FOXF1 antibody - N-terminal region (ARP31691_T100)
- Known as:
- FOXF1 (anti-) - N-terminal region (ARP31691_T100)
- Catalog number:
- arp31691_t100
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- FOXF1 antibody - N-terminal region (ARP31691_T100)
Related genes to: FOXF1 antibody - N-terminal region (ARP31691_T100)
- Gene:
- FENDRR NIH gene
- Name:
- FOXF1 adjacent non-coding developmental regulatory RNA
- Previous symbol:
- FOXF1-AS1
- Synonyms:
- lincFOXF1, onco-lncRNA-21
- Chromosome:
- 16q24.1
- Locus Type:
- RNA, long non-coding
- Date approved:
- 2012-04-25
- Date modifiied:
- 2018-07-25
- Gene:
- FOXF1 NIH gene
- Name:
- forkhead box F1
- Previous symbol:
- FKHL5
- Synonyms:
- FREAC1
- Chromosome:
- 16q24.1
- Locus Type:
- gene with protein product
- Date approved:
- 1995-06-05
- Date modifiied:
- 2016-10-05
Related products to: FOXF1 antibody - N-terminal region (ARP31691_T100)
Related articles to: FOXF1 antibody - N-terminal region (ARP31691_T100)
- Large scale sequencing efforts have defined up to 27 diagnostic entities in B-ALL, leaving few samples without subtype assignment. Extended genomic and transcriptomic profiling in routine diagnostics broadens the sample collection and holds the potential to identify novel B-ALL subtypes. By analyzing an aggregated set of 4,857 B-ALL patients from three cohorts, we identified a novel group of twenty cases (age 18-66 years, median: 34 years) characterized by a previously undescribed IGH::FENDRR rearrangement exclusive to this subtype (n=17/20), KRAS p.A146T/V/P mutations (n=17/20 vs. n=86/4,857; p<0.001) and distinct DNA-methylation/gene expression profiles, including overexpression of the lncRNA FENDRR and the transcription factor FOXF1 ('FOXF1/FENDRR') as well as JAK/STAT and RAS signaling signatures. A gene expression machine learning classifier identified FOXF1/FENDRR cases in two independent cohorts with high accuracy. Patients treated according to GMALL/GRAALL protocols showed very poor chemotherapy response with n=8/13 having induction failure or MRD ≥10-3 and n=8/12 remaining MRD positive after 1st consolidation / salvage. MRD-stratified intensification including blinatumomab (n=10) and/or allogenic stem cell transplantation (n=12) resulted in ongoing molecular remission in 13/16 cases. FOXF1/FENDRR patients represent a novel B-ALL subtype which might benefit from early immunotherapeutic treatment or targeted interventions. - Source: PubMed
Publication date: 2026/03/27
Bendig SonjaHartmann Alina MWessels WiebkeBeder ThomasKim RathanaPasset MarieGao QingsongWolgast NadineHorns Johanna MAlves Santos LeonardoIben KatharinaSteffen Fabio DCantoni LoredanaKehden BrittaChitadze GurandaKünstner AxelBusch HaukeBornhauser BeatBourquin Jean-PierreLeguay Thibaut TlBoissel NicolasGökbuget NicolaIacobucci IlariaMullighan Charles GClappier EmmanuelleBaldus Claudia DBrüggemann MonikaBastian Lorenz - Despite great progress in understanding the genomic basis of immature T-cell acute lymphoblastic leukemia/lymphoblastic lymphoma (T-ALL) and acute leukemias of ambiguous lineage (ALAL), there are still cases that lack defining genetic markers, complicating risk stratification and limiting targeted therapeutic options. Recent studies have shown that enhancer hijacking drives oncogene activation in approximately half of T-ALL cases, with the BCL11B enhancer frequently involved. Here, we describe a subtype of leukemia with a distinct gene expression signature, and immunophenotype characterized by positivity for immature (CD38), myeloid (CD13), T-lymphoid (cytoplasmic (c)CD3, CD7), and B-lymphoid markers (CD19, CD79a, CD10). This subtype is defined by the t(14;16)(q32;q24) translocation, which places the FOXF1 gene and its antisense long noncoding RNA gene FENDRR under the regulatory control of the BCL11B enhancer, leading to their ectopic transcriptional activation. Common concomitant genetic lesions are loss-of-function alterations of GATA3, CDKN2A/CDKN2B deletion and activating JAK/STAT and NOTCH1 pathway mutations. Patients were predominantly children and adolescents/young adults (AYA) and experienced poor treatment outcome. High-throughput drug screening of 176 compounds demonstrated efficacy of combined BCL2-family proteins and JAK/STAT signaling inhibitors. Additionally, the clinical use of tyrosine kinase inhibitors in some of these cases showed therapeutic efficacy. Collectively, these findings identify BCL11B-enhancer mediated deregulation of FOXF1/FENDRR as a hallmark of a subtype of high-risk lineage ambiguous leukemia that is potentially amenable to targeted therapeutic intervention. - Source: PubMed
Publication date: 2026/03/06
