rHuman FLt3 Active
- Known as:
- rHuman FLt3 Active
- Catalog number:
- RF00394041-5
- Product Quantity:
- 5
- Category:
- -
- Supplier:
- Agren
- Gene target:
- rHuman FLt3 Active
Related genes to: rHuman FLt3 Active
- 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
Related articles to: rHuman FLt3 Active
- Acute myeloid leukemia (AML) remains a molecularly heterogeneous malignancy with poor prognosis, necessitating robust biomarkers for risk stratification. By integrating single-cell RNA-seq and multiomics data from 2,680 AML samples across 10 cohorts, we demonstrate that dysregulated programmed cell death (PCD) pathways are significantly elevated in AML cells and correlate with adverse outcomes. Unsupervised clustering identified two PCD-driven subtypes: Subtype A exhibits high PCD activity, an immunosuppressive microenvironment (M2 macrophages, upregulated PD-L1/HAVCR2), increased somatic mutations (NPM1/DNMT3A/FLT3), and poor survival, while Subtype B shows lower PCD activity, immune-active features, and better prognosis. As an exploratory analysis, subtype-specific therapeutic vulnerabilities were revealed: Subtype A displays predicted sensitivity to immune checkpoint inhibitors (anti-PD-1) and tipifarnib, whereas Subtype B responds better to cytarabine/doxorubicin. We developed PCDRScore-a prognostic model incorporating 13 PCD-related genes via machine learning-which outperformed existing models (higher C-index) in 10 validation cohorts and remained independent of clinicopathological factors. A nomogram combining PCDRScore, age, and cytogenetic risk enhanced clinical applicability. Crucially, experimental validation confirmed significant upregulation of key model genes (HIP1, SQLE, VNN1) in AML patient samples and cell lines (P < 0.05), reinforcing the model's biological relevance. These findings establish PCD dysregulation as a central axis of AML heterogeneity, providing a framework for precision risk stratification and hypothesis-generating immunophenotype-guided therapy. - Source: PubMed
Publication date: 2026/06/15
Liu JingZhong FangminWang XiaozhongXu LiuqingTu ZanweiCheng XiaofangZhang LinlinKong Guangyao - Acute myeloid leukemia (AML) in the pediatric population can present significant diagnostic and therapeutic challenges, especially when immunophenotypic or genetic findings indicate mixed lineage features. Here, we present the case of an 11-year-old female patient who was initially diagnosed with AML (FLT3-ITD negative) and central nervous system (CNS-3) involvement. The leukemic blasts co-expressed myeloid markers (MPO, CD33, and CD13) as well as a low-intensity B-lymphoid antigen (CD19). Despite receiving two standard induction regimens (MEC and ADE), minimal residual disease (MRD) persisted. Next-generation sequencing (Illumina MiSeq; SOPHiA DDM Myeloid Plus) was performed on bone marrow aspirate collected after the second induction cycle (ADE), at which point MRD had become negative by flow cytometry but persistent MRD had been documented after the first induction (MEC). Post-induction NGS revealed a TCF3::ZNF384 fusion with a fusion read support of 75.04% (supported by 21,262 reads and 80.56% unique molecular coverage). This aberration is more commonly associated with B-ALL or mixed-phenotype acute leukemia (MPAL-B/M), which are both characterized by lineage plasticity and a higher risk of relapse. These results highlight the importance of comprehensive molecular testing and the need for therapeutic strategies that integrate both myeloid- and lymphoid-directed approaches, as well as meticulous MRD surveillance. - Source: PubMed
Publication date: 2026/05/28
Alonso-Carballo AserMateos NataliaGómez PaulaMontolio SaraSalinas Jose AntonioGutiérrez AntonioSampol AntoniaMartínez-Serra Jordi - Acute myeloid leukemia (AML) is a molecularly diverse hematologic malignancy, with clinical outcomes driven by patient fitness, disease biology, and the depth of remission. Over the past decade, the increasing use of molecular studies has enabled genotype-directed therapy and accelerated the incorporation of targeted agents into both intensive and lower-intensity treatment regimens. FLT3 inhibitors are now well established across a wide disease spectrum, including frontline settings, relapsed/refractory disease, and post-allogeneic hematopoietic cell transplantation maintenance, with emerging evidence supporting measurable residual disease (MRD)-adapted maintenance approaches. IDH1/2 inhibitors offer therapy for specific molecular subsets, particularly in older or unfit patients, and are increasingly being evaluated in doublet and triplet combinations. Venetoclax-based regimens have become a cornerstone for older or unfit patients with AML and are being optimized through response-adapted dosing and careful partner selection to mitigate cytopenias while deepening remission. Menin inhibitors represent a major therapeutic advance for KMT2A-rearranged and NPM1-mutated AML and are rapidly moving into combination and earlier-line treatment strategies. In parallel, immune and cellular therapies, including antibody-drug conjugates, immune checkpoint modulation, bispecific engagers, and chimeric antigen receptor T-cell and chimeric antigen receptor natural killer constructs, are under investigation, although durable, practice-changing benefits outside select settings remain limited to date. This review synthesizes pivotal clinical data and translational principles informing emerging targeted, immune-based, and cellular strategies in AML, with an emphasis on remission depth, MRD-driven decision-making, and relapse prevention. - Source: PubMed
Publication date: 2026/06/13
Simkhada ShaileshJoshi UtsavDhakal Prajwal - Chromosomal microarray analysis (CMA) is an essential tool in modern cytogenetics for detecting copy number alterations and copy-neutral loss of heterozygosity (CN-LOH). As optical genome mapping (OGM) emerges as a potential replacement for traditional cytogenetic methods, the extent to which CMA remains necessary in routine diagnostic workflows remains to be elucidated. - Source: PubMed
Publication date: 2026/06/04
Marr Alexander RGonzales Patrick RGolem Shivani - 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