rHuman FLt3 Active, Human cytokinesand growth factors
- Known as:
- rHuman FLt3 Active, Human cytokinesand growth factors
- Catalog number:
- RF0041-50
- Product Quantity:
- 50
- Category:
- -
- Supplier:
- Agren
- Gene target:
- rHuman FLt3 Active Human cytokinesand growth factors
Related genes to: rHuman FLt3 Active, Human cytokinesand growth factors
- 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: rHuman FLt3 Active, Human cytokinesand growth factors
Related articles to: rHuman FLt3 Active, Human cytokinesand growth factors
- Resistance to venetoclax-based therapy in acute myeloid leukemia (AML) includes genetic (i.e., mutations in N/KRAS, FLT3-ITD, TP53) and phenotypic (i.e., monocytic differentiation) features. Whether monocytic differentiation contributes to clinical venetoclax resistance secondary to a genetic bias remains unknown. This multimodal, multicenter, international analysis inclusive of 678 patients comprehensively characterized the prognostic role of monocytic differentiation in AML patients treated with hypomethylating agents combined with venetoclax. AML genetics and monocytic differentiation (HR: 1.89, 95% CI: 1.35-2.66, p < 0.001) in NPM1 wild-type cases correlated with an increased risk of death. Clustering of centralized quantitative multiparameter flow cytometry data, evaluation of RNA sequencing-derived AML maturation stage, and single-cell proteogenomics linked driver mutations with AML phenotype and anti-apoptotic gene expression. This comprehensive analysis of AML genetics, phenotype, and anti-apoptotic protein expression highlights the complementary role these factors impart following venetoclax-based therapy. - Source: PubMed
Publication date: 2025/05/21
Lachowiez Curtis AHeiblig MaelAspas Requena GasparTavernier-Tardy EmmanuelleDai FangyanAshango Amenech BPeters Daniel TFang JacobKaempf AndyLong NicolaEide Christopher AKurtz Stephen EXie WeiAgarwal AnupriyaSahasrabudhe AishwaryaMcMahon Christine MAmaya Maria LMeyers GabrielleGandhi ArpitaLeonard JessicaHayes-Lattin BrandonMaziarz Richard TTraer ElieCook Rachel JSwords RonanBraun Theodore PSaultz Jennifer NEckel Ashley MLoken Michael RZeidner Joshua FTyner Jeffrey WPollyea Daniel A - - Source: PubMed
Publication date: 2025/05/20
Wang XiaoyangYao HangChen JiaohaoLiu Xiaogu - This study explores the molecular distinctions between myelodysplastic neoplasms (MDS) and acute myeloid leukemia (AML) with RUNX1 mutations (RUNX1mut), aiming to elucidate factors influencing the progression from MDS to AML. Analyzing 1520 patients (773 AML and 747 MDS cases), RUNX1mut were present in 10 % of MDS and 13 % of AML cases. Interestingly, RUNX1mut were associated with higher blast counts in MDS, suggesting a potential role in disease progression. Despite similar overall survival across subgroups, significant differences in variant allele frequency (VAF) were observed, correlating with blast count. Our study highlights a unique genetic signature in both RUNX1mut MDS and AML: Cytogenetic analysis showed a higher frequency of normal karyotypes in RUNX1mut-MDS compared to RUNX1mut-AML. While only trisomy 8 was found in MDS, trisomies 8, 11, and 13 were detected in RUNX1mut-AML. Notably, MECOM rearrangements, KMT2A-PTD, and FLT3-ITD alterations were exclusive to RUNX1mut-AML. RUNX1 mutations were strongly associated with spliceosome gene mutations, especially in RUNX1mut-MDS. Copy neutral loss of heterozygosity (CN-LOH) involving RUNX1 was detected in 22 % of RUNX1mut-AML cases but was absent in RUNX1mut-MDS. These findings highlight the distinct genetic landscape of RUNX1mut-MDS and AML. Understanding these molecular determinants may enhance monitoring and early intervention strategies for MDS patients at risk of progression to AML. - Source: PubMed
Publication date: 2025/05/15
Stengel AnnaHörst KatharinaKühn ConstanzeMeggendorfer ManjaKern WolfgangHaferlach TorstenHaferlach Claudia - This study aims to develop a clinical prediction model for sensitivity to Bcl-2 inhibitors combined with hypomethylating agents (HMAs) in elderly/unfit patients with acute myeloid leukemia (AML). - Source: PubMed
Publication date: 2025/05/20
Du YufengLi ChunhongChen YonghongXie FangYan Jinsong - Acute myeloid leukemia (AML) and DNMT3A mutations (DNMT3A) are considered to carry intermediate risk under the 2022 European LeukemiaNet (ELN-2022) classification in the absence of other co-mutations or cytogenetic abnormalities. However, this group is highly heterogeneous. In this study, the genomic and transcriptomic features influencing outcomes in DNMT3A-mutated AML were examined in a cohort of 884 patients with AML receiving standard chemotherapy. Stratification by NPM1 and FLT3-ITD status revealed worse survival among patients with NPM1 mutations and wild-type FLT3-ITD (NPM1/FLT3-ITD) than patients in the ELN-2022 favorable risk group. The other three subgroups (NPM1/FLT3-ITD, NPM1/FLT3-ITD, and NPM1/FLT3-ITD) exhibited worse prognoses than patients in the ELN-2022 intermediate risk group. Additionally, the presence of TET2 in patients with AML and DNMT3A/NPM1/FLT3-ITD led to reclassification from favorable risk to intermediate risk in the ELN-2022. RNA-sequencing analysis revealed a distinct transcriptomic profile in patients with TET2, highlighting the enrichment of leukemic stem cell signatures and dendritic cell migration, with MMP14, CD200, and CT45A5 identified as key differentially expressed genes. In conclusion, co-mutation patterns strongly affected AML outcomes in patients with DNMT3A. Patients with TET2 constituted a unique subgroup within the ELN-2022 favorable DNMT3A/NPM1/FLT3-ITD group, characterized by distinct transcriptomic features and an unfavorable prognosis. - Source: PubMed
Publication date: 2025/05/20
Ni Sao-ChihYao Chi-YuanTsai Xavier Cheng-HongLo Min-YenChen Chien-YuanLee Wan-HsuanLin Chien-ChinKuo Yuan-YehPeng Yen-LingTseng Mei-HsuanWu Yu-SinLiu Ming-ChihLin Liang-InChuang Ming-KaiKo Bor-ShengYao MingTang Jih-LuhTien Feng-MingChou Wen-ChienHou Hsin-AnTien Hwei-Fang