Di Giacomo DanikaPölönen PetriBardelli ValentinaKimura ShunsukePierini ValentinaPagliaro LucaArniani SilviaChang YunchaoGao QingsongMontefiori Lindsey EWu YimingPark Chun ShikWright William CVento FedericaWei HuimeiMatteucci CaterinaLei ShaohuaRosikiewicz WojciechNardelli CarlottaLema Fernandez Anair GracielaØstergaard AnnaBackhaus Emily ABaviskar PradyumnaCerrano MarcoLeoncin MatteoManabe AtsushiHirabayashi ShinsukeTakita JunkoHasegawa DaisukeMiyamoto SatoshiMacchiarulo AntonioXu JasonTeachey David TrentRoti GiovanniIacobucci IlariaLa Starza RobertaMecucci CristinaMullighan Charles G - The molecular classification of T-cell acute lymphoblastic leukemia (T-ALL) remains incomplete, limiting risk stratification and the development of targeted therapies. Enhancer hijacking is a critical oncogenic mechanism that deregulates proto-oncogenes by repositioning cis-regulatory regions via structural variants. Here, we performed an integrated analysis of pediatric and adult T-ALL and mixed phenotype acute leukemias (MPALs), using whole-genome and whole-transcriptome sequencing. This analysis identified a group of 14 patients with predominantly T-lineage neoplasms driven by a t(14;16)(q32;q24) translocation, harboring universal GATA3 mutations and CDKN2A/B deletions. Mechanistically, this translocation repositions the ThymoD locus downstream of BCL11B, causing monoallelic, ectopic overexpression of FENDRR and mesenchymal transcription factor genes FOXF1 and FOXC2, activating epithelial-mesenchymal transition (EMT) transcription signatures. Immunophenotypic and single-cell RNA-seq analyses revealed marked lineage ambiguity with myeloid and B-cell differentiation potentials specific to this subtype. Furthermore, functional analyses in CD34-positive cord blood cells demonstrated that FOXF1 overexpression promotes myeloid differentiation while suppressing T-cell differentiation, serving as a key factor for lineage specification. Clinically, this subtype was detected in 0.15-4.0% of T-ALL/MPAL cases depending on the cohort, showing a median age of 15 years and enrichment in adolescents and young adults (AYA). Importantly, patients with t(14;16)(q32;q24) have an extremely poor prognosis, showing a trend toward worse outcomes than high-risk groups such as KMT2A-rearranged early T-cell progenitor (ETP)-like, SPI1-rearranged, and LMO2 γδ-like T-ALLs. The unique molecular landscape and poor prognosis of patients with the t(14;16)(q32;q24) translocation underscore the need for the development of novel subtype-specific therapeutic approaches. - Source: PubMed
Publication date: 2026/03/05
Mimura KaitoKaino AkiraOchi YotaroChang Yu-HsuanSeki MasafumiTakeda JuneKatayama SaoriNiizuma HidetakaSasahara YojiMizoguchi YokoShimomura MaikoKoyamada RyosukeOno RintaroHasegawa DaisukeMitani KazukiKubota HirohitoYoshihara SatoshiHiramoto NobuhiroOtsuki AkihitoOkamura YasunobuKatsuoka FumikiKinoshita KengoHasegawa MasatakaTogo-Ohno MarinaMaeda HironaKakiuchi NobuyukiTakeuchi MaiSato-Otsubo AikoKato ShotaWatanabe KentaroKatayama KotoeImoto SeiyaShiraishi YuichiKoh KatsuyoshiSuenobu SouichiHiyama EisoGoyama SusumuKikuchi AtsuoOgawa SeishiKato MotohiroNannya YasuhitoTakita JunkoYoshida Kenichi - Pathogenic single-nucleotide variants (SNVs) and copy-number variant (CNV) deletions involving the transcription factor gene or CNV deletions of its distant lung-specific enhancer are responsible for alveolar capillary dysplasia with misalignment of pulmonary veins (ACDMPV), a rarely diagnosed lethal lung developmental disorder in neonates. In contrast to SNVs within and CNV deletions involving only the enhancer, larger-sized deletions involving and the adjacent, oppositely oriented lncRNA gene have additionally been associated with hypoplastic left heart syndrome and single umbilical artery (SUA). Here, in an ACDMPV infant without any congenital heart defect or SUA, we identified a small 5 kb CNV deletion that removed the paternal allele of and its promoter, leaving and its promoter intact. Reporter assay in the IMR-90 fetal cell line implied that the deletion may indeed not have significantly affected expression. It also showed a polarization of the - inter-promoter region consisting of its ability to increase the transcription of but not . Interestingly, this transcription-stimulating activity was suppressed in the presence of the promoter. Our data shed more light on the interactions between neighboring promoters of - and possibly other divergently transcribed mRNA-lncRNA gene pairs. - Source: PubMed
Publication date: 2023/10/09
Szafranski PrzemyslawStankiewicz Paweł - Genetically abnormal fibroblasts are notably more prevalent in colorectal cancer (CRC) than in adjacent normal tissue, emphasizing their significance in driving the heterogeneity of the tumor microenvironment. Functioning as a significant regulatory gene in the context of fibrosis, FOXF1 adjacent non-coding developmental regulatory RNA (FENDRR) has exhibited abnormal expression in colorectal cancer and interstitial localization in our experiments. However, current research on the role of FENDRR in cancer has focused solely on its impact on cancer cells. Its crucial role in the tumor stroma is yet to be explored. The goal of this study was to understand the relationship between atypical FENDRR expression, its distinct localization, and genetically abnormal fibroblasts in CRC. We aimed to establish the function of FENDRR within the stromal compartment of patients through bioinformatics. Our study confirmed that FENDRR suppresses cancer-associated fibroblasts by inhibiting their activation and collagen generation in CRC. Furthermore, our findings suggest that low FENDRR expression indicates a poor prognosis. Therefore, we propose that FENDRR is a promising therapeutic target for future studies in CRC. - Source: PubMed
Publication date: 2023/07/22
Li FengxiaYang JingLi YankunTan ZhenyuLi HuiZhang Nong