FLT3 (CD135) Antibody (N_term)
- Known as:
- FLT3 (CD135) Antibody (N_term)
- Catalog number:
- AP7644a
- Product Quantity:
- 0.1 mg
- Category:
- -
- Supplier:
- Abgen
- Gene target:
- FLT3 (CD135) Antibody (N_term)
Related genes to: FLT3 (CD135) Antibody (N_term)
- 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 (CD135) Antibody (N_term)
Related articles to: FLT3 (CD135) Antibody (N_term)
- Older or medically unfit patients with newly diagnosed FLT3-mutated acute myeloid leukemia (AML) have poor outcomes with hypomethylating agent (HMA) monotherapy. Venetoclax plus HMA is a modern lower-intensity standard, but FLT3-mutated AML remains biologically heterogeneous, and triplet regimens combining HMA, venetoclax, and a FLT3 inhibitor are increasingly used despite limited randomized comparative evidence. PubMed/MEDLINE, Embase, Cochrane CENTRAL, Web of Science, Scopus, and major hematology/oncology conference proceedings were searched from inception to 12 June 2026 in accordance with PRISMA 2020 and MOOSE guidance. Eligible studies reported primary clinical outcomes for newly diagnosed FLT3-ITD and/or FLT3-TKD AML treated with frontline lower-intensity HMA alone, VEN-HMA doublet, HMA/LIC plus FLT3 inhibitor, or HMA/LIC plus VEN plus FLT3 inhibitor therapy. Comparative effect estimates and single-arm proportions were synthesized only when clinical and statistical assumptions were defensible. Thirteen eligible records were retained. Direct VEN + AZA versus AZA evidence came from one FLT3-mutated pooled subgroup comparison (42 vs. 22 patients), showing CRc 67% versus 36%, RR 1.83 (95% CI 1.01-3.32), and median OS 12.5 versus 8.6 months. The randomized non-venetoclax LACEWING trial showed higher CRc with gilteritinib + AZA than AZA (58.1% vs. 26.5%; HR for OS 0.916; p = 0.753), illustrating that improved remission does not guarantee survival benefit. The principal comparative triplet evidence was one retrospective study: CR/CRi 93% versus 70%, RR 1.32 (95% CI 1.09-1.61), with median OS not reached versus 9.5 months. Prospective and long-term triplet reports described CR/CRi rates of 93%-96%, deep FLT3-ITD MRD negativity, and median OS up to 38.5 months; several reports derive from overlapping institutional series and non-randomized designs, limiting independent corroboration and causal inference. VEN + AZA improves remission compared with AZA in the FLT3-mutated subgroup, but the evidence base is underpowered for FLT3-specific survival conclusions. Triplet therapy produces the strongest remission-depth and MRD signals but has not shown superiority over VEN-HMA in a randomized frontline comparison. On current evidence, triplets are a promising biologically rational strategy requiring direct randomized validation against the contemporary VEN-HMA standard. - Source: PubMed
Shaik Mahboob YounusPatel JayAggarwal VaishaliKakadia SunilDivers Stephen - -mutated acute myeloid leukemia (AML) represents one of the most frequent and biologically distinct AML entities, characterized by the aberrant cytoplasmic localization of the NPM1 mutant protein. The recent advances in molecular biology and translational research have progressively redefined the clinical management of this disease. This narrative review summarizes the evolution of -mutated AML over the last two decades, focusing on the transition from immunohistochemical observations to modern genetics-based and measurable residual disease (MRD)-driven approaches. We discuss the biological role of mutant NPM1, the prognostic impact of co-occurring genetic alterations, and the integration of molecular monitoring into routine clinical practice. Particular attention is given to the prognostic and therapeutic implications of the co-mutational landscape. We also discuss emerging targeted therapies directed against key pathogenic pathways, including the menin-KMT2A axis and nuclear export machinery. Despite significant advances in risk stratification and treatment, considerable heterogeneity in clinical outcomes persists among patients with -mutated AML, indicating that genomic information obtained at diagnosis alone is insufficient to fully capture prognostic differences. Future advances will likely depend on the integration of genetic, transcriptional, and broader cellular-state information to better define biologically relevant disease states and guide more personalized therapeutic strategies. - Source: PubMed
