Please use this identifier to cite or link to this item: https://dspace.iiti.ac.in/handle/123456789/11873
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dc.contributor.authorMahapatra, Subhasmitaen_US
dc.contributor.authorJonniya, Nisha Amarnathen_US
dc.contributor.authorKoirala, Sumanen_US
dc.contributor.authorUrsal, Kapil Dattatrayen_US
dc.contributor.authorKar, Parimalen_US
dc.date.accessioned2023-06-20T15:33:49Z-
dc.date.available2023-06-20T15:33:49Z-
dc.date.issued2023-
dc.identifier.citationMahapatra, S., Jonniya, N. A., Koirala, S., Ursal, K. D., & Kar, P. (2023). The FGF/FGFR signalling mediated anti-cancer drug resistance and therapeutic intervention. Journal of Biomolecular Structure and Dynamics, doi:10.1080/07391102.2023.2191721en_US
dc.identifier.issn0739-1102-
dc.identifier.otherEID(2-s2.0-85152254806)-
dc.identifier.urihttps://doi.org/10.1080/07391102.2023.2191721-
dc.identifier.urihttps://dspace.iiti.ac.in/handle/123456789/11873-
dc.description.abstractABSTRACT : Fibroblast Growth Factor (FGF) ligands and their receptors are crucial factors driving chemoresistance in several malignancies, challenging the efficacy of currently available anti-cancer drugs. The Fibroblast growth factor/receptor (FGF/FGFR) signalling malfunctions in tumor cells, resulting in a range of molecular pathways that may impact its drug effectiveness. Deregulation of cell signalling is critical since it can enhance tumor growth and metastasis. Overexpression and mutation of FGF/FGFR induce regulatory changes in the signalling pathways. Chromosomal translocation facilitating FGFR fusion production aggravates drug resistance. Apoptosis is inhibited by FGFR-activated signalling pathways, reducing multiple anti-cancer medications’ destructive impacts. Angiogenesis and epithelial-mesenchymal transition (EMT) are facilitated by FGFRs-dependent signalling, which correlates with drug resistance and enhances metastasis. Further, lysosome-mediated drug sequestration is another prominent method of resistance. Inhibition of FGF/FGFR by following a plethora of therapeutic approaches such as covalent and multitarget inhibitors, ligand traps, monoclonal antibodies, recombinant FGFs, combination therapy, and targeting lysosomes and micro RNAs would be helpful. As a result, FGF/FGFR suppression treatment options are evolving nowadays. To increase positive impacts, the processes underpinning the FGF/FGFR axis’ role in developing drug resistance need to be clarified, emphasizing the need for more studies to develop novel therapeutic options to address this significant problem.  Communicated by Ramaswamy H. Sarma. © 2023 Informa UK Limited, trading as Taylor & Francis Group.en_US
dc.language.isoenen_US
dc.publisherTaylor and Francis Ltd.en_US
dc.sourceJournal of Biomolecular Structure and Dynamicsen_US
dc.subjectanti-cancer drugsen_US
dc.subjectchemoresistanceen_US
dc.subjectFGF/FGFR signallingen_US
dc.subjecttherapeutic approachesen_US
dc.titleThe FGF/FGFR signalling mediated anti-cancer drug resistance and therapeutic interventionen_US
dc.typeReviewen_US
Appears in Collections:Department of Biosciences and Biomedical Engineering

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