Fibroblast growth factors (FGFs) and their receptors (FGFRs) have been extensively investigated in solid malignancies. In various solid tumors, FGF/FGFR genomic alterations, such as gene amplification, rearrangements or mutations are relevant oncogenic drivers and therefore attractive therapeutic targets.
FGFR Tyrosine Kinase Inhibitors (TKIs) have recently received FDA approval for the treatment of intrahepatic cholangiocarcinomas and urothelial cancers with susceptible FGFR2 or FGFR3 alterations. However, clinical trials testing FGFR TKIs in other solid malignancies, such as breast cancer (BC) with gene amplification, have delivered disappointing results.
FGFR tyrosine kinase inhibitors demonstrated a relevant efficacy in solid cancers harboring FGFRs rearrangements, but these alterations are very rare in BCs. Instead, BCs, particularly ER+ BCs, harbor FGFR1-4 amplification. Further preclinical investigation is required to better dissect the role of FGFR signaling in breast cancer and the impact of such genomic alterations in these cancers.
This Research Topic aims to create a platform to discuss the role of FGFR signaling in breast cancer. We welcome manuscripts focused on, but not limited to:
- studies exploring the efficacy of FGFR inhibitors in FGFR1-4-amplified BCs;
- the role of non-genomic alterations of FGFRs, such as overexpression of the receptors in the nucleus of cancer cells;
- reviews aiming to synthesize the current knowledge about FGFR signaling in breast cancer and challenges for the development of future treatment strategies.
Please note: manuscripts consisting solely of bioinformatics or computational analysis of public genomic or transcriptomic databases which are not accompanied by validation (independent cohort or biological validation in vitro or in vivo) are out of scope for this section and will not be accepted as part of this Research Topic.
Fibroblast growth factors (FGFs) and their receptors (FGFRs) have been extensively investigated in solid malignancies. In various solid tumors, FGF/FGFR genomic alterations, such as gene amplification, rearrangements or mutations are relevant oncogenic drivers and therefore attractive therapeutic targets.
FGFR Tyrosine Kinase Inhibitors (TKIs) have recently received FDA approval for the treatment of intrahepatic cholangiocarcinomas and urothelial cancers with susceptible FGFR2 or FGFR3 alterations. However, clinical trials testing FGFR TKIs in other solid malignancies, such as breast cancer (BC) with gene amplification, have delivered disappointing results.
FGFR tyrosine kinase inhibitors demonstrated a relevant efficacy in solid cancers harboring FGFRs rearrangements, but these alterations are very rare in BCs. Instead, BCs, particularly ER+ BCs, harbor FGFR1-4 amplification. Further preclinical investigation is required to better dissect the role of FGFR signaling in breast cancer and the impact of such genomic alterations in these cancers.
This Research Topic aims to create a platform to discuss the role of FGFR signaling in breast cancer. We welcome manuscripts focused on, but not limited to:
- studies exploring the efficacy of FGFR inhibitors in FGFR1-4-amplified BCs;
- the role of non-genomic alterations of FGFRs, such as overexpression of the receptors in the nucleus of cancer cells;
- reviews aiming to synthesize the current knowledge about FGFR signaling in breast cancer and challenges for the development of future treatment strategies.
Please note: manuscripts consisting solely of bioinformatics or computational analysis of public genomic or transcriptomic databases which are not accompanied by validation (independent cohort or biological validation in vitro or in vivo) are out of scope for this section and will not be accepted as part of this Research Topic.
