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Binding of\nFGF to fibroblast growth factor receptor (FGFR), a tyrosine kinase receptor, is facilitated by a glycosaminoglycan,\nheparin. Activated FGFRs phosphorylate the tyrosine kinase residues that mediate\ninduction of downstream signaling pathways, such as RAS-MAPK, PI3K-AKT, PLC\u03b3, and\nSTAT. Dysregulation of the FGF\/FGFR signaling occurs frequently in cancer due to gene amplification,\nFGF activating mutations, chromosomal rearrangements, integration, and oncogenic fusions.\nAberrant FGFR signaling also affects organogenesis, embryonic development, tissue homeostasis,\nand has been associated with cell proliferation, angiogenesis, cancer, and other pathophysiological\nchanges.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Objective::<\/jats:title>\n                    <jats:p>This comprehensive review will discuss the biology, chemistry, and functions of FGFs,\nand its current applications toward wound healing, diabetes, repair and regeneration of tissues, and\nfatty liver diseases. In addition, specific aberrations in FGFR signaling and drugs that target FGFR\nand aid in mitigating various disorders, such as cancer, are also discussed in detail.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion::<\/jats:title>\n                    <jats:p>Inhibitors of FGFR signaling are promising drugs in the treatment of several types of\ncancers. The clinical benefits of FGF\/FGFR targeting therapies are impeded due to the activation\nof other RTK signaling mechanisms or due to the mutations that abolish the drug inhibitory activity\non FGFR. Thus, the development of drugs with a different mechanism of action for FGF\/FGFR\ntargeting therapies is the recent focus of several preclinical and clinical studies.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.2174\/1389450121999201012201926","type":"journal-article","created":{"date-parts":[[2020,10,13]],"date-time":"2020-10-13T03:17:07Z","timestamp":1602559027000},"page":"214-240","update-policy":"https:\/\/doi.org\/10.2174\/bsp_crossmark_policy","source":"Crossref","is-referenced-by-count":26,"title":["Targeting Drugs Against Fibroblast Growth Factor(s)-Induced Cell Signaling"],"prefix":"10.2174","volume":"22","author":[{"given":"Shilpi","family":"Agrawal","sequence":"first","affiliation":[{"name":"Department of Chemistry and Biochemistry, University of Arkansas, Fayetteville, Arkansas, United States"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sanhita","family":"Maity","sequence":"additional","affiliation":[{"name":"Department of Chemistry and Biochemistry, University of Arkansas, Fayetteville, Arkansas, United States"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Zeina","family":"AlRaawi","sequence":"additional","affiliation":[{"name":"Department of Chemistry and Biochemistry, University of Arkansas, Fayetteville, Arkansas, United States"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Musaab","family":"Al-Ameer","sequence":"additional","affiliation":[{"name":"Department of Chemistry and Biochemistry, University of Arkansas, Fayetteville, Arkansas, United States"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-7574-3226","authenticated-orcid":true,"given":"Thallapuranam Krishnaswamy Suresh","family":"Kumar","sequence":"additional","affiliation":[{"name":"Department of Chemistry and Biochemistry, University of Arkansas, Fayetteville, Arkansas, United States"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"965","reference":[{"key":"ref=1","doi-asserted-by":"publisher","first-page":"121","DOI":"10.1093\/jb\/mvq121","volume":"149","author":"Itoh N.","year":"2011","unstructured":"Itoh N.; Ornitz D.M.; Fibroblast growth factors: from molecular evolution to roles in development, metabolism and disease. 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