{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,13]],"date-time":"2026-10-13T00:33:32Z","timestamp":1791851612213,"version":"4.3.4"},"reference-count":193,"publisher":"Portland Press Ltd.","issue":"2","content-domain":{"domain":["portlandpress.com"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2011,7,15]]},"abstract":"<jats:p>FGFs (fibroblast growth factors) and their receptors (FGFRs) play essential roles in tightly regulating cell proliferation, survival, migration and differentiation during development and adult life. Deregulation of FGFR signalling, on the other hand, has been associated with many developmental syndromes, and with human cancer. In cancer, FGFRs have been found to become overactivated by several mechanisms, including gene amplification, chromosomal translocation and mutations. FGFR alterations are detected in a variety of human cancers, such as breast, bladder, prostate, endometrial and lung cancers, as well as haematological malignancies. Accumulating evidence indicates that FGFs and FGFRs may act in an oncogenic fashion to promote multiple steps of cancer progression by inducing mitogenic and survival signals, as well as promoting epithelial\u2013mesenchymal transition, invasion and tumour angiogenesis. Therapeutic strategies targeting FGFs and FGFRs in human cancer are therefore currently being explored. In the present review we will give an overview of FGF signalling, the main FGFR alterations found in human cancer to date, how they may contribute to specific cancer types and strategies for therapeutic intervention.<\/jats:p>","DOI":"10.1042\/bj20101603","type":"journal-article","created":{"date-parts":[[2011,6,29]],"date-time":"2011-06-29T08:23:05Z","timestamp":1309335785000},"page":"199-213","update-policy":"https:\/\/doi.org\/10.1042\/crossmark_policy","source":"Crossref","is-referenced-by-count":469,"title":["Fibroblast growth factors and their receptors in cancer"],"prefix":"10.1042","volume":"437","author":[{"given":"J\u00f8rgen","family":"Wesche","sequence":"first","affiliation":[{"name":"Centre for Cancer Biomedicine, Faculty of Medicine, University of Oslo, Oslo, Norway and Department of Biochemistry, Institute for Cancer Research, The Norwegian Radium Hospital, Oslo University Hospital, Montebello, 0310 Oslo, Norway"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kaisa","family":"Haglund","sequence":"additional","affiliation":[{"name":"Centre for Cancer Biomedicine, Faculty of Medicine, University of Oslo, Oslo, Norway and Department of Biochemistry, Institute for Cancer Research, The Norwegian Radium Hospital, Oslo University Hospital, Montebello, 0310 Oslo, Norway"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ellen\u00a0Margrethe","family":"Haugsten","sequence":"additional","affiliation":[{"name":"Centre for Cancer Biomedicine, Faculty of Medicine, University of Oslo, Oslo, Norway and Department of Biochemistry, Institute for Cancer Research, The Norwegian Radium Hospital, Oslo University Hospital, Montebello, 0310 Oslo, Norway"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"288","published-online":{"date-parts":[[2011,6,28]]},"reference":[{"key":"2021112214484118600_B1","doi-asserted-by":"crossref","first-page":"57","DOI":"10.1016\/S0092-8674(00)81683-9","article-title":"The hallmarks of cancer","volume":"100","author":"Hanahan","year":"2000","journal-title":"Cell"},{"key":"2021112214484118600_B2","doi-asserted-by":"crossref","first-page":"646","DOI":"10.1016\/j.cell.2011.02.013","article-title":"Hallmarks of cancer: the next generation","volume":"144","author":"Hanahan","year":"2011","journal-title":"Cell"},{"key":"2021112214484118600_B3","doi-asserted-by":"crossref","first-page":"220","DOI":"10.1038\/nrm2858","article-title":"Genomic instability: an evolving hallmark of cancer","volume":"11","author":"Negrini","year":"2010","journal-title":"Nat. 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