CD114 _ G_CSFR _ GCSFR Antibody
- Known as:
- CD114 _ G_CSFR _ GCSFR Antibody
- Catalog number:
- 10218-MM01
- Product Quantity:
- 100
- Category:
- -
- Supplier:
- Smart Serology
- Gene target:
- CD114 _ G_CSFR GCSFR Antibody
Related genes to: CD114 _ G_CSFR _ GCSFR Antibody
- Gene:
- CSF3R NIH gene
- Name:
- colony stimulating factor 3 receptor
- Previous symbol:
- CD114
- Synonyms:
- GCSFR
- Chromosome:
- 1p34.3
- Locus Type:
- gene with protein product
- Date approved:
- 1990-12-10
- Date modifiied:
- 2019-04-23
Related products to: CD114 _ G_CSFR _ GCSFR Antibody
Related articles to: CD114 _ G_CSFR _ GCSFR Antibody
- Quizartinib is a FMS-like tyrosine kinase 3 (FLT3) inhibitor indicated for FLT3 internal tandem duplication (FLT3-ITD)-positive acute myeloid leukemia (AML). We aimed to evaluate quizartinib resistance mechanisms, in addition to efficacy and safety outcomes, in patients with relapsed or refractory FLT3-ITD-positive AML. This multicenter, single-arm study in Japan (jRCTs071200015) enrolled 18 patients between May 2020 and December 2022. Of these, 15 patients received oral quizartinib (up to 53 mg once daily) for up to 12 cycles of 28 days each, then were followed for 12 months. The primary endpoint was to evaluate the type and rate of quizartinib resistance mutations; secondary endpoints included composite complete remission (CRc) rate, overall response rate (ORR), hematopoietic stem cell transplantation (HSCT) rate, relapse-free survival (RFS), overall survival (OS), and adverse events (AEs). Among seven evaluable patients, acquired mutations were detected in four patients (NF1 [R2616X], CSF3R [Q754X], NRAS [G13R], and FLT3 [D835Y] in one patient each), while loss of FLT3-ITD was observed in two patients. In efficacy analyses (n = 15), CRc rate was 66.7% (95% confidence interval [CI], 38.4-88.2), ORR was 73.3% (44.9-92.2), and median OS was 13.6 months (5.4-not evaluable). Three patients (20.0%) received HSCT directly after quizartinib; in these patients, median RFS was 8.5 months (95% CI, 6.2-not evaluable). Grade ≥ 3 non-hematologic AEs and grade 1 QT prolongation were each reported in three patients (20.0%). These data offer additional information on potential resistance mechanisms in patients with relapsed or refractory FLT3-ITD-positive AML. Trial Registration: Japan Registry of Clinical Trials (jRCTs071200015). - Source: PubMed
Publication date: 2026/08/12
Semba YuichiroMiyamoto ToshihiroKasahara SenjiKikushige YoshikaneMaeda TakahiroYoshimoto GoichiOta ShuichiSaito AkioNajima YuhoHosoi HirokiNiiya DaigoKato KojiNagafuji KojiAkasaka TakashiKamimura TomohikoTakita AtsushiNarahara MaikoToki TadashiIwanaga KoichiYonemoto KojiHarada MineAkashi Koichi - Fulvic acid (FA) is a mineral-based traditional Chinese medicine, which is commonly used to treat gastrointestinal diseases. The aim of this study is to investigate the protective effects of FA against 5-FU-induced intestinal injury in vivo and elucidate its potential mechanisms. - Source: PubMed
Publication date: 2026/07/27
Wang LeiDai WeifengYuan ChengQin YiChen YonggangChen JieZhang Mi - Myeloid/lymphoid neoplasms with tyrosine kinase fusions are rare but important because many are highly sensitive to targeted therapy. PDGFRB rearrangements are well-established drivers, whereas TPM3 is an exceptionally rare fusion partner. - Source: PubMed
Publication date: 2026/08/04
Lambert FrédéricKoopmansch BenjaminCarazo Rafael FernandezDardenne ElisaKeutgens AuroreVanstraelen GaëtanCollins PatrickMenten CatherineVertenoeil Gaëlle - This study investigated how cytosine-cytosine-adenine-adenine-thymine (CCAAT)/enhancer-binding protein alpha (CEBPA) mutation sites and types affect the prognosis of acute myeloid leukaemia (AML). It specifically analysed the clinical and genetic features of AML patients harbouring CEBPA basic leucine zipper in-frame insertion/deletion (CEBPA bZIP-InDel-inf) mutations and identified prognostic factors in this subtype. Prognostic factors in CEBPA bZIP-InDel-inf subgroup were examined in depth. Overall survival (OS) and relapse-free survival (RFS) censoring models were built, informative censoring was adjusted using inverse probability of censoring weighting, and stabilized weights were applied in weighted Cox regression analyses. Risk scores for OS and RFS were then developed from multivariable results. Ninety-three patients with CEBPA mutation, 56 had CEBPA bZIP-InDel-inf. Compared with CEBPA bZIP-InDel-inf, CEBPA non-InDel had a worse prognosis. Within the bZIP region, bZIP-InDel-inf also showed better outcomes than other mutation types, especially in double-mutated cases. In weighted multivariate analysis, higher white blood cell count, blast cell count and M4/M5 phenotype independently predicted worse OS, while higher variant allele frequency (VAF), colony stimulating factor 3 receptor (CSF3R) mutation and lower haemoglobin predicted worse RFS. These variables enabled clear OS and RFS risk stratification. CEBPA bZIP-InDel-inf is a favourable CEBPA-mutated AML subtype. Further research is needed to elucidate the role of bZIP-domain-mutated proteins. - Source: PubMed
Publication date: 2026/07/23
Yang YankunTang YuqianYang KunZhang YingTang JiruiLiang MeitingGong Yuping - This study describes a case of severe congenital neutropenia (SCN) harboring biallelic CSF3R variants and presenting with a novel inflammatory bowel disease (IBD) phenotype that responded remarkably to thalidomide. We performed functional studies to reveal the pathogenicity of the CSF3R and to elucidate the potential mechanisms underlying the therapeutic effects of thalidomide. A comprehensive review of the literature identified 18 reported cases of SCN associated with CSF3R variants. We subsequently validated the pathogenicity of the variants in the patient's peripheral blood by flow cytometry, which demonstrated reduced granulocyte colony-stimulating factor (G-CSF) receptor (G-CSFR) expression and markedly decreased phosphorylation of signal transducer and activator of transcription (STAT)3 (p-STAT3) following stimulation with recombinant human G-CSF (rhG-CSF). Thalidomide augmented rhG-CSF-induced STAT3 phosphorylation in HEK293T cells harboring the CSF3R Q257 or R308G/Q257 variants, and this effect was suppressed by a Janus kinase (JAK)1 inhibitor. Thus, IBD might represent a novel phenotype of SCN caused by CSF3R variants, and thalidomide could potentially alleviate the symptoms by modulating the JAK1/STAT3 signaling pathway. - Source: PubMed
Wang YanqiuWang LinPan ChunHuang ZhihengLi PingQiu XiaoxiaZheng CuifangHuang Ying