rHuman FLt3 Active, Human cytokinesand growth factors
- Known as:
- rHuman FLt3 Active, Human cytokinesand growth factors
- Catalog number:
- RF0040-50
- 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
- Depletion of CD4 cells during an anti-tumor immune response promotes tumor regression and accelerates proliferation of tumor-antigen-specific CD8 T cells in draining lymph nodes (dLNs). However, the effect of the depletion on inter-organ kinetics of antigen presentation and qualitative changes in dendritic cells (DCs) are not yet understood. Here, we established a novel approach for simultaneous detection of cellular movement and cell cycle phase by KikGR/Fucci mice and used it to examine migratory and LN resident DC (LNDC) dynamics after CD4 cell depletion. We found that CD4 cell depletion enhanced migration of CD11c MHC class II migratory DCs from tumor to dLNs and induced activation-associated phenotypic changes, such as increased MHC class II expression. Despite reduced overall cellularity in tumor dLNs, LNDC numbers were relatively maintained. Within the LNDC compartment, CD4 depletion increased the relative abundance of a CD8αCD11b subset and promoted influx and cell-cycle activity among newly recruited LNDCs. Publicly available single-cell RNA sequencing data further delineated ligand-receptor expression relationships, including and axes, within tumor dLNs. These findings reveal remodeling of DC migration, activation, and LNDC turnover within tumor dLNs in the context of CD4 cell depletion, which enhanced anti-tumor immunity. - Source: PubMed
Publication date: 2026/06/10
Moriya TaikiHashimoto MayukoUeda MizukiAoyagi TatsuyaKawaguchi AyakoTakahashi KentaroTsukasa KobayashiDoi KazukiHemmi HiroakiKaisho TsuneyasuUeha SatoshiMatsushima KojiKusumoto YutakaChtanova TatyanaTomura Michio - Although core-binding factor acute myeloid leukemia (CBF-AML) is generally considered a favorable-risk subtype in children, disease relapse remains a significant concern. The prognostic relevance of co-occurring mutations, particularly KIT and FLT3-ITD, remains debatable, and treatment intensity may modulate their impact. This multicenter analysis included 289 children (< 14 years) with newly diagnosed CBF-AML enrolled in the C-HUANAN-AML-15 study (2015-2023). KIT and FLT3-ITD mutations were identified via cytogenetic analysis and targeted sequencing. Measurable residual disease (MRD) was evaluated by multiparameter flow cytometry (MFC) and quantitative polymerase chain reaction (PCR) following induction chemotherapy. Survival analyses were performed using Kaplan-Meier and Cox regression methods. This multicenter analysis included 289 children (< 14 years) with newly diagnosed CBF-AML enrolled in the C-HUANAN-AML-15 study (2015-2023). KIT and FLT3-ITD mutations were identified via cytogenetic analysis and targeted sequencing. Measurable residual disease (MRD) was evaluated by multiparameter flow cytometry (MFC) and quantitative polymerase chain reaction (PCR) following induction chemotherapy. Survival analyses were performed using Kaplan-Meier and Cox regression methods. KIT mutations were detected in 103 patients (35.6%), predominantly involving exon 17 (69.9%), and were associated with extramedullary disease, sex chromosome loss, and trisomy 22. No significant differences in 5-year event-free survival (EFS), overall survival (OS), or cumulative incidence of relapse (CIR) were observed between patients with and without KIT mutations. FLT3-ITD mutations (5.5% of patients) did not adversely affect outcomes. Neither mutation independently predicted survival. MRD positivity (MFC-MRD ≥ 0.1%) after the second induction cycle strongly predicted inferior EFS and OS and higher CIR, with corresponding results observed for molecular MRD and parallel findings for PCR-based MRD. In this large multicenter cohort, KIT and FLT3-ITD mutations did not adversely affect the prognosis of pediatric CBF-AML treated according to the C-HUANAN-AML-15 protocol. MRD after induction was the most powerful predictor of relapse and survival, underscoring its importance for risk stratification in future pediatric AML trials. - Source: PubMed
Publication date: 2026/06/10
Zheng YongzhiYu LihuaLe ShaohuaLi NainongFeng XiaoqinLi ChunfuZheng MincuiMai HuirongJiang HuaHe XianglingWen HongXu HongguiChen ChunYang Lihua - Waldenström macroglobulinemia (WM) is a low-grade non-Hodgkin lymphoplasmacytic lymphoma of the bone marrow, characterized by production of monoclonal immunoglobulin M (IgM) protein. Smoldering Waldenström macroglobulinemia (SWM) is asymptomatic and exhibits an increased risk of progression to WM. Myelodysplastic syndrome (MDS) arises from blood cancer in the hematopoietic stem cell compartment, featuring dysplastic changes in bone marrow and blood cells, along with cytopenias, including anemia, neutropenia, or thrombocytopenia. Their coexistence is extremely rare. We report a 74-year-old woman with IgM monoclonal gammopathy, anemia, and