| Literature DB >> 33352931 |
Alessio Ardizzone1, Sarah A Scuderi1, Dario Giuffrida2, Cristina Colarossi2, Caterina Puglisi3, Michela Campolo1, Salvatore Cuzzocrea1, Emanuela Esposito1, Irene Paterniti1.
Abstract
Despite pharmacological treatments and surgical practice options, the mortality rate of astrocytomas and glioblastomas remains high, thus representing a medical emergency for which it is necessary to find new therapeutic strategies. Fibroblast growth factors (FGFs) act through their associated receptors (FGFRs), a family of tyrosine kinase receptors consisting of four members (FGFR1-4), regulators of tissue development and repair. In particular, FGFRs play an important role in cell proliferation, survival, and migration, as well as angiogenesis, thus their gene alteration is certainly related to the development of the most common diseases, including cancer. FGFRs are subjected to multiple somatic aberrations such as chromosomal amplification of FGFR1; mutations and multiple dysregulations of FGFR2; and mutations, translocations, and significant amplifications of FGFR3 and FGFR4 that correlate to oncogenesis process. Therefore, the in-depth study of these receptor systems could help to understand the etiology of both astrocytoma and glioblastoma so as to achieve notable advances in more effective target therapies. Furthermore, the discovery of FGFR inhibitors revealed how these biological compounds improve the neoplastic condition by demonstrating efficacy and safety. On this basis, this review focuses on the role and involvement of FGFRs in brain tumors such as astrocytoma and glioblastoma.Entities:
Keywords: Fisogatinib; Futibatinib; astrocytoma; brain tumors; fibroblast growth factors (FGFs); fibroblast growth factors receptors (FGFRs); glioblastoma
Year: 2020 PMID: 33352931 PMCID: PMC7766440 DOI: 10.3390/cancers12123825
Source DB: PubMed Journal: Cancers (Basel) ISSN: 2072-6694 Impact factor: 6.639