Fibroblast growth factor 3 _ FGF3
- Known as:
- Fibroblast growth factor 3 _ FGF3
- Catalog number:
- GTX19894
- Product Quantity:
- 100 µg
- Category:
- -
- Supplier:
- ACR
- Gene target:
- Fibroblast growth factor 3 _ FGF3
Related genes to: Fibroblast growth factor 3 _ FGF3
- Gene:
- FGF3 NIH gene
- Name:
- fibroblast growth factor 3
- Previous symbol:
- INT2
- Synonyms:
- HBGF-3
- Chromosome:
- 11q13.3
- Locus Type:
- gene with protein product
- Date approved:
- 1986-01-01
- Date modifiied:
- 2019-04-23
Related products to: Fibroblast growth factor 3 _ FGF3
"Recombinant Mouse epidermal growth factor_EGF""Recombinant Mouse epidermal growth factor_EGF""Recombinant Mouse epidermal growth factor_EGF""Recombinant Mouse epidermal growth factor_EGF""Recombinant Mouse Vascular endothelial growth factor D_VEGFD ""Recombinant Mouse Vascular endothelial growth factor D_VEGFD ""Recombinant Mouse Vascular endothelial growth factor D_VEGFD ""Recombinant Mouse Vascular endothelial growth factor D_VEGFD "α-Mating Factor Pheromone, yeastα-Mating Factor Pheromone, yeast(-)-Indolactam V-combined with growth factors, can direct the differentiation of hESCs to Pdx1-expressing pancreatic progenitors(-)-Indolactam V-combined with growth factors, can direct the differentiation of hESCs to Pdx1-expressing pancreatic progenitors(Ala1)-PAR-4 (1-6) (mouse)
(Ala1)-Thrombin Receptor-Like 3 (1-6) (mouse), (Ala1)-Proteinase Activated Receptor 4 (1-6) (mouse), (Ala1)-Coagulation Factor II Receptor-Like 3 (1-6) (mouse), AYPGKF 98%(Ala1)-PAR-4 (1-6) amide (mouse)
AYPGKFamide, (Ala1)-Thrombin Receptor-Like 3 (1-6) amide (mouse), (Ala1)-Coagulation Factor II Receptor-Like 3 (1-6) amide (mouse), (Ala1)-Proteinase Activated Recepto(Ala1)_PAR_4 (1_6) (mouse) Salt Trifluoroacetate Binding _ Synonym (Ala1)_Thrombin Receptor_Like 3 (1_6) (mouse), (Ala1)_Proteinase Activated Receptor 4 (1_6) (mouse), (Ala1)_Coagulation Factor II Related articles to: Fibroblast growth factor 3 _ FGF3
- Lung squamous cell carcinoma (LUSC) is a prevalent subtype of lung cancer, which is primarily characterized by poor prognosis due to the lack of targeted therapies, while a large proportion of patients show limited response to chemotherapy. The present study aimed to identify predictive chemotherapy biomarkers based on genomic alterations in LUSC. Non-negative matrix factorization clustering was applied to classify patients with LUSC into distinct subgroups based on genomic alterations. Subsequently, chemotherapy efficacy was predicted via exploring gene signatures, and the results were validated using The Cancer Genome Atlas database (TCGA). A total of four distinct clusters were classified. Cluster 1 and loss-of-function ( LOF) variations were each independently associated with poor prognosis, irrespective of clinical stage. Based on the molecular characteristics of the initial clusters, the classification was further refined by further incorporating LOF and gene amplification (amp). Patients without LOF, who harbored amplification of at least one of nine specified genes [ and ] displayed the longest progression-free survival (PFS). By contrast, patients with LOF but lacking amplification of at least one of nine genes [Amp(9G)] exhibited the worst overall survival compared with the other subgroups. Validation in the TCGA database confirmed the prognostic significance of this classification, with Amp(9G) without LOF predicting the most favorable PFS, and LOF without Amp(9G) indicating the least favorable PFS. Therefore, a composite biomarker integrating Amp(9G) and LOF was identified as a prognostic indicator for patients with LUSC treated with first-line chemotherapy. Overall, the results of the present study suggest that the absence of LOF combined with the presence of Amp(9G) could be associated with improved response to first-line chemotherapy in LUSC. - Source: PubMed
Publication date: 2026/05/11
Li YuliHou TingLiu HongjieDu HaiweiQiu LiZhang YajingZhang GuipingTang Yuan - Vulvar squamous cell carcinoma (VSCC) comprises biologically distinct subtypes with divergent molecular profiles and clinical behaviors. In this study, we performed comprehensive genomic profiling of 48 primary VSCCs, integrating mutational and copy number data with HPV status and clinicopathological parameters. Tumors were stratified into HPV-associated (HPVA), HPV-independent (HPVI), and a third proposed subgroup characterized by HPV negativity and wild-type TP53 status. Overall, 650 somatic mutations were identified, with TP53, TERT promoter, NOTCH1, PIK3CA, and CDKN2A being the most frequently altered genes. HPVA VSCCs exhibited a higher mutational burden and enrichment of PIK3CA, NOTCH1, and MLL2 mutations, consistent with APOBEC-driven mutagenesis. HPVI VSCCs showed frequent TP53, TERTp, and CDKN2A mutations, along with an age-related mutational signature. Copy number alterations were more common in HPVI tumors, with recurrent amplifications in CCND1, FGF3/4/19, and CDK pathway genes. Six VSCCs lacked both HPV association and TP53 mutations, supporting the existence of a third molecular subtype, with frequent TERTp mutations and limited additional alterations. No significant survival differences were observed between subtypes, although nodal status remained prognostically relevant. These findings refine the molecular taxonomy of VSCC, support the recognition of a third genomic subgroup, and highlight subtype-specific therapeutic targets. - Source: PubMed
Publication date: 2026/05/11
Choschzick MHoesli LStergiou CRüschoff J H - Copy number variation (CNV), including genomic gains or losses of DNA segments ranging from kilobases to megabases, represents a major source of genetic diversity and can substantially alter gene dosage, regulation, and phenotype. Although CNVs have been catalogued across many dog breeds in prior large-scale efforts, breed-specific CNVs, defined as copy-number changes that are highly prevalent within one breed but rare or absent across others, have not been systematically investigated. To address this gap, we analyzed whole-genome sequencing data from 436 dogs representing 105 modern breeds and constructed a high-resolution catalog of breed-specific CNVs. - Source: PubMed
Publication date: 2026/04/27
Wang ShiyingLi ZichengBargmann WalkerChen ZhiyuanGruen JefferyHoh Josephine - Esophagogastric junction adenocarcinomas (EGJA) pose a serious threat to health and are increasing in incidence. The Siewert classification is the recognized anatomical classification system for guiding the surgical approaches in EGJA. However, the definition of EGJA and its optimal resection strategy remain controversial. This study aims to investigate the distinct molecular relationship between EGJA subtypes and other upper gastrointestinal cancers at the molecular level. - Source: PubMed
Publication date: 2026/03/24
Qin XiaoXu LinWang XiaozhenQi YouchaoZhong WeiShang BinWang ZhouChen Gang - Anaplastic lymphoma kinase () rearrangement has been identified in approximately 1% of lung squamous cell carcinomas (LUSCCs). Due to its rarity, the efficacy of anaplastic lymphoma kinase-tyrosine kinase inhibitors in the treatment of -positive LUSCCs is poorly characterized. - Source: PubMed
Publication date: 2026/03/24
Li ShengshuDu XiaosongZhang XinxinMa HaixiaYang YanliLi YuanWei QinChen YanLi HongweiBu PengLiu DujuanHan SongyanChen Deyi