Publication date: 2026/09/19
Cimino GaetanoCaridi MatteoCelenza RosannaMillucci FrancescoCrocioni MartinaSciabolacci SofiaCardinali ValeriaMartelli Maria Paola - Cytarabine is a cornerstone of acute myeloid leukemia (AML) therapy; however, acquired resistance remains a major clinical challenge. FMS-like tyrosine kinase 3 internal tandem duplication (FLT3-ITD), a common genetic alteration in AML, is associated with high relapse rates and poor outcomes. Here, we investigated the cellular and molecular mechanisms of acquired cytarabine resistance in FLT3-ITD AML. Cytarabine-resistant MV4-11-CR and MOLM-13-CR cells were generated from parental MV4-11 and MOLM-13 cells, respectively, by stepwise drug selection. Both models exhibited markedly elevated cytarabine IC values and enhanced proliferation. FLT3 expression and activation increased in MV4-11-CR cells but decreased in MOLM-13-CR cells. Midostaurin pretreatment failed to restore cytarabine sensitivity, indicating that altered FLT3 signaling is not a shared mechanism of resistance. Cytogenetic analyses and interphase FISH revealed greater numerical and structural chromosomal heterogeneity in the resistant cells than in their parental counterparts, including the presence of polyploid and near-tetraploid subpopulations. RNA sequencing identified common transcriptional alterations, with among the most significantly downregulated genes. Reduced expression was confirmed at the mRNA and protein levels. knockdown in parental MV4-11 cells attenuated cytarabine-induced cytotoxicity, whereas its re-expression in MV4-11-CR cells partially restored cytarabine sensitivity, supporting the functional contribution of downregulation to acquired resistance. Gene set enrichment analysis demonstrated shared enrichment of G2/M checkpoint and mitotic spindle pathways. Notably, combined TTK/Mps1 and FLT3 inhibition with luvixasertib and midostaurin synergistically suppressed cell viability in both resistant cell lines. These findings identify divergent FLT3 regulation, downregulation, increased chromosomal heterogeneity, and enrichment of mitotic regulatory programs as key features associated with acquired cytarabine resistance. They also support the combined inhibition of TTK/Mps1 and FLT3 as a potential therapeutic strategy for cytarabine-resistant FLT3-ITD AML. - Source: PubMed
Publication date: 2026/09/21
Yen Jui-HungChen Zi-AnLin Yu-XuanJiang Hui-YuLin Liang-InLi Chi-ChengChen Pei-Yi - Sweet syndrome (acute febrile neutrophilic dermatosis) is characterized by fever, leukocytosis, and tender erythematous skin lesions with neutrophilic infiltrate. Although associated with granulocyte colony-stimulating factor (G-CSF) use, its occurrence with pegfilgrastim-the pegylated form-is rare, with fewer than five reported cases. Sweet syndrome has also been rarely linked to FLT3 inhibitors such as quizartinib. We report a 71-year-old male with acute myeloid leukemia who developed bullous Sweet syndrome following concurrent exposure to pegfilgrastim and quizartinib. - Source: PubMed
Publication date: 2026/10/01
London JonathanPatresan JohnBelkin AlexanderElnair Radowan - Juvenile myelomonocytic leukemia (JMML) is a rare and very aggressive pediatric myelodysplastic/myeloproliferative neoplasm with molecular heterogeneity and constitutive activation of the RAS signaling pathway. The aim of this study was to identify the mutational landscape, driver genes, mutational signatures, functional pathways, and therapeutic targets of mutations that affect receptor tyrosine kinases (RTKs) and RAS pathways in JMML. - Source: PubMed
Publication date: 2026/09/18
Goel HarshMajhi Ravi KumarMeena Jagdish PrasadChopra AnitaBakhshi SameerSingh LataSeth RachnaKar BibekanandaTanwar PranayGupta Aditya Kumar