FGFR2
- Known as:
- FGFR2
- Catalog number:
- Y214020
- Product Quantity:
- 200ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- FGFR2
Related genes to: FGFR2
- Gene:
- FGFR2 NIH gene
- Name:
- fibroblast growth factor receptor 2
- Previous symbol:
- KGFR, BEK, CFD1, JWS
- Synonyms:
- CEK3, TK14, TK25, ECT1, K-SAM, CD332
- Chromosome:
- 10q26.13
- Locus Type:
- gene with protein product
- Date approved:
- 1991-05-09
- Date modifiied:
- 2019-04-23
Related products to: FGFR2
Related articles to: FGFR2
- The target-oriented synthesis of diethylene glycol-linked bis-imidazo- and bis-thiazolo ring-fused mono-, bi-, and tricyclic derivatives was accomplished using inexpensive reagents, bis-phenacyl bromide derivative 4, and thiosemicarbazone 6. The diethylene glycol-linked architectures included bis(thiazolo[3,2-a]pyrimidinone) derivatives 8a,b, bis(imidazo-azole) derivatives 12-14, bis(imidazo-thiazole) derivatives 17,18, and bis-thiazoles 20a-g. Cytotoxic evaluation against liver, lung, colon, and prostate human tumor cell lines found remarkable selectivity to hepatocellular carcinoma (HepG2) cells. The most potent bis-imidazo- and bis-thiazolo-fused derivatives 8a,b, 12 and 13 demonstrated cytotoxicity against HepG2 cells (IC 6.8-17.8 µM) with exceptional selectivity (SI 5.6-14.6) compared with cisplatin (SI 2.4). Further screening of their VEGFR-2 TK and FGFR-2 TK inhibition showed that 8a had moderate activity, whereas phenyl-substituted derivative 8b displayed promising anti-VEGFR-2 and remarkable anti-FGFR-2 activities, with IC 0.19 ± 0.01 and 0.03 ± 0.01 µM, respectively, compared with the reference drugs sorafenib (IC 0.12 ± 0.01) and staurosporine (IC 0.03 ± 0.01 µM). The inhibition of VEGFR-2 and FGFR-2 TKs was supported by molecular docking studies, with compound 8b showing binding affinity to the VEGFR-2 and FGFR-2 ATP binding pockets. Pharmacokinetics and ADMET drug-likeness evaluation indicated that bis(thiazolo[3,2-a]pyrimidinone) derivatives 8a and 8b have drug-like properties. - Source: PubMed
Al-Hussain Sami AAlharbi Abdulrahman SMuhammad Zeinab AHalim Alyaa S AbdelZaki Magdi E ABagley Mark CKassab Refaie M - Skeletal Class III malocclusions are frequently associated with craniosynostosis syndromes, resulting in distinctive facial and dental anomalies. Among these, Crouzon syndrome is characterised by mutations in the FGFR2 gene, leading to premature fusion of the cranial vault, cranial base, orbital and maxillary sutures. The phenotypic expression of this congenital condition varies according to the timing and pattern of sutural fusion. This report details the clinical features and management of a 16-year-old male patient presenting with moderate skeletal Class III malocclusion as a manifestation of Crouzon syndrome. The present case fell within the spectrum of conventional non-surgical management. Adjunctive chin cup therapy initiated after rapid maxillary expansion aided in controlling residual mandibular growth, contributing to a favourable outcome in a hypodivergent pattern. Functional and aesthetic outcomes were markedly enhanced, and the results remained stable at the one-year follow-up assessment. Excellent compliance over 36 months contributed to treatment success and stability. - Source: PubMed
Publication date: 2026/09/25
Kumar SnigdhaShastri DiptiSingh Gulshan K - Fibroblast growth factor receptor 2 (FGFR2) fusions are identified in approximately 10-16% of patients with intrahepatic cholangiocarcinoma (iCCA) and represent actionable targets, with several FGFR inhibitors approved for clinical use. To evaluate the clinical utility and assay performance of an amplicon-based next-generation sequencing (NGS) approach in this setting, we assessed fusion detection using the Oncomine Comprehensive Assay Plus (OCA-P). A total of 75 formalin-fixed paraffin-embedded (FFPE) specimens from biliary, pancreatic, and ampullary malignancies submitted for FGFR2 fusion testing between 1 March 2023 and 30 June 2024 were retrospectively analyzed, including 40 cases of iCCA. All iCCA specimens were successfully analyzed. fusions were detected exclusively in iCCA, yielding a detection rate of 20%. RNA concentrations in iCCA specimens ranged from 0.02 ng/µL to 104 ng/µL; six cases (15%) exhibited yields below 1 ng/µL and 10 cases (25%) ranged between 1 and 2 ng/µL. Despite limited RNA input, OCA-P demonstrated robust performance, successfully identifying fusions at concentrations below 2 ng/µL, levels typically considered suboptimal for partner-agnostic NGS approaches. These findings support the robustness and clinical utility of the OCA-P assay for reliable fusion detection in iCCA, particularly in specimens with limited RNA input. - Source: PubMed
