Ask about this productRelated genes to: FLT3 protein
- Gene:
- FLT3 NIH gene
- Name:
- fms related tyrosine kinase 3
- Previous symbol:
- -
- Synonyms:
- STK1, FLK2, CD135
- Chromosome:
- 13q12.2
- Locus Type:
- gene with protein product
- Date approved:
- 1990-07-30
- Date modifiied:
- 2019-04-23
Related products to: FLT3 protein
Related articles to: FLT3 protein
- After many years of stagnation in the treatment of acute myeloid leukemia (AML), there is currently a rapid move towards personalized medicine. Improvements in molecular diagnostics, risk assessment tools, targeted therapies, overall patient fitness assessments, and quality-of-life assessments have significantly changed how patients are treated. Genetic and molecular analyses, risk and health assessments, and measurable residual disease (MRD) monitoring are now integral to the treatment plan for evaluating patient responses and recurrence. In this regard, lower-intensity treatments are provided to older or unfit individuals. On the other hand, younger patients are usually subjected to curative therapies such as intensive chemotherapy to induce remission. Depending on their fitness and disease risk, they can be considered for hematopoietic cell transplantation, which is done after close observation for MRD. In addition, newer therapeutic drugs and immunotherapy techniques are being applied for patient management. Tremendous strides have been made in improving the efficiency of treatment programs in the relatively new area of personalized AML therapy, with a focus on functionality. - Source: PubMed
Publication date: 2026/05/15
Niscola PasqualeGianfelici ValentinaGiovannini MarcoMazzone CarlaPrincipe Maria Ilaria Del - Acute myeloid leukemia (AML) harboring KMT2A rearrangement (KMT2Ar) was generally associated with poor prognosis. We enrolled 490 patients with KMT2Ar from the East China Leukemia Alliance between March 2013 and August 2025. KMT2A::MLLT3 was the most frequent KMT2Ar (31.6%), followed by KMT2A::MLLT4 (25.1%), KMT2A::ELL (20%), and KMT2A::MLLT10 (12.7%). KMT2A::MLLT4 showed an inferior prognosis. The most co-occurring gene mutations were KRAS (20.1%), NRAS (19.0%), TET2 (10.2%), WT1 (8.6%), and PTPN11 (7.4%). Trisomy 8 was more common in patients < 60 years, while FLT3-ITD was only detected in patients < 60 years. With a median follow-up time of 42.6 months, the median overall survival (OS) of all patients was 30.9 months, and the 3-year OS rate was 49.9%. Patients treated with venetoclax plus intensive chemotherapy (Ven+IC) showed the best composite complete remission (CRc) rate and OS compared to intensive chemotherapy, venetoclax plus reduced-intensive chemotherapy, and reduced-intensive chemotherapy (CRc rate: 89.5% vs. 62.4% vs. 57.3% vs. 61.4%; median OS: not reached vs. 39.9 months vs. 34.8 months vs. 12.7 months). Multivariate analysis identified multiparameter flow cytometry minimal residual disease negativity post-induction therapy, allogeneic hematopoietic stem cell transplantation, and Ven+IC as independent favorable prognostic factors for event-free survival (EFS), and KMT2A::MLLT4 fusion, EVI1 overexpression were independent unfavorable prognostic factors for EFS. In summary, our study showed characteristics and prognostic implications in newly diagnosed KMT2Ar AML in China. - Source: PubMed
Publication date: 2026/05/26
Pan JiajiaFu ChunmeiLing QingLu YingShi YifenZhang YunxiangWang ShaoyuanJi ChunyanQian ShenxianHuang ZhenqiGe ZhengZhang JingchengOuyang GuifangJin ChenghaoLu QuanyiHuang LiKong HongweiZhu YuYan ZhilingLiu DebinJiang HuaweiChen NianciLin XiangjieZhou YileZhang YiLi XiaTong HongyanJin JieChen SuningWang Huafeng - - Source: PubMed
Publication date: 2026/05/13
Yang JieZhang YvyinLi QingshanWang Peihong - The efficacy of FLT3 inhibitors in acute myeloid leukemia (AML) is severely limited by resistance mutations, particularly the recalcitrant gatekeeper F691L and activation loop D835V/Y variants. Herein, through the structure-guided optimization of our previously reported lead , we identified , a highly potent type II FLT3 inhibitor capable of overcoming these recalcitrant mutants. exhibited single-digit nanomolar potency against Ba/F3-FLT3-ITD-F691L (IC = 9.09 nM) and subnanomolar activity against Ba/F3-FLT3-ITD-D835Y (IC = 4.64 nM) and Ba/F3-FLT3-ITD-D835V (IC = 0.76 nM). , induced profound tumor regression (TGI = 125%) in the MV4-11 xenograft model (10 mg/kg) and achieved robust tumor growth suppression (TGI = 68.6%) in the Ba/F3-FLT3-ITD-F691L model (50 mg/kg), where quizartinib was ineffective. Mechanistic studies confirmed that effectively blocked FLT3 signaling and induced apoptosis without observable toxicity. Collectively, represents a promising lead candidate for drug-resistant AML. - Source: PubMed
Publication date: 2026/05/23
Yang JinZhang Ling-YuNi Xing-FengBai Ming-YuWang XuFu An-QiChen Min-HuiZhang Meng-YuanQiao NuoWang Zi-XuanLi Qing-QingCai ShuWang YingYao Yu-ShengYu Yan-ChengChen Wei-DongSun Shan-LiangZhang ZhangLi Nian-GuangShi Zhi-Hao - Pediatric acute myeloid leukemia (AML) is a heterogeneous hematologic malignancy that accounts for about 15%-20% of childhood leukemias. Despite therapeutic advances, relapses remain common, and survival for high-risk patients is below 60%. Unlike adult AML, pediatric AML displays distinct genetic mutations, including FLT3-ITD, NPM1, KMT2A rearrangements, and core-binding factors (CBF) fusions, as well as extensive epigenetic dysregulation. Aberrant DNA methylation, histone modifications, and altered non-coding RNA expressions disrupt hematopoietic differentiation and activate oncogenic transcriptional networks. Recent advances in silico transcriptomic analysis have transformed the study of pediatric AML by integrating gene expression and epigenetic data to identify molecular drivers and regulatory networks. Computational RNA-seq pipelines and pathway analyses have highlighted key epigenetic regulators, including DNMT3A, TET2, and HDACs, as potential therapeutic targets. Multi-omics approaches combining transcriptomic, methylomic, and chromatin accessibility data are increasingly used to define biomarkers for diagnosis, prognosis, and therapeutic response. This review provides a comprehensive overview of the molecular and epigenetic landscape of pediatric AML, emphasizing the power of in silico transcriptome analysis to uncover disease mechanisms, refine patient stratification, and guide the development of precision-based epigenetic therapies aimed at improving long-term outcomes in children with AML. - Source: PubMed
Publication date: 2026/05/22
Salah Akram NMansour Reda MEl-Sayyad Gharieb SMoustafa Hebatallah Ahmed MohamedSayed Ghadir AMohamed Hend HElshami Nourhan HAlFarsi KareemFahim AhmedMohammed Osama ARudayni Hassan ADoghish Ahmed S