FLT3 (Phospho_Tyr591) Antibody
- Known as:
- FLT3 (Phospho_Tyr591) Antibody
- Catalog number:
- E012078-1
- Product Quantity:
- 50ug
- Category:
- Antibodies
- Supplier:
- EnoGene
- Gene target:
- FLT3 (Phospho_Tyr591) Antibody
Related genes to: FLT3 (Phospho_Tyr591) Antibody
- 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 (Phospho_Tyr591) Antibody
Related articles to: FLT3 (Phospho_Tyr591) Antibody
- Leukemic stem cells (LSCs) are the cellular reservoir most strongly implicated in relapse of acute myeloid leukemia, yet their operational detection by multiparameter flow cytometry remains challenging because of immunophenotypic overlap with normal progenitors and variability across assays. Including CD45RA in the CD34⁺CD38⁻ gating strategy substantially improves discrimination between malignant and normal stem/progenitor populations and thus enables more precise LSC enumeration in a single-tube format. Given the clinical importance of accurately quantifying the LSC compartment, we evaluated a refined single-tube flow cytometry assay that incorporates CD45RA within the CD34 + CD38- gate to increase specificity for the leukemic stem compartment. - Source: PubMed
Publication date: 2026/05/02
Navidinia Amir AbbasRostami ShahrbanooKarami NajibeShemshadinia MohammadrezaPatekhor Habibeh SabriHajaliaskari AkramMohammadi SaeedRostami TaherehBarkhordar MaryamVaezi MohammadJanbabaei GhasemChahardouli Bahram - Acute myeloid leukemia (AML) blasts often have high CD135 (FLT3 receptor) expression, but its clinical impact is unclear. We analyzed CD135 expression, and the clinical characteristics and outcomes of 214 patients with de novo AML diagnosed between October 2022 and May 2024. Subsequently, we collected data on additional 78 patients, diagnosed with AML at four medical centers from June to December 2024, for external validation. The high-CD135-expression group had significantly lower CD34 surface expression (p = 0.003) and higher CD33 expression (p = 0.014) on AML blasts. The high-CD135-expression group also showed a higher frequency of NPM1 (p < 0.001) and DNMT3A (p = 0.032) mutations, but was not significantly associated with CD135 expression (p = 0.229). The patients in the high-CD135-expression group had lower initial induction therapy response rates than those in the low-CD135-expression group (p < 0.001). High CD135 expression was independently associated with poorer OS and PFS. In the subgroup of patients with high CD135 expression and FLT3-ITD mutations, those who received TKI combined with chemotherapy had significantly better OS (p = 0.007). Then we developed a prognostic nomogram incorporating CD135 expression. This model performed well both in the development cohort (area under the curve [AUC] = 0.817) and multicenter validation cohort (AUC = 0.722). CD135 expression on AML blasts is a pivotal marker that integrates molecular pathogenesis with clinical outcomes, highlighting its dual role as a prognostic indicator and therapeutic target in precision clinical approaches for AM. - Source: PubMed
Publication date: 2026/05/02
Nie JinhongGao LuShao YingchunYang LiCao JunjieXu JingeWang YuhangZhang YuqiCui TongZhou ShiyuanZhu WenjuanZhu MingqingMa XiaoWu DepeiWu Xiaojin - Conventional type-1 dendritic cells (cDC1) are the main mediators of crosspresentation of tumor antigens to CD8+ T cells and provide a context of costimulatory molecules and cytokines that lead to cytotoxic T lymphocyte (CTL) responses. We analyzed bulk RNA sequences from 7 key clinical trials testing checkpoint inhibitors across multiple cancer types. cDC1- and CD8-associated gene signatures were analyzed. Multiplex tissue immunofluorescence was used to quantify cDC1 in melanoma, urothelial cancer, and non-small-cell lung cancer (NSCLC) samples and assess cDC1 tissue neighborhoods. Melanoma samples were studied with Xenium spatial transcriptomics (ST) and one series of NSCLC was analyzed using GeoMX-DSP. Strong associations across tumor types were found between cDC1 and CD8+ T cell transcripts with clinical outcomes. As mechanistically expected, transcripts for the CCL4 and CCL5 chemokines and the growth factor FLT3-L showed associations with cDC1 abundance. Tissue immunofluorescence showed a strong correlation of cDC1 and CD8+ T cell infiltration with clinical benefit upon treatment with checkpoint inhibitors (CPIs). Moreover, short distance between cDC1 and CD8+ T cells was found to define tissue niches associated with favorable outcomes. ST revealed recent T cell activation within immune cDC1-rich niches. cDC1 abundance, which determines CD8+ T lymphocyte density and activation in tumor tissues across cancer types, is strongly associated with clinical response to CPI-based immunotherapies. - Source: PubMed
Publication date: 2026/05/01
Lopez-Janeiro AlvaroGonzález-Gomariz JoséIssa FadiHester JoannaPorciuncula AngeloTeijeira AlvaroLuri-Rey CarlosRuiz-Guillamon DavidPerez-Gracia Jose LuisPerez-Ruiz ElisabethBarragan IsabelMartín-Algarra SalvadorSanmamed Miguel FOrtego IgnacioRodriguez-Ruiz Maria EAlexandru RalucaRodriguez InmaculadaArrieta-Aranzueque SaioaRimm DavidAung ThazinSchalper Kurt Ade Andrea Carlos EMelero Ignacio - Second generation tyrosine kinase inhibitors (TKIs) such as gilteritinib, characterized by minimal EGFR and absent VEGFR inhibition, are in theory associated with low dermatologic toxicity. This case report brings to the awareness that the opposite may occur and emphasize the need for attentive pharmacovigilance. - Source: PubMed
Publication date: 2026/04/12
Seki Jack TSibai JadPerusini Maria AgustinaSibai Hassan - Acute promyelocytic leukemia (APL) is a distinct subtype of acute myeloid leukemia defined by the t(15;17)(q24;q21)-derived fusion. However, a small subset of patients harbor cryptic or atypical rearrangements that escape detection by routine real-time quantitative RT-PCR (qRT-PCR). We report a 34-year-old man presenting typical APL in whom repeated testing for the canonical long, short, and variant transcripts yielded negative results. RNA sequencing subsequently identified a previously unreported in-frame fusion linking exon 8 to a 58-base pair-deleted exon 3. The resulting chimeric transcript retained the coiled-coil domain as well as the DNA- and ligand-binding domains of , suggesting preserved sensitivity to retinoid-based therapy. Consistent with this prediction, induction therapy with all-trans retinoic acid (ATRA) and arsenic trioxide (ATO) resulted in achievement of complete molecular remission. Molecular relapse occurred three months after premature discontinuation of maintenance therapy, underscoring the leukemogenic potential of this novel fusion. This observation expands the molecular spectrum of APL and highlights the potential value of incorporating RNA sequencing into the diagnostic workflow for morphologically suspected but PCR-negative APL. - Source: PubMed
Publication date: 2026/04/14
Chen Jia-PingHou Jun-JieChen Xiao-YongCao Yi-XuanKe PengZhou Ji-HaoHu Li-Na