic lungs. This study investigated the possibility that the macrophage-produced growth factors might modulate the expression of basic fibroblast growth factor (bFGF) by lung fibroblasts. To evaluate this question, bFGF gene expression and protein production were evaluated in normal adult human lung fibroblast cell lines. Under normal culture conditions, the fibroblasts expressed the bFGF gene as two major transcripts (7.1, 3.7 kb). The addition of fetal calf se

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21

Fabisiak, J. P., M. Absher, J. N. Evans, and J. Kelley. "Spontaneous production of PDGF A-chain homodimer by rat lung fibroblasts in vitro." American Journal of Physiology-Lung Cellular and Molecular Physiology 263, no. 2 (1992): L185—L193. http://dx.doi.org/10.1152/ajplung.1992.263.2.l185.

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Platelet-derived growth factor (PDGF) is considered a decisive mediator of fibroblast growth and phenotype within the lung. The cellular sources of PDGF within the lung remain undefined. The ability of lung fibroblasts themselves to produce PDGF in vitro was therefore investigated. Northern and Western blot analyses revealed the expression of PDGF-A mRNA and secretion of A-chain containing proteins by fibroblasts derived from adult and fetal rat lung. PDGF-A gene or protein expression were below the limits of detection in two human lung fibroblast lines examined in a similar manner. PDGF-B tra

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22

Manetti, F., F. Corelli, and M. Botta. "Fibroblast Growth Factors and Their Inhibitors." Current Pharmaceutical Design 6, no. 18 (2000): 1897–924. http://dx.doi.org/10.2174/1381612003398528.

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23

Baker, Kevin P., and Gerrit Los. "Targeting fibroblast growth factors in cancer." Oncotarget 4, no. 7 (2013): 952–53. http://dx.doi.org/10.18632/oncotarget.1054.

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24

Galzie, Zoya, Anne R. Kinsella, and John A. Smith. "Fibroblast growth factors and their receptors." Biochemistry and Cell Biology 75, no. 6 (1997): 669–85. http://dx.doi.org/10.1139/o97-091.

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Fibroblast growth factors (FGFs) represent a group of polypeptide mitogens eliciting a wide variety of responses depending upon the target cell type. The knowledge of the cell surface receptors mediating the effects of FGFs has recently expanded remarkably. The complexity of the FGF family and the FGF-induced responses is reflected in the diversity and redundancy of the FGF receptors. In this review, a number of biochemical characteristics and biological properties of the FGF family and its receptors are described and their expression both in normal tissues and in tumours is discussed. Finally

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25

Gnatenko, D. A., E. P. Kopantsev, and E. D. Sverdlov. "Fibroblast growth factors and pancreas organogenesis." Biochemistry (Moscow), Supplement Series B: Biomedical Chemistry 11, no. 4 (2017): 341–48. http://dx.doi.org/10.1134/s1990750817040023.

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26

Jane Robinson, C. "Tailoring and targeting fibroblast growth factors." Trends in Biotechnology 9, no. 1 (1991): 147–48. http://dx.doi.org/10.1016/0167-7799(91)90049-n.

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27

Partanen, Juha, Satu Vainikka, Jaana Korhonen, Elina Armstrong, and Kari Alitalo. "Diverse receptors for fibroblast growth factors." Progress in Growth Factor Research 4, no. 1 (1992): 69–83. http://dx.doi.org/10.1016/0955-2235(92)90005-3.

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28

GOSPODAROWICZ, DENIS. "Biological Activities of Fibroblast Growth Factors." Annals of the New York Academy of Sciences 638, no. 1 The Fibroblas (1991): 1–8. http://dx.doi.org/10.1111/j.1749-6632.1991.tb49012.x.

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29

Yamaguchi, Terry P., and Janet Rossant. "Fibroblast growth factors in mammalian development." Current Opinion in Genetics & Development 5, no. 4 (1995): 485–91. http://dx.doi.org/10.1016/0959-437x(95)90053-j.

