Ask about this productRelated genes to: FGFR2 antibody
- 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 antibody
Related articles to: FGFR2 antibody
- - Source: PubMed
- Exposure to fine particulate matter (PM.) is increasingly recognized as a breast cancer risk factor, yet its combined effect with genetic susceptibility is unclear. This study examined the effects of PM. and genetic variants ESR1 (Estrogen Receptor 1) rs2046210 and FGFR2 (Fibroblast Growth Factor Receptor 2) rs2981582 on breast cancer risk. - Source: PubMed
Publication date: 2026/04/17
Liaw Yi-ChingWu Chih-DaLiaw Yi-ChiaHsu Shu-YiChao Mu-RongHu Chiung-WenLiaw Yung-Po - The hallmarks of cancer, first proposed in 2000, have since provided a unified framework for understanding the complexity of carcinogenesis. This conceptual model has profoundly influenced the treatment landscape of primary liver cancer, which includes hepatocellular carcinoma (HCC, ∼85%) and intrahepatic cholangiocarcinoma (iCCA, 10%)-malignancies with high mortality. Key hallmarks exhibited by HCC include sustaining proliferative signaling, inducing or accessing vasculature, and avoiding immune detection. Over the past two decades, outcomes for patients with advanced HCC have significantly improved with immunotherapies. iCCA is characterized by hallmarks such as sustaining proliferative signaling, deregulating cellular metabolism, and avoiding immune detection. Unlike HCC, roughly 45% of iCCA harbor alterations amenable to precision oncology approaches, including fibroblast growth factor receptor 2 (FGFR2) fusions, isocitrate dehydrogenase 1 (IDH1) mutations, ERBB2 alterations, and BRAF mutations. In this review, we explore how this framework has reshaped liver cancer care and discuss the resulting breakthroughs in management and emerging directions that may further improve therapeutic strategies. - Source: PubMed
Llovet Josep MPinyol RoserAffo SilviaYarchoan MarkGores Gregory JKelley Robin KateLowe Scott WSia DanielaVillanueva Augusto - Gulf War Illness (GWI) is a chronic neuroimmune condition affecting veterans of the 1990-91 Gulf War. Current treatments primarily target symptom relief, and the biological mechanisms underlying GWI remain poorly understood. Using a validated mouse model of Gulf War Illness (GWI) combining corticosterone (CORT) and diisopropyl fluorophosphate (DFP) exposure to induce stress- and toxicant-related neuroimmune priming, we examined how prior exposure alters molecular responses to a subsequent immune challenge. Male mice were exposed to CORT and DFP with repeated intermittent CORT, followed by lipopolysaccharide (LPS) or saline to assess transcriptional and epigenetic changes in brain and blood. We analysed transcript abundance, chromatin accessibility, and DNA methylation in the hippocampus, frontal cortex, and blood at 6 h, 12 h and 24hrs after LPS challenge (3-4 mice per group). We identified widespread transcriptional changes and dynamic chromatin accessibility following LPS exposure, with DNA methylation modifications that persisted in the hippocampus and blood. Thirty-three genes, including , , , and , were differentially expressed and methylated in both hippocampus and blood across all time points. These genes clustered in immune- and glial-related pathways. Transcription factor analysis revealed enrichment of NF-κB, CREB1, EGR1, JUN, and MYC binding motifs in regions with differential methylation. Our findings identify novel candidate biomarkers in peripheral blood that reflect brain molecular changes, providing a new framework for elucidating the long-term epigenetic impacts of stress and toxicant exposure in GWI. - Source: PubMed
Publication date: 2026/03/11
Sasaki AKelly K AMichalovicz L TAshbrook D GWijenayake SO'Callaghan J PMcGowan P O - Characterization of molecular features of cholangiocarcinoma (CCA) has questioned the traditional, anatomy-based classification scheme and has alternatively suggested biology-based classifications. Intrahepatic CCA has been classified into small-duct and large-duct types, and the latter is histologically and molecularly almost identical to perihilar CCA. Although distal and perihilar CCA have been classified together, they have different molecular abnormalities, with MDM2 amplification observed in 15% of perihilar CCA cases but in none of the distal CCA cases. FGFR2 and IDH1 are two main drug targets in small-duct intrahepatic CCA, and mismatch repair (MMR) deficiency is most common in small-duct intrahepatic CCA. In contrast, HER2 is a promising target for extrahepatic CCA and gallbladder cancer, as HER2 overexpression is seen in 17%-30% of cases. Classification of intrahepatic CCA is often challenging on biopsy specimens; however, recognition of pitfalls (e.g., hybrid morphology) will help avoid misclassification. Staining for ancillary markers, including CRP, albumin-ISH, and S100P, is also useful. Accurate distinction between distal CCA and pancreatic head cancer has become increasingly important, particularly in unresectable or borderline resectable cases, as systemic treatment strategies differ between these entities. Although these two neoplasms share many morphological and immunohistochemical features, the presence of clear or foamy cancer cells in biopsy specimens is uncommon in dCCA and may favour pancreatic ductal carcinoma. - Source: PubMed
Publication date: 2026/04/16
Zen Yoh