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An In Vitro Dormancy Model of Estrogen-sensitive Breast Cancer in the Bone Marrow: A Tool for Molecular Mechanism Studies and Hypothesis Generation
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FGFR signalling in women's cancers.

Abbie E Fearon1, Charlotte R Gould, Richard P Grose

  • 1Centre for Tumour Biology, Barts Cancer Institute - A Cancer Research UK Centre of Excellence, Queen Mary University of London, John Vane Science Centre, Charterhouse Square, London EC1M 6BQ, United Kingdom.

The International Journal of Biochemistry & Cell Biology
|October 24, 2013
PubMed
Summary

Fibroblast Growth Factors (FGFs) and their receptors (FGFRs) are crucial for cell functions and are implicated in various diseases, including cancers. Understanding FGFR signaling is key to developing targeted therapies for women

Keywords:
AuNPCCCCINCISHCLCCancerDCISEECERFGFFGFRFISHFibroblast growth factor (FGF)Fibroblast growth factor receptor (FGFR)GWASGenome Wide Association StudyHPVHSIDCIHCMSINEECPDGFRPRRTKSCSNPSaethre ChotzenSignallingTICTKITMATherapyVEGFRcervical intraepithelial neoplasiachromogenic in situ hybridisationclassic lobular carcinomaclear cell carcinomaductal carcinoma in situendometrioid endometrial carcinomafibroblast growth factorfibroblast growth factor receptorfluorescence in situ hybridisationgold nanoparticleheparan sulfatehuman papilloma virusimmunohistochemistryinvasive ductal carcinomamAbmicrosatellite instabilitymonoclonal antibodynon-endometrioid endometrial carcinomaoestrogen receptorplatelet-derived growth factor receptorprogesterone receptorreceptor tyrosine kinasesmall nucleotides polymorphismtissue microarraytumour initiating celltyrosine kinase inhibitorvascular endothelial growth factor receptor

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Area of Science:

  • Molecular Biology
  • Oncology
  • Cell Signaling

Background:

  • Fibroblast Growth Factors (FGFs) complex with Fibroblast Growth Factor Receptors (FGFRs) and heparan sulfate (HS) to regulate critical cellular functions like embryogenesis and metabolism.
  • Germline and somatic mutations in FGFRs are associated with developmental disorders (e.g., craniosynostosis, dwarfism) and cancer.
  • FGFR signaling promotes cell proliferation, migration, and survival, making it a target for cancer cells.

Purpose of the Study:

  • To elucidate the molecular mechanisms of FGFR signaling.
  • To discuss the role of FGFR signaling in the pathogenesis and progression of female cancers.
  • To review preclinical and clinical data for FGFR-targeted therapies in women's cancers.

Main Methods:

  • Review of molecular mechanisms underlying FGFR signaling pathways.
  • Analysis of existing preclinical and clinical data concerning FGFRs in female cancers.
  • Discussion of therapeutic intervention strategies targeting FGFRs.

Main Results:

  • FGFR mutations and amplifications are prevalent in various cancers, particularly impacting female cancers.
  • FGFR signaling plays a significant role in the development and advancement of breast, endometrial, ovarian, and cervical carcinomas.
  • Preclinical and clinical studies demonstrate the potential of FGFR-targeted therapies.

Conclusions:

  • FGFR signaling is a critical pathway in normal physiology and is frequently dysregulated in women's cancers.
  • Targeting FGFRs offers a promising therapeutic strategy for female cancers.
  • Selective FGFR-targeted therapy is essential to mitigate effects on normal physiological processes.