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
- 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 - Non-small cell lung cancer (NSCLC) remains a leading cause of cancer-related mortality worldwide, largely due to the supportive role of the tumor microenvironment (TME). Tumor-associated macrophages, particularly the M2 phenotype, are pivotal in promoting NSCLC progression. Exosomes, key mediators of intercellular communication, can transfer functional cargo from M2 macrophages to cancer cells, thereby regulating malignant behaviors. However, the specific mechanisms by which M2 macrophage-derived exosomes modulate NSCLC progression are not fully understood. - Source: PubMed
Publication date: 2026/08/11
Zhang DanWu WeiGe PengCao XiaQin YuanDong DanfengYang Jin - The fibroblast growth factor (FGF)/FGF receptor (FGFR) signaling system regulates tissue repair, angiogenesis, extracellular matrix remodeling, fibrosis, and bone metabolism. Although FGF/FGFR biology has been extensively studied in oncology, development, and fibrotic lung disease, its relevance to systemic autoimmune rheumatic diseases remains scattered across disease-specific and unevenly supported literatures. This narrative, evidence-informed review synthesizes current evidence on FGF/FGFR signaling in rheumatoid arthritis (RA), systemic lupus erythematosus/lupus nephritis (SLE/LN), systemic sclerosis (SSc), spondyloarthritis/psoriatic arthritis (SpA/PsA), and Sjögren's disease. We explicitly distinguish mechanistically supported axes from biomarker-level associations and extrapolated regenerative concepts. In RA, FGF10/FGFR1 and FGF2/FGFR3 have the strongest tissue-level support, linking relapse-prone synovial fibroblast niches, fibroblast-like synoviocyte activation, angiogenesis, and bone erosion. In SLE/LN, FGF23/Klotho is best interpreted as an emerging renal-metabolic and inflammatory biomarker axis rather than a validated therapeutic target, although reported associations with urinary MCP-1/CCL2 suggest testable links to renal chemokine-mediated inflammation. In SSc-ILD, nintedanib demonstrates that FGFR-containing multi-kinase networks are clinically tractable, but the FGFR-specific contribution remains unresolved. In SpA/PsA, FGF2-mediated angiogenesis-osteogenesis coupling and FGF7/FGFR2IIIb signaling provide candidate mechanisms for entheseal remodeling, whereas direct human entheseal validation is still lacking. In Sjögren's disease, FGF7/FGF10/FGFR2b signaling supports a regenerative hypothesis derived mainly from salivary gland developmental biology and organoid studies. We propose an axis-prioritization translational framework that specifies ligand-receptor pairs, patient subgroups, validation tissues, delivery strategies, pharmacodynamic endpoints, and clinical or imaging readouts. This review is not a systematic review or meta-analysis; rather, it provides a structured roadmap for tissue-level validation, longitudinal biomarker studies, and short-course proof-of-mechanism trials before clinical translation. - Source: PubMed
Publication date: 2026/07/22
Zhong ShengMeng XiaohuiXiang ZhengQiu GuoweiSun SongtaoXie JunXiao Lianbo - Doxorubicin (DOX) is a potent anthracycline chemotherapeutic agent, but its clinical use is limited by cumulative cardiotoxicity. Exercise, particularly high-intensity interval training (HIIT), has emerged as an effective non-pharmacological strategy to counteract chemotherapy-induced cardiac injury. However, the molecular mechanisms underlying the cardioprotective effects of HIIT remain unclear. This study aimed to determine whether HIIT attenuates DOX-induced cardiotoxicity via activation of the fibroblast growth factor 21 (FGF21)/sirtuin 1 (SIRT1) signalling pathway in rats. Thirty-three male Wistar rats (200-250 g) were randomly assigned to three groups (n = 11 each): control (CONTROL), DOX-treated sedentary (DOX-Sed) and DOX-treated HIIT (DOX-HIIT). DOX-induced cardiotoxicity was induced by intraperitoneal DOX injections (12 mg/kg cumulative dose over 12 days). After confirmation of cardiac dysfunction by echocardiography, the DOX-HIIT group completed an 8 week treadmill HIIT programme (three sessions per week, five intervals of 4 min at 85%-90% of maximal O uptake separated by 2 min at 50%-60% of maximal O uptake). Cardiac function, oxidative stress markers, inflammatory cytokines, plasma levels of FGF21 and protein expression of FGFR1 and the SIRT1/AMPK/Nrf2 pathway were assessed. HIIT improved survival (81.8% vs. 63.6% in DOX-Sed), prevented weight loss and ameliorated left ventricular systolic dysfunction, as evidenced by increased ejection fraction and fractional shortening (P < 0.05). HIIT reduced cardiac interleukin-6, tumor necrosis factor-α, interleukin-1β and malondialdehyde levels while elevating antioxidant enzyme activities. Mechanistically, HIIT increased plasma FGF21 and phosphorylated FGFR1 and upregulated SIRT1, LKB1 and phosphorylated AMPK, leading to activation of the Nrf2/HO-1 antioxidant pathway. Therefore, HIIT-induced FGF21 has a potential therapeutic effect on cardiac function in DOX-induced cardiotoxicity through activation of the FGF21/SIRT1/LKB1/AMPK/Nrf2/HO-1 signalling pathway. - Source: PubMed
Publication date: 2026/08/04
Farahani MahdiyehGaeini Abbas AliGhardashi Afousi AlirezaBorjian Fard Mahboobeh