Ask about this productRelated genes to: FGFR1OP Blocking Peptide
- Gene:
- FGFR1OP NIH gene
- Name:
- FGFR1 oncogene partner
- Previous symbol:
- -
- Synonyms:
- FOP
- Chromosome:
- 6q27
- Locus Type:
- gene with protein product
- Date approved:
- 2003-05-21
- Date modifiied:
- 2014-11-19
Related products to: FGFR1OP Blocking Peptide
Related articles to: FGFR1OP Blocking Peptide
- Chemical carcinogen induced mouse models closely mimic environmentally driven human cancers and provide platforms for studying tumor initiation and progression. However, the behavior and diagnostic value of cell-free DNA (cfDNA) in such models remain poorly understood, limiting their translational utility for biomarker development. Considering the increasing clinical relevance of cfDNA for early detection and treatment monitoring, this study aimed to systematically characterize cfDNA dynamics and genomic alterations in B(a)P induced lung cancer and DMH induced colon cancer mouse models. The aim was to evaluate cfDNA as a minimally invasive biomarker that reflects tumor burden and its potential use in preclinical diagnostic and therapeutic studies. Mouse lung and colon cancers were induced using B(a)P and DMH, respectively. Plasma was collected at defined time points, cfDNA was isolated, quantified, and analyzed for integrity profiles. Real time assessment was performed using liquid biopsies of cell free DNA using NGS-WGS platform for non-invasive tumor detection in live animals, reserving histopathology for post-mortem analysis. Our results reveal circulating cell-free DNA mutations similar to those found in humans (Lung cancer: ALK, NRAS, NF1, BRAF, FGFR1OP, FGFR1, STK11ip, AKT1 & AK1S1; Colon cancer: APC, MYC, KRAS). We have performed gene enrichment and protein-protein interactions and found various cancer related genes. The histopathological examination revealed neoplastic changes that corroborated with genomic studies. This study establishes cfDNA as a potential surrogate biomarker in chemical carcinogen induced lung and colon cancer models, supporting its utility for early detection, disease monitoring, and preclinical therapeutic assessment. - Source: PubMed
Publication date: 2026/01/31
Trivedi Devangkumar DShaikh Aafrinbanu MPatel Saumya KDalai Sarat KumarBakshi Sonal R - The oral mucosa mirrors a range of latent systemic disorders, with potential clinical associations noted between autoimmune thyroid disease (AITD) and oral lichen planus (OLP). This study aims to explore the genetic relationship and underlying mechanisms mediating these conditions. - Source: PubMed
Publication date: 2024/12/31
Ni JieYe XinjianChen YitongFu HaizhouWu ZiqiongLu HaipingChen Qianming - Recent advances in human genetics have shed light on the genetic factors contributing to inflammatory diseases, particularly Crohn's disease (CD), a prominent form of inflammatory bowel disease. Certain risk genes associated with CD directly influence cytokine biology and cell-specific communication networks. Current CD therapies primarily rely on anti-inflammatory drugs, which are inconsistently effective and lack strategies for promoting epithelial restoration and mucosal balance. To understand CD's underlying mechanisms, we investigated the link between CD and the FGFR1OP gene, which encodes a centrosome protein. FGFR1OP deletion in mouse intestinal epithelial cells disrupted crypt architecture, resulting in crypt loss, inflammation, and fatality. FGFR1OP insufficiency hindered epithelial resilience during colitis. FGFR1OP was crucial for preserving non-muscle myosin II activity, ensuring the integrity of the actomyosin cytoskeleton and crypt cell adhesion. This role of FGFR1OP suggests that its deficiency in genetically predisposed individuals may reduce epithelial renewal capacity, heightening susceptibility to inflammation and disease. - Source: PubMed
Publication date: 2024/06/27