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30

Suzuki, Satoshi, Yutaka Ota, Kazuo Ozawa, and Toru Imamura. "Controlling Fibroblast Growth Factors for Hair Growth Regulation." Journal of Society of Cosmetic Chemists of Japan 35, no. 3 (2001): 231–36. http://dx.doi.org/10.5107/sccj.35.3_231.

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31

De Luca, Francesco, and Jeffrey Baron. "Control of Bone Growth by Fibroblast Growth Factors." Trends in Endocrinology & Metabolism 10, no. 2 (1999): 61–65. http://dx.doi.org/10.1016/s1043-2760(98)00120-9.

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32

Walters, J. D., R. J. Nakkula, and P. Maney. "Modulation of Gingival Fibroblast Minocycline Accumulation by Biological Mediators." Journal of Dental Research 84, no. 4 (2005): 320–23. http://dx.doi.org/10.1177/154405910508400405.

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Gingival fibroblasts actively accumulate tetracyclines, thereby enhancing their redistribution from blood to gingiva. Since growth factors and pro-inflammatory cytokines regulate many fibroblast activities, they could potentially enhance fibroblast minocycline accumulation. To test this hypothesis, we treated gingival fibroblast monolayers for 1 or 6 hours with platelet-derived growth factor-BB (PDGF), fibroblast growth factor-2 (FGF), transforming growth factor-β1 (TGF), or tumor necrosis factor-α (TNF). Minocycline uptake was assayed at 37° by a fluorescence method. All 4 factors significant

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33

Sieuwerts, Anieta, Joan Bolt-de Vries, Peter Bosma, et al. "Aging of stromal-derived human breast fibroblasts might contribute to breast cancer progression." Thrombosis and Haemostasis 89, no. 02 (2003): 393–404. http://dx.doi.org/10.1055/s-0037-1613457.

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SummaryAge is an important factor in the development and spread of breast cancer. Stromal cells also contribute to breast cancer growth and metastasis through the production of extracellular matrix (ECM) modifiers such as urokinase type plasminogen activator (uPA), its receptor (uPAR), its inhibitors (PAI-1 and PAI-2), matrix metalloproteinases (MMPs), and growth factors, including the fibroblast and insulin-like growth factors (FGF’s and IGF’s). In the present study we have investigated whether breast fibroblasts aged in vitro through passage in culture display altered levels of the plasminog

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34

Tunyogi-Csapo, Miklos, Tamas Koreny, Csaba Vermes, Jorge O. Galante, Joshua J. Jacobs, and Tibor T. Glant. "Role of fibroblasts and fibroblast-derived growth factors in periprosthetic angiogenesis." Journal of Orthopaedic Research 25, no. 10 (2007): 1378–88. http://dx.doi.org/10.1002/jor.20449.

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35

Iwasaki, Kengo, Keiko Akazawa, Mizuki Nagata, et al. "Angiogenic Effects of Secreted Factors from Periodontal Ligament Stem Cells." Dentistry Journal 9, no. 1 (2021): 9. http://dx.doi.org/10.3390/dj9010009.

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Periodontal disease is a chronic inflammation of tooth-supporting tissues, and the destruction of these tissues results in tooth loss. Regeneration of periodontal tissues is the ultimate goal of periodontal treatment. We previously reported that transplantation of conditioned medium (CM) of periodontal ligament stem cells (PDLSCs) demonstrated the enhancement of periodontal tissue regeneration, compared to CM from fibroblasts (Fibroblast-CM). We hypothesized that the angiogenic effects of PDLSC-CM might participate in the enhanced wound healing of periodontal tissues. The aim of this study was

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36

Burhan Rafiq, Shvan, Heshu Sulaiman Rahman, and Kawa Amin. "The Estimate of Cytokines and Fibroblast Growth Factors in Patients with Breast Cancer." Journal of Zankoy Sulaimani - Part A 22, no. 2 (2020): 9–16. http://dx.doi.org/10.17656/jzs.10803.

