Ask about this productRelated genes to: FGFR1 antibody
- Gene:
- FGFR1 NIH gene
- Name:
- fibroblast growth factor receptor 1
- Previous symbol:
- FLT2, KAL2
- Synonyms:
- H2, H3, H4, H5, CEK, FLG, BFGFR, N-SAM, CD331
- Chromosome:
- 8p11.23
- Locus Type:
- gene with protein product
- Date approved:
- 1992-02-25
- Date modifiied:
- 2019-04-23
Related products to: FGFR1 antibody
Related articles to: FGFR1 antibody
- Fibroblast growth factor 5 (FGF5) has been implicated in catagen induction, but its downstream mechanism remains unclear. Transforming growth factor-β2 (TGF-β2), another catagen-inducing factor, contributes to follicular epithelial cell apoptosis and regression of the lower portion of the hair follicle during catagen. This study examined whether TGF-β2 acts downstream of FGF5 signaling in human dermal papilla cells. FGF5 did not reduce keratinocyte viability, whereas TGF-β2 markedly decreased viability. In dermal papilla cells, FGF5 increased TGF-β2 expression, whereas FGF1 and FGF2 did not. These findings suggest that FGF5 may act upstream of TGF-β2 rather than as a direct final effector of follicular epithelial cell death. FGF5-induced TGF-β2 upregulation was suppressed by FGFR1 inhibition, p38 MAPK and Akt inhibition, and ETS-1 knockdown, but not by MEK/ERK inhibition. FGF5 did not markedly increase STAT3 phosphorylation. Cyclosporine A, which prolongs anagen in human hair follicles, reduced FGF5 expression in dermal papilla cells but not in outer root sheath cells. Together, these findings suggest that FGF5 may contribute to catagen induction indirectly by upregulating TGF-β2 expression in dermal papilla cells through FGFR1-dependent signaling involving p38 MAPK, Akt, and ETS-1. - Source: PubMed
Publication date: 2026/08/13
Hagiwara KentaKitamura HiroakiTsuchiya YukaYamanishi HaruyoIwabuchi Tokuro - Aberrant activation of fibroblast growth factor receptors (FGFRs) due to gene rearrangements or fusions, single-nucleotide variants, and copy number amplifications has been linked to several human cancers. Therefore, FGFRs increasingly recognized as a significant cancer therapy target. We herein designed and synthesized a series of quinoline derivatives as new type II covalent pan-FGFRs inhibitors based on our previous pan-FGFRs I-5. Of which, 18 exhibited a significant improvement in prominent pan-tumor inhibitory activities when substantially inhibited the kinase activities of FGFRs (FGFR1: IC = 5.70 nM, FGFR2: IC = 2.37 nM, FGFR3: IC = 3.78 nM, FGFR4: IC = 7.67 nM). Additionally, 18 blocked cellular FGFR phosphorylation and exhibited highly potent anti-tumor efficacy in vitro. Moreover, in vivo pharmacokinetic profiles and the safety property of 18 were found to be excellent (F % = 41.70%). Nevertheless, Oral administration of 18 significantly suppressed the tumor growth of the HuH-7 (TGI = 92.71%; 60 mg/kg, QD), SNU-16 (TGI = 49.80%; 30 mg/kg, QD) and RT112 (TGI = 67.61%; 30 mg/kg, QD) xenograft mouse models without obvious changes in body weight. - Source: PubMed
Publication date: 2026/08/16
Hu ShiheJiang CuihuaZhang XiaoyangChen KeLi XinJin Qiaomei - Pediatric gliomas constitute the largest group of pediatric brain tumors and are biologically distinct from adult gliomas. The 2021 fifth edition of the World Health Organization Classification of Tumors of the Central Nervous System (WHO CNS5) introduced a molecularly integrated classification system and recognized pediatric-type gliomas as distinct entities. In pediatric low-grade gliomas, activation of the MAPK pathway is a common molecular hallmark, with BRAF V600E mutations, BRAF fusions, FGFR1 alterations, and NF1-associated abnormalities representing major driver events. These discoveries have supported the development of targeted therapies, including dabrafenib plus trametinib, tovorafenib, and MEK inhibitors. In pediatric high-grade gliomas, diffuse midline glioma, H3 K27-altered, remains one of the most devastating tumors, although recent advances have led to the approval of dordaviprone in the United States. In addition, infant-type hemispheric gliomas frequently harbor NTRK, ROS1, or ALK fusions and may respond markedly to corresponding targeted therapies. Comprehensive molecular diagnostics have therefore become essential for accurate classification and treatment selection. This review summarizes the current WHO CNS5 classification of pediatric gliomas and highlights recent advances in molecularly guided therapeutic strategies. - Source: PubMed
Terashima Keita - Primary breast neuroendocrine carcinomas (NECs) are rare, high-grade malignancies that are frequently grouped with invasive breast carcinomas with neuroendocrine differentiation (IBC-NED), despite uncertain biological equivalence. We sought to define the clinicopathologic, immunophenotypic, and genomic features of breast NEC and to determine whether they represent a biologically distinct entity. - Source: PubMed
Publication date: 2026/08/13
Schwartz Christopher JMack TannerTravis WilliamZhang HongAbuhadra NourKiernan RisaMontagna GiacomoBrogi EdiPareja FresiaWen Hannah YRoss Dara S - Lung squamous cell carcinoma (LUSC) represents a predominant subtype of non-small cell lung cancer (NSCLC) with scarce effective targeted therapeutic options, rendering immune checkpoint inhibitor (ICI)-based regimens the standard first-line treatment for advanced-stage disease. Fibroblast growth factor receptor 1 (FGFR1) copy number (CN) gain is a prevalent genomic aberration in LUSC; nevertheless, the correlation between FGFR1 CN gain and ICI therapeutic efficacy has not yet been clarified. This retrospective single-center study aimed to explore the predictive value of FGFR1 CN gain in advanced LUSC patients receiving first-line ICI monotherapy or combination regimens. - Source: PubMed
Publication date: 2026/07/29
Mu ShuyaLi XingyuanSun YingjiaYu Yongfeng