FLT3 (Ab_591) Antibody
- Known as:
- FLT3 (Ab_591) Antibody
- Catalog number:
- E021187-1
- Product Quantity:
- 50ug
- Category:
- Antibodies
- Supplier:
- EnoGene
- Gene target:
- FLT3 (Ab_591) Antibody
Related genes to: FLT3 (Ab_591) 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 (Ab_591) Antibody
Related articles to: FLT3 (Ab_591) Antibody
- Gilteritinib (GIL)-based venetoclax regimens are active in relapsed or refractory (R/R) fms-like tyrosine kinase 3 (FLT3)-mutated acute myeloid leukemia (AML), but real-world delivery after prior targeted therapy remains challenging. - Source: PubMed
Publication date: 2026/07/29
Chen MeilingChen YuanzhongWang ShaoyuanYang Feng'eZheng JingFu DanhuiLin JiaLi XiaofanLi Nainong - Acute myeloid leukemia (AML) is a genetically heterogeneous and dynamically evolving malignancy in which morphologic remission does not necessarily indicate eradication of disease. Bone marrow examination remains central to diagnosis and response assessment, yet repeated aspiration is invasive, may be affected by hemodilution and spatial sampling, and provides only intermittent snapshots of an evolving clonal process. Liquid biopsy offers a complementary strategy by interrogating circulating cell-free DNA (cfDNA), the leukemia-derived fraction termed circulating tumor DNA (ctDNA), extracellular vesicles, exosomal nucleic acids, and circulating leukemic cells. Among the analytical platforms applicable to these materials, droplet digital polymerase chain reaction (ddPCR) is attractive because it partitions a specimen into thousands of reactions and enables highly precise absolute quantification without a calibration curve. This narrative review critically examines the biological rationale, analytical performance, and clinical evidence supporting ddPCR-based liquid biopsy in AML. The strongest current evidence concerns molecular measurable residual disease (MRD), particularly for NPM1 mutations and selected patient-specific variants, with additional applications in IDH1/2, FLT3-TKD, KIT, CEBPA, DNMT3A, and fusion-transcript monitoring. We discuss the roles of peripheral blood and plasma cfDNA at diagnosis, during induction and consolidation, before and after allogeneic hematopoietic stem-cell transplantation, and at suspected molecular relapse. We also compare ddPCR with multiparameter flow cytometry, reverse-transcription quantitative PCR, and error-corrected next-generation sequencing, emphasizing that analytical sensitivity alone does not establish clinical validity. Major barriers include pre-analytical variation, low and fluctuating ctDNA abundance, assay-specific false-positive droplets, incomplete target coverage, clonal hematopoiesis, and the absence of harmonized thresholds. Emerging multi-analyte strategies that combine mutation tracking, methylation, exosomal RNA, chimerism, and computational modeling may improve robustness. At present, ddPCR is best positioned as a rapid, targeted, and complementary tool embedded in a multimodal MRD framework rather than as a universal replacement for bone marrow or broad genomic profiling. - Source: PubMed
Publication date: 2026/08/20
El-Sehrawy Amr Ali Mohamed AbdelgawwadAbohassan MohammadShonazarov IskandarAbd Haitham HassanBaig Mirza RMenon Soumya VSharma RaviMishra SwatiBainsal NeerajSmerat Aseel - While the FLT3 inhibitor gilteritinib is initially effective in patients with FLT3-mutated acute myeloid leukemia (AML), patients invariably relapse within months of treatment. Gilteritinib resistance is commonly driven by the emergence of NRAS mutations and a shift towards a more monocytic cell state. We hypothesized that directly targeting and depleting NRAS protein would reverse these adaptive differentiation changes and restore therapeutic sensitivity. To test this, we utilized a mutation-agnostic antisense oligonucleotide (ASO) to selectively knock down NRAS expression across gilteritinib-resistant AML cell lines, in vivo cell-line-derived xenografts, and primary patient samples. NRAS ASO successfully resensitized gilteritinib resistant cells with multiple distinct NRAS mutations, displaying superior efficacy compared to downstream MEK inhibition. This therapeutic efficacy was independent of NRAS mutant variant allele frequency, suggesting that wild-type NRAS may also contribute to resistance. Comprehensive multi-omic profiling (transcriptomics, proteomics, phosphoproteomics) revealed that NRAS knockdown consistently reversed monocytic phenotype, shifting cells back toward a more primitive cell state. Monocytic differentiation and NRAS mutations are established drivers of resistance to diverse targeted regimens in AML, including FLT3, IDH, and BCL2 inhibitors, so we also tested venetoclax resistant primary cells with NRAS mutations. Resistant cells were resensitized to venetoclax after NRAS knockdown, suggesting that NRAS knockdown may be more broadly applicable in overcoming monocytic cell state and drug resistance in AML. - Source: PubMed
Publication date: 2026/08/11
Joshi Sunil KMaazi HadiPittsenbarger JanétGarana Belinda BKaempf AndyHuang ArianeGritsenko Marina AHutchinson-Bunch ChelseaWeitz Karl KChu Rosalie KGosline Sara J CPiehowski Paul DEisfeld Ann-KathrinCarroll Martin PPerl Alexander ERodland Karin DChang Bill HRevenko Alexey STyner Jeffrey WDruker Brian JTraer Elie - FLT3-ITD mutations in acute myeloid leukemias (AMLs) cause ligand-independent signaling. One way signaling pathways potently and immediately influence cell fates is by phosphorylating key fate-determining proteins to trigger their proteolysis. We investigated the master transcription factor (MTF) driver of granulo-monocytic lineage-fates, CEBPA, for regulation by this mechanism because we found high CEBPA mRNA but little CEBPA protein in versus -wildtype AML cells, and inhibiting FLT3-ITD signaling with tyrosine kinase inhibitors (TKI) rapidly rescued CEBPA protein. Mass spectrometry revealed that CEBPA interacts with major ubiquitin-proteasome pathway (UPP) components: the ubiquitin-ligase UHRF1 and the deubiquitinase USP7. TKI treatment decreased the phosphorylation of CEBPA (Ser21) and USP7 (Ser18) alongside shifts in CEBPA interactions from degradative UHRF1 to protective USP7, stabilizing CEBPA and activating differentiation. Similarly, TKIs and UPP inhibitors stabilized the USP7 client p53, triggering apoptosis specifically in FLT3-ITD cells. Notably, UPP inhibitors (such as bortezomib) successfully stabilized CEBPA and p53 even in TKI-resistant cells. Because FLT3-ITD signaling functionally suppresses CEBPA and p53, genetic mutations in or were mutually exclusive with FLT3-ITD in clinical series. In summary, FLT3-ITD drives the UPP-mediated destruction of CEBPA and p53, positioning UPP inhibitors as promising therapeutic candidates acting downstream of TKIs. - Source: PubMed
Publication date: 2026/07/30
Saunthararajah YogenGu XiaorongBiswas SudiptaZahran ZeinabBae SongaBalusu RameshJha BabalMaciejewski Jaroslaw - Treatment options for older adults with -mutated AML who are unfit for intensive chemotherapy have evolved substantially. The combination of hypomethylating agent (HMA) and venetoclax is the current standard-of-care regimen for these patients, though outcomes remain suboptimal, particularly in -ITD mutated AML. More recently, encouraging data have emerged supporting the safety and efficacy of frontline HMA + venetoclax + FLT3 inhibitor 'triplet' regimens. - Source: PubMed
Publication date: 2026/08/18
Arora SankalpDaver NavalRavandi FarhadShort Nicholas J