Literature DB >> 19874848

De-regulated FGF receptors as therapeutic targets in cancer.

Victoria Knights1, Simon J Cook.   

Abstract

Fibroblast growth factors (FGFs) acting through their cognate receptors (FGFRs) play vital roles in development and de-regulation of FGF/FGFR signalling is associated with many developmental syndromes. In addition there is much interest in inhibiting FGF/FGFR signalling as a therapeutic approach to cancer. FGF/FGFR signalling is certainly important in tumour angiogenesis but studies in the last few years have uncovered increasing evidence that FGFRs are driving oncogenes in certain cancers and act in a cell autonomous fashion to maintain the malignant properties of tumour cells. These observations make FGFRs increasingly attractive as targets for therapeutic intervention in cancer. In this article, we review FGFR signalling and describe recent advances in cancer genomics and cancer cell biology that demonstrate that specific tumour types are dependent upon or addicted to de-regulated FGFR. We also describe the range of therapeutic strategies currently employed or in development to antagonise de-regulated FGFRs including antibodies and small molecule tyrosine kinase inhibitors.

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Year:  2009        PMID: 19874848     DOI: 10.1016/j.pharmthera.2009.10.001

Source DB:  PubMed          Journal:  Pharmacol Ther        ISSN: 0163-7258            Impact factor:   12.310


  56 in total

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Journal:  Tumour Biol       Date:  2014-07-26

5.  Twist1 correlates with poor differentiation and progression in gastric adenocarcinoma via elevation of FGFR2 expression.

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Review 6.  Metabolic derivatives of alcohol and the molecular culprits of fibro-hepatocarcinogenesis: Allies or enemies?

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7.  Fibroblast growth factor receptor 3 (FGFR3) is a strong heat shock protein 90 (Hsp90) client: implications for therapeutic manipulation.

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8.  FGFR1 gene amplification in squamous cell carcinomas of the lung: a potential favorable prognostic marker for women and for patients with advanced cancer.

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9.  The role of human papillomavirus type 16 E6/E7 oncoproteins in cervical epithelial-mesenchymal transition and carcinogenesis.

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10.  Oncogenic RAS pathway activation promotes resistance to anti-VEGF therapy through G-CSF-induced neutrophil recruitment.

Authors:  Vernon T Phan; Xiumin Wu; Jason H Cheng; Rebecca X Sheng; Alicia S Chung; Guanglei Zhuang; Christopher Tran; Qinghua Song; Marcin Kowanetz; Amy Sambrone; Martha Tan; Y Gloria Meng; Erica L Jackson; Franklin V Peale; Melissa R Junttila; Napoleone Ferrara
Journal:  Proc Natl Acad Sci U S A       Date:  2013-03-25       Impact factor: 11.205

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