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37

Zucali, J. R., H. E. Broxmeyer, M. A. Gross, and C. A. Dinarello. "Recombinant human tumor necrosis factors alpha and beta stimulate fibroblasts to produce hemopoietic growth factors in vitro." Journal of Immunology 140, no. 3 (1988): 840–44. http://dx.doi.org/10.4049/jimmunol.140.3.840.

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Abstract The influences of TNF alpha and TNF beta were evaluated for their stimulatory and inhibitory effects on in vitro colony formation by human bone marrow granulocyte-macrophage (CFU-GM), erythroid (BFU-E), and multipotential (CFU-GEMM) progenitor cells. Both TNF alpha and TNF beta induced fibroblasts to produce stimulators of CFU-GM, BFU-E, and CFU-GEMM in a dose-dependent fashion. Similar results were seen when equivalent concentrations of TNF alpha and TNF beta were used. Prior incubation of the TNF alpha and TNF beta with their respective antibodies inactivated the ability of the TNF

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38

Nakamura, Y., L. Tate, R. F. Ertl, et al. "Bronchial epithelial cells regulate fibroblast proliferation." American Journal of Physiology-Lung Cellular and Molecular Physiology 269, no. 3 (1995): L377—L387. http://dx.doi.org/10.1152/ajplung.1995.269.3.l377.

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Chronic bronchitis frequently leads to irreversible airway obstruction. Alteration of airway architecture with abnormal airway connective tissue is thought to play an important role in this process. We hypothesized that the epithelial cells that line the airways modulate the development of peribronchial fibrosis and fixed airway obstruction by directing fibroblast proliferation. To assess this, we examined stimulatory activities for human lung fibroblast proliferation in bovine bronchial epithelial cell-conditioned medium. The conditioned medium stimulated the proliferation of fibroblasts in a

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39

Ihn, H., K. Kikuchi, Y. Soma, et al. "The stimulatory effects of PDGF and TGF-beta 1 on dermal fibroblast attachment." Acta Dermato-Venereologica 75, no. 5 (1995): 367–71. http://dx.doi.org/10.2340/0001555575367371.

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We investigated the effects of various growth factors (platelet-derived growth factor (PDGF), epidermal growth factor (EGF), basic fibroblast growth factor (bFGF), transforming growth factor-alpha (TGF-alpha), transforming growth factor-beta 1 (TGF-beta 1), tumor necrosis factor-alpha (TNF-alpha), keratinocyte growth factor (KGF)) on fibroblast attachment to plastic plates. It is thought that cell attachment to plastic plates in vitro may represent the step between cell migration and proliferation in vivo during wound healing. Among the growth factors examined, only PDGF and TGF-beta 1 signifi

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40

Rogers, Mary-Louise, David A. Belford, Geoffrey L. Francis, and F. John Ballard. "Identification of fibroblast growth factors in bovine cheese whey." Journal of Dairy Research 62, no. 3 (1995): 501–7. http://dx.doi.org/10.1017/s0022029900031198.

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SummaryAcidic and basic fibroblast growth factors (FGF) were identified in bovine cheese whey after partial purification using a two step procedure. Cation-exchange chromatography produced a mitogen-rich extract which was loaded on to a heparin-sepharose column and eluted stepwise with 0·8, 1·2 and 2·0 M-NH4HC03. Mitogenic activity was found in all three fractions by cell growth assays using Balb/c-3T3 fibroblasts. Immunoblotting identified acidic FGF in the 1·2 M-eluate and basic FGF in the 2·0 M-eluate, but neither acidic nor basic FGF was detected in the 0·8 M-fraction. Quantitative radiore

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41

Korc, M., and R. Friesel. "The Role of Fibroblast Growth Factors in Tumor Growth." Current Cancer Drug Targets 9, no. 5 (2009): 639–51. http://dx.doi.org/10.2174/156800909789057006.