Publication date: 2026/09/15
Guertin SimonSina NiloofarKron KenCraddock Kenneth JMcCarty AmyHwang David MHuang Weei-Yuarn - Basal cell carcinosarcomas (BCCSs) are rare, aggressive biphasic epithelial-mesenchymal neoplasms typically occurring in elderly patients. Their nonspecific clinical presentation may mimic inflammatory disorders, necessitating histopathological examination. We characterize a novel cutaneous BCCS with prominent trichoblastic differentiation, clinically mimicking ulcerative pyoderma gangrenosum. Although morphologically resembling trichoblastic carcinosarcoma (TBCS), the tumor retained a BCC-associated genetic signature, supporting a basal cell rather than a primary trichoblastic lineage. We therefore propose the provisional designation "basal cell carcinosarcoma with divergent trichoblastic differentiation (BCCS-DTB)", suggesting acquired follicular lineage plasticity within a Hedgehog-driven, UV-mutagenized BCC clone. Shared molecular alterations across epithelial and sarcomatous components support monoclonality and an inside-out epithelial-mesenchymal transition (EMT) model, with progressive acquisition of trichoblastic and sarcomatous features. The patient's young age, unusual tumor location, and development during the COVID-19 pandemic raise the hypothesis of additional environmental influences. Detection of associated spike protein and Snail expression is hypothesis-generating given their reported association with EMT. Further cases are required to validate the molecular profile for diagnostic and therapeutic relevance involving Hedgehog, FGFR2, and mTOR signaling. - Source: PubMed
Publication date: 2026/09/16
Georg PaulBlum RolandHunger RobertDislich BastianWolf Ronald - Cholangiocarcinoma (CCA) includes a heterogeneous group of malignancies arising from the biliary epithelium, anatomically classified into intrahepatic, perihilar, and distal disease, with subtype-specific molecular features and treatment implications. Intrahepatic CCA is further subclassified into small- and large-duct variants. Most patients present with advanced, unresectable disease, and 5-year survival rates remain poor. For over a decade, gemcitabine-cisplatin (Gem-Cis) combination chemotherapy was the only established first-line standard of care. More recently, the addition of immune checkpoint inhibitors (IO), durvalumab and pembrolizumab, to Gem-Cis in the TOPAZ-1 and KEYNOTE-966 trials, respectively, improved overall survival, establishing chemoimmunotherapy as the new first-line therapy. Given the high prevalence of actionable alterations in CCA, comprehensive molecular profiling has become indispensable for second-line treatment selection and front-line clinical trial eligibility. fusions, mutations, and amplification are among the most relevant, with several targeted agents now available in the second-line setting. Despite this progress, most patients exhaust treatment options within the first year, highlighting the need for further therapeutic advances. Emerging strategies include novel targeted agents, antibody-drug conjugates, locoregional approaches for liver-limited disease, and circulating tumor DNA monitoring for real-time treatment adaptation. The immunosuppressive tumor microenvironment and the absence of reliable predictive biomarkers for IO response remain key challenges that ongoing research aims to address. This review summarizes current evidence for the management of advanced CCA, focusing on molecular profiling, treatment sequencing, and emerging therapies. - Source: PubMed
Publication date: 2026/09/23
Saj FenXavier Camila BragancaGoyal LipikaJavle MilindPant Shubham