Ask about this productRelated genes to: FIP1L1 antibody
- Gene:
- FIP1L1 NIH gene
- Name:
- factor interacting with PAPOLA and CPSF1
- Previous symbol:
- -
- Synonyms:
- DKFZp586K0717, FIP1
- Chromosome:
- 4q12
- Locus Type:
- gene with protein product
- Date approved:
- 2003-03-03
- Date modifiied:
- 2015-08-25
Related products to: FIP1L1 antibody
Related articles to: FIP1L1 antibody
- FIP1-like-1-platelet-derived growth factor receptor-α (FIP1L1-PDGFRA)-positive hypereosinophilic syndrome (HES) is a rare myeloproliferative neoplasm characterized by persistent eosinophilia and occurs predominantly in middle-aged adults. We report a 15-year-old boy with FIP1L1-PDGFRA-associated chronic eosinophilic leukemia who initially presented with persistent hemorrhagic crusts on the lower lip, an uncommon mucocutaneous manifestation resulting from thrombotic aggregates of eosinophil granule proteins. This case is followed by a systematic literature review of pediatric FIP1L1-PDGFRA-positive HES to further characterize its clinical features and outcomes in children. - Source: PubMed
Publication date: 2026/04/21
Chiang Yi-KuanHo Yi-Hsin - Accurate detection of driver gene fusions is essential for the diagnosis, treatment, and prognostic prediction of hematologic malignancies. Despite increasing reliance on RNA sequencing (RNA-seq) for fusion detection, its algorithms have not been sufficiently examined for their ability to detect clinically relevant driver fusions. We evaluated 12 algorithms using conventional RNA-seq from 170 cell lines and targeted RNA-seq from 26 cell lines and 165 clinical samples. The true positive rate, based on 61 and 24 driver fusion-cell line pairs for conventional and targeted RNA-seq, varied between 0.41-1 (median 0.81) and 0-1 (median 0.85), respectively. Many algorithms failed to detect fusions resulting from small deletions (including STIL::TAL1 and FIP1L1::PDGFRA), lowly expressed fusions, and IGH fusions (DUX4::IGH and IGH::NSD2). Targeted RNA-seq more sensitively detected driver fusions than conventional RNA-seq, especially lowly expressed ones. One algorithm, Arriba, detected all driver fusions. These findings will inform algorithm selection in clinical settings. - Source: PubMed
Publication date: 2026/04/04
Tamura ZenSaito YukiKogure YasunoriOshikawa-Kumade YujiFukuhara SuguruShingaki SumitoKariyazono HirokazuKikukawa YoshiyaIto YutaMizuno KotaShiraishi YuichiKatayama KotoeImoto SeiyaIzutsu KojiMurakami KoichiKoya JunjiKataoka Keisuke - Benralizumab, an eosinophil-depleting anti-IL-5 receptor α antibody, has demonstrated efficacy in severe eosinophilic asthma and eosinophilic granulomatosis with polyangiitis and shown promising results in hypereosinophilic syndrome (HES). NATRON was a randomized, double-blind placebo-controlled phase 3 study evaluating the efficacy and safety of benralizumab in FIP1L1::PDGFRA-negative HES. The primary endpoint was time to first HES flare. In total, 133 patients (median (range) age 51 (14-87) years, 62% female) were randomized (1:1) to receive benralizumab 30 mg every 4 weeks or placebo for 24 weeks, in addition to background therapy. Benralizumab significantly reduced the risk of first flare versus placebo (hazard ratio 0.35, 95% CI 0.18 to 0.69, P = 0.0024). Adverse events occurred in 64.2% and 66.7% of benralizumab- and placebo-treated patients, respectively. Benralizumab's safety was consistent with its known profile. These results demonstrate the efficacy and safety of add-on benralizumab in the treatment of HES. ClinicalTrials.gov identifier: NCT04191304 . - Source: PubMed
Publication date: 2026/03/31
Ogbogu Princess URoufosse FlorenceAkuthota PraveenKuna PiotrGroh MatthieuReiter AndreasYokota AkiraSiddiqui Salman HMutsaers Pim G N JLi BingKhoury PaneezBahadori Lila MBednarczyk ArturBouma GerbenBrooks Laura GFerreira JorgeGrindebacke HannaHo Calvin NJain PriyaPalmer Rebecca LJison Maria LKlion Amy D - This review examines the rapidly evolving landscape of myeloproliferative hypereosinophilic syndromes (HES) and related neoplasms. We aim to synthesize current understanding of their diverse molecular drivers, evaluate the efficacy of established and novel targeted therapies, and identify critical research gaps. The goal is to provide a clinically relevant update on how molecular precision is reshaping the diagnosis and management of these rare, often aggressive hematologic malignancies beyond the established standard of imatinib. - Source: PubMed
Publication date: 2026/03/07
Hanna ColetteRizkallah JoeCharbel NicoleSakkal ShereenHaddad Fadi G - Myeloid neoplasms harboring the FIP1L1-PDGFRA fusion gene infrequently manifest as acute cerebral infarction. The F/P fusion gene induces proliferation within the eosinophilic lineage, resulting in a clonal hypereosinophilic syndrome that may lead to cerebral infarction. This condition demonstrates a high responsiveness to imatinib therapy. - Source: PubMed
Publication date: 2026/02/10
Cheng MinShi WenjieXu JinWei DoudouSun YueJiang QianLi Yongjie