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42

Bidey, SP, DJ Hill, and MC Eggo. "Growth factors and goitrogenesis." Journal of Endocrinology 160, no. 3 (1999): 321–32. http://dx.doi.org/10.1677/joe.0.1600321.

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By combining data from studies of multinodular non-toxic goitre (MNTG) with data from rat models of goitre induction and in vitro models, a map of the growth factors involved in goitrogenesis has been constructed. We have addressed the roles of the insulin-like growth factors, transforming growth factors, fibroblast growth factors, endothelins, etc. We hypothesise that an imbalance in the interactions between the various growth factor axes exists in MNTG which favours cell replication. Thyrotrophin, although not significantly elevated in MNTG, exerts critical effects through interactions with

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43

Trautmann, Axel, Georg Krohne, Eva-B. Bröcker, and C. Eberhard Klein. "Human Mast Cells Augment Fibroblast Proliferation by Heterotypic Cell-Cell Adhesion and Action of IL-4." Journal of Immunology 160, no. 10 (1998): 5053–57. http://dx.doi.org/10.4049/jimmunol.160.10.5053.

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Abstract Mast cells have been implicated in the pathogenesis of fibrosis because of their increased number in chronic inflammatory reactions. In a previous study, we had shown that human mast cells readily attach and form heterotypic cell-cell contacts when seeded on top of fibroblast monolayers. Here, we report that human mast cells stimulate fibroblast proliferation after cell-cell contact. Proliferation was measured by 5-bromo-2′-deoxyuridine or [3H]thymidine uptake of subconfluent fibroblast monolayers after attachment of mast cells that had been preincubated with mitomycin C. An 18-h cocu

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44

Labanca, Estefania, Elba S. Vazquez, Paul G. Corn, et al. "Fibroblast growth factors signaling in bone metastasis." Endocrine-Related Cancer 27, no. 7 (2020): R255—R265. http://dx.doi.org/10.1530/erc-19-0472.

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Many solid tumors metastasize to bone, but only prostate cancer has bone as a single, dominant metastatic site. Recently, the FGF axis has been implicated in cancer progression in some tumors and mounting evidence indicate that it mediates prostate cancer bone metastases. The FGF axis has an important role in bone biology and mediates cell-to-cell communication. Therefore, we discuss here basic concepts of bone biology, FGF signaling axis, and FGF axis function in adult bone, to integrate these concepts in our current understanding of the role of FGF axis in bone metastases.

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45

Ray, L. B. "Enabling Endocrine Action of Fibroblast Growth Factors." Science's STKE 2007, no. 382 (2007): tw133. http://dx.doi.org/10.1126/stke.3822007tw133.

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46

Terwisscha van Scheltinga, Afke F., Steven C. Bakker, René S. Kahn, and Martien J. H. Kas. "Fibroblast Growth Factors in Neurodevelopment and Psychopathology." Neuroscientist 19, no. 5 (2013): 479–94. http://dx.doi.org/10.1177/1073858412472399.

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47

Krejci, P., P. B. Mekikian, and W. R. Wilcox. "The fibroblast growth factors in multiple myeloma." Leukemia 20, no. 6 (2006): 1165–68. http://dx.doi.org/10.1038/sj.leu.2404202.

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48

Baird, A. "Fibroblast growth factors: what's in a name?" Endocrinology 132, no. 2 (1993): 487–88. http://dx.doi.org/10.1210/endo.132.2.8425469.

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49

Jeffers, Michael, William J. LaRochelle, and Henri S. Lichenstein. "Fibroblast growth factors in cancer: therapeutic possibilities." Expert Opinion on Therapeutic Targets 6, no. 4 (2002): 469–82. http://dx.doi.org/10.1517/14728222.6.4.469.

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50

Sensenbrenner, M. "The neurotrophic activity of fibroblast growth factors." Progress in Neurobiology 41, no. 6 (1993): 683–704. http://dx.doi.org/10.1016/0301-0082(93)90031-m.

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