Literature DB >> 26463732

Dysregulated FGF signalling in neoplastic disorders.

Yasmine Tanner1, Richard P Grose2.   

Abstract

The fibroblast growth factor (FGF) signalling pathway contributes to the regulation of a multitude of cellular functions, impacting on proliferation, survival, differentiation and migration. This biological importance is reflected by its prominent role in carcinogenesis; often being hijacked by cancer cells to offer growth or survival advantage. FGF signalling can contribute a driving force in the malignancy of different cancer types; through alterations in ligands, receptors or regulatory molecules. The dramatic advances in genomics technologies have highlighted how mutation, amplification, translocation or loss of elements in the FGF signalling network can contribute to cancer. Added to this are the stromal influences of FGF signalling. Dissection of the mechanisms that underlie the pro-tumourigenic effects resulting from perturbations to the FGF signalling network will be of utmost importance to the development of therapeutic approaches to treat FGF receptor (FGFR)-driven cancers. In this review, we will focus on the mechanisms of FGF deregulation, the prevalence of aberrations in different cancer types, and how we are progressing in the development of targeted therapies.
Copyright © 2015 Elsevier Ltd. All rights reserved.

Entities:  

Keywords:  Cancer; Cell signalling; Fibroblast growth factor; Fibroblast growth factor receptor; Neoplastic disorders

Mesh:

Substances:

Year:  2015        PMID: 26463732     DOI: 10.1016/j.semcdb.2015.10.012

Source DB:  PubMed          Journal:  Semin Cell Dev Biol        ISSN: 1084-9521            Impact factor:   7.727


  30 in total

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10.  Intrinsic fluorescence of the clinically approved multikinase inhibitor nintedanib reveals lysosomal sequestration as resistance mechanism in FGFR-driven lung cancer.

Authors:  Bernhard Englinger; Sebastian Kallus; Julia Senkiv; Daniela Heilos; Lisa Gabler; Sushilla van Schoonhoven; Alessio Terenzi; Patrick Moser; Christine Pirker; Gerald Timelthaler; Walter Jäger; Christian R Kowol; Petra Heffeter; Michael Grusch; Walter Berger
Journal:  J Exp Clin Cancer Res       Date:  2017-09-07
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