bone marrow dysplasia. Initially treated as WM, persistent cytopenias prompted reevaluation, leading to a revised diagnosis of SWM with MDS-IB-1 MDS with increased blasts-1. After six cycles of azacitidine, she achieved remission of MDS but rapidly progressed to AML and ultimately died. This case provides a key clinical lesson: persistent cytopenias during ibrutinib therapy were attributable to MDS progression rather than SWM, underscoring the importance of re-evaluation. Furthermore, it completely documents clonal evolution from 2.5% blasts (MDS with low blasts) to 6% blasts (MDS with increased blasts-1) and ultimately to AML (66% blasts), and it introduces the emergence of an FLT3-ITD mutation that rapidly drove the disease into AML even after the patient had achieved MDS remission. We also review the rare coexistence of WM and MDS/AML, and MGUS with MDS. - Source: PubMed
Publication date: 2026/05/25
Wang HuanyuanTan ShuaiLi YumengSun Wanling - Pancreatic ductal adenocarcinoma (PDAC) remains a therapeutic challenge, and the aggressive basal-like/mesenchymal subtype is particularly refractory to chemotherapy, underscoring the need for novel therapies. Leveraging genetic screens, we identified protein phosphatase 2A (PP2A) catalytic subunit PPP2CA as a target. Pharmacological PP2A inhibition selectively impaired the growth of mesenchymal PDAC cells. To delineate the mechanisms underlying sensitivity to the PP2A inhibitor LB100, we employed a dual-pronged strategy. Functional characterization revealed metabolic reprogramming coupled with endoplasmic reticulum (ER) stress and cell death induction. Genome-wide genetic screens identified key modifiers of LB100 sensitivity, implicating transcriptional regulators, mRNA processing, translation, and metabolism. Based on expression data linking PP2A to splicing and transcriptional regulation, we prioritized these processes for validation. Mesenchymal PDAC cells exhibited enhanced splicing following PP2A inhibition. Notably, we identified enhanced transcriptional elongation upon LB100 treatment, particularly of short genes, driven by cyclin-dependent kinase 9 (CDK9). Our findings support a reciprocal regulatory relationship between PP2A and CDK9 that connects to the activation of ER stress response factors, including activating transcription factor 4 (ATF4). These results establish PP2A as a druggable target in mesenchymal PDAC cells and reveal a role of LB100-induced transcriptional elongation and splicing, providing a mechanistic basis to guide future therapy development. - Source: PubMed
Publication date: 2026/06/07
Murr JanineSchneider CarolinDuan NingjunKöse HazalRajamani AnantharamananHe XueyangBuchloh JonasHintze ChristianNaik AtharvaGoeke DanielRjasanow NicoleKrauß LukasNguyen AlexandraWidholz Sebastian ASchneeweis ChristianTrozzo RiccardoOrben FelixMueller SebastianÖllinger RupertMontero Juan JDudek MichaelKnolle PercyKong BoEllenrieder VolkerContreras Constanza TapiaHessmann ElisabethGrade MarianGhadimi MichaelBraun Christian JRad RolandReichert MaximillianKeller UlrichSchmid Roland MBoutz Paul LSaur DieterWirth MatthiasKrämer Oliver HSchneider Günter - In acute myeloid leukemia (AML), the insertion site of internal tandem duplications (ITDs) within the FLT3 gene critically determines the sensitivity to tyrosine kinase inhibitors (TKIs). Despite recent advances, patients harboring ITDs in the tyrosine kinase domain (TKD) still lack effective therapeutic options. To elucidate the molecular basis underlying the differential TKI sensitivity of FLT3-ITD cells, we integrated high-resolution mass spectrometry-based (phospho)proteomics with subcellular fractionation. Our analysis revealed that midostaurin induces the subcellular redistribution of approximately 2500 proteins involved in crucial biological processes, including cell cycle control, autophagy, and metabolism. Functional analyses further demonstrated that the ITD insertion site determines the autophagy response to midostaurin and modulates mitochondrial metabolism, influencing organelle architecture and ATP production, even at steady state. Importantly, by integrating subcellular proteomic dataset with functional metabolic assays, we uncovered a lipid-dependent vulnerability of FLT3-ITD cells: lipid restriction enhances FLT3 trafficking to the plasma membrane, and markedly reduces cell viability, restoring midostaurin sensitivity of resistant FLT3-ITD cells. Together, our findings reveal that the FLT3-ITD insertion site orchestrates a coordinated remodeling of subcellular protein organization, autophagy, and metabolism, and identify lipid-mediated control of FLT3 compartmentalization as a therapeutically actionable mechanism to overcome TKI resistance in FLT3-ITD AML. - Source: PubMed
Publication date: 2026/06/09
Bica ValeriaPacilè Anna FrancescaBoettcher MartinMarano ValentinaMarabitti VeronicaNazio FrancescaCortese MirkoFischer ThomasPerfetto LiviaMougiakakos DimitriosMassacci GiorgiaSacco Francesca