FGF3 siRNA_Lentivectors
- Known as:
- FGF3 siRNA_Lentivectors
- Catalog number:
- i007885d
- Product Quantity:
- 500ng
- Category:
- -
- Supplier:
- ABM
- Gene target:
- FGF3 siRNA_Lentivectors
Ask about this productRelated genes to: FGF3 siRNA_Lentivectors
- 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: FGF3 siRNA_Lentivectors
Related articles to: FGF3 siRNA_Lentivectors
- 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
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