Trsan TihanaPeng VincentKrishna ChiragOhara Takahiro EBeatty Wandy LSudan RakiKanai MasahiroKrishnamoorthy PraveenRodrigues Patrick FernandesFachi Jose LGrajales-Reyes GaryJaeger NataliaFitzpatrick James A JCella MarinaGilfillan SusanNakata ToruJaiswal AlokStappenbeck Thaddeus SDaly Mark JXavier Ramnik JColonna Marco - Prostate cancer (PC) is a fatally aggressive urogenital cancer killing millions of men, globally. Thus, this study aims to identify key miRNAs, target genes, and drug targets associated with prostate cancer metastasis. The miRNA and mRNA expression datasets of 148 prostate tissue biopsies (39 tumours and 109 normal tissues), were analysed by differential gene expression analysis, protein interactome mapping, biological pathway analysis, miRNA-mRNA networking, drug target analysis, and survival curve analysis. The dysregulated expression of 53 miRNAs and their 250 target genes involved in Hedgehog, ErbB, and cAMP signalling pathways connected to cell growth, migration, and proliferation of prostate cancer cells was detected. The subsequent miRNA-mRNA network and expression status analysis have helped us in narrowing down their number to 3 hub miRNAs (hsa-miR-455-3p, hsa-miR-548c-3p, and hsa-miR-582-5p) and 9 hub genes (, ). Further investigations with different systems biology methods have prioritized and as potential genes involved in prostate cancer metastasis owing to their high mutation load and expression status. Interestingly, down regulation of seems to improve the prostate cancer patient survival rate beyond 150 months. The and genes are predicted to be targeted by hsa-miR-582-5p, besides some antibodies, PROTACs and inhibitory molecules. This study identified key miRNAs (miR-548c-3p and miR-582-5p) and target genes ( and ) as potential biomarkers for metastatic prostate cancers from large-scale gene expression data using systems biology approaches. - Source: PubMed
Publication date: 2022/11/16
Shinawi ThoraiaNasser Khalidah KhalidMoradi Fatima AmanullahMujalli AbdulrahmanAlbaqami Walaa FAlmukadi Haifa SElango RamuShaik Noor AhmadBanaganapalli Babajan - Primary biliary cholangitis (PBC) is a chronic cholestatic autoimmune liver disease that appears to be strongly influenced by genetic factors. Recently, an international meta-analysis of genome-wide association studies (GWAS) identified CC-Motif Chemokine Receptor-6 (CCR6) and FGFR1 Oncogene-Partner (FGFR1OP) as PBC-susceptibility genes. However, the lead single nucleotide polymorphisms (SNPs) of CCR6/FGFR1OP showed low linkage disequilibrium with each other in East Asian and European populations. Additionally, the primary functional variants and the molecular mechanisms responsible for PBC-susceptibility remain unclear. Here, among the PBC-susceptibility SNPs identified by high-density association mapping in our previous meta-GWAS (Patients: n = 10,516; healthy controls: n = 20,772) within the CCR6/FGFR1OP locus, rs9459874 and rs1012656 were identified as primary functional variants. These functional variants accounted for the effects of GWAS-identified lead SNPs in CCR6/FGFR1OP. Additionally, the roles of rs9459874 and rs1012656 in regulating FGFR1OP transcription and CCR6 translation, respectively, were supported by expression quantitative trait loci (eQTL) analysis and gene editing technology using the CRISPR/Cas9 system. Immunohistochemistry showed higher expression of CCR6 protein in the livers of patients with PBC than in those of a non-diseased control. In conclusion, we identified primary functional variants in CCR6/FGFR1OP and revealed the molecular mechanisms by which these variants confer PBC-susceptibility in an eQTL-dependent or -independent manner. The approach in this study is applicable for the elucidation of the pathogenesis of other autoimmune disorders in which CCR6/FGFR1OP is known as a susceptibility locus, as well as PBC. - Source: PubMed
Publication date: 2021/12/02
Hitomi YukiAiba YoshihiroUeno KazukoNishida NaoKawai YosukeKawashima MinaeYasunami MichioGervais OlivierIto MasahiroCordell Heather JMells George FNagasaki MasaoTokunaga KatsushiTsuiji MakotoNakamura Minoru