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
- Pediatric acute myeloid leukemia (AML) is a heterogeneous hematologic malignancy that accounts for about 15%-20% of childhood leukemias. Despite therapeutic advances, relapses remain common, and survival for high-risk patients is below 60%. Unlike adult AML, pediatric AML displays distinct genetic mutations, including FLT3-ITD, NPM1, KMT2A rearrangements, and core-binding factors (CBF) fusions, as well as extensive epigenetic dysregulation. Aberrant DNA methylation, histone modifications, and altered non-coding RNA expressions disrupt hematopoietic differentiation and activate oncogenic transcriptional networks. Recent advances in silico transcriptomic analysis have transformed the study of pediatric AML by integrating gene expression and epigenetic data to identify molecular drivers and regulatory networks. Computational RNA-seq pipelines and pathway analyses have highlighted key epigenetic regulators, including DNMT3A, TET2, and HDACs, as potential therapeutic targets. Multi-omics approaches combining transcriptomic, methylomic, and chromatin accessibility data are increasingly used to define biomarkers for diagnosis, prognosis, and therapeutic response. This review provides a comprehensive overview of the molecular and epigenetic landscape of pediatric AML, emphasizing the power of in silico transcriptome analysis to uncover disease mechanisms, refine patient stratification, and guide the development of precision-based epigenetic therapies aimed at improving long-term outcomes in children with AML. - Source: PubMed
Publication date: 2026/05/22
Salah Akram NMansour Reda MEl-Sayyad Gharieb SMoustafa Hebatallah Ahmed MohamedSayed Ghadir AMohamed Hend HElshami Nourhan HAlFarsi KareemFahim AhmedMohammed Osama ARudayni Hassan ADoghish Ahmed S - Mixed-phenotype acute leukemia (MPAL) with BCR::ABL1 fusion is rare, and its clinicopathologic features, genetic landscape, therapeutic response, and patient outcomes remain incompletely defined, as does its relationship to blast-phase chronic myeloid leukemia (CML). In this multicenter study of 44 patients, 86.4% had B/myeloid MPAL, 72.7% showed lymphoid predominance, 40.9% had complex karyotypes (CK), and 68.3% harbored somatic mutations, most commonly RUNX1 mutations (46.3%). RUNX1 mutations frequently co-occurred with AML-associated alterations, whereas DNMT3A, TET2, and BCORL1 mutations were restricted to RUNX1-mutated cases. In contrast, ALL-associated alterations (IKZF1 mutation/deletion and ETV6 mutations) were confined to RUNX1-wild-type patients. TP53 and signaling-pathway mutations (NRAS, KRAS, PTPN11, and FLT3) were not detected. Forty-two patients received induction chemotherapy and/or immunotherapy combined with tyrosine kinase inhibitors: 74.2% of lymphoid-predominant and 63.6% of myeloid-predominant patients receiving ALL- and AML-type therapies, respectively. Ten patients relapsed and 2 had primary refractory disease; some exhibited dynamic shift in predominant lineage immunophenotype, chromosomal alterations, and somatic mutations at relapse or refractory stage. The overall remission rate was 86.8%, with no significant differences across ALL-, AML-, or hybrid-type regimens. After a median follow-up of 24.2 months, the median overall survival (OS) was 52.5 months. CK was associated with inferior OS compared with cases lacking additional chromosomal alterations (p=0.02), whereas RUNX1 mutations were not. No significant differences in genetic profiles, treatment response, or outcomes were observed between patients with and without CML-like features. This study provides a comprehensive genomic and clinical characterization of BCR::ABL1-positive MPAL, supporting improved risk stratification and future therapeutic strategies. - Source: PubMed
Publication date: 2026/05/21
Shen QiudanHuang XiaoyanWang XiaoqiongShuai WenFang HongJabbour ElliasChen WeinaTashakori MehrnooshKhanlari MahsaWu XiaojunShao LinaZhang LingEl Hussein SibaKonoplev SergejKhoury Joseph DTang GuilinWang WeiWang Sa AMedeiros L JeffreyHu Shimin - Myeloid/lymphoid neoplasms with eosinophilia and tyrosine kinase gene fusions (M/LN-eo-TK) are diverse, with most cases showing a combination of lymphoblastic leukemia/lymphoma and myeloproliferative features. Various tyrosine kinase fusion genes have been identified, including FLT3 fusions. RNA based next generation sequencing studies offer an effective approach to detect such pathogenic fusion genes, including the novel SSBP2::FLT3 fusion described here. Timely identification of this fusion gene led to targeted management of our patient, who achieved complete resolution of his FDG-avid lymphadenopathy only after the addition of gilteritinib. Two years after successful bone marrow transplant, the patient remains in complete remission. Clinicians and pathologists should have a low index of suspicion for a M/LN-eo-TK when evaluating patients with and without unexplained eosinophilia in the context of extramedullary lymphoid or myeloid disease or unusual myeloproliferative disorders. - Source: PubMed
Publication date: 2026/05/22
Cook James RAstbury CarolineBosler David SMolina John CRogers Heesun JSobecks Ronald MOwczarczyk Anna B - Standard therapy for elderly patients with acute myeloid leukemia (AML) consists of hypomethylating agents (HMAs) combined with venetoclax (VEN), administered long term until disease progression. However, several retrospective studies have shown that patients in complete remission (CR) who discontinued treatment electively or because of poor tolerance did not experience a negative impact on relapse-free or overall survival. Therefore, after obtaining informed consent, we offered treatment discontinuation to patients in CR after six months of HMA-VEN therapy. Here, we report the outcomes of seven consecutively treated patients who achieved CR between May 2021 and June 2025 and opted for discontinuation of therapy. Five of the seven patients showed clearance of somatic mutations to < 1% and resolution of cytogenetic abnormalities. Six of the seven patients remain in continuous remission for 7-50 months. One patient with FLT3-ITD experienced relapse after 14 months and achieved a second hematologic remission after resuming HMA-VEN therapy. These findings suggest that treatment-free remission after time-limited HMA-VEN therapy may be a feasible approach in selected patients. - Source: PubMed
Publication date: 2026/05/22
Lindemann AlbrechtGöckel GerhardGarcia-Pardillos Guillermo - FLT3 internal tandem duplications (FLT3-ITD) are major genetic events in acute myeloid leukemia (AML). Although the clinical impact of FLT3-ITD "macroclones" (allelic ratio [AR] ≥0.05) is well established, the significance of low-level FLT3-ITD subclones ("microclones") remains uncertain. We conducted a post-hoc analysis of 1 733 patients with newly diagnosed AML enrolled in the BIG-1 trial (NCT02416388). Using next-generation sequencing (NGS), we detected FLT3-ITD microclones (AR between 0.0004 and 0.05) in 17.4% of patients without FLT3-ITD macroclones. Microclones and macroclones (low and high AR) were independently associated with increased relapse risk (sHR 1.50 [95% CI 1.18-1.91], 1.98 [1.50-2.62], and 2.33 [1.69-3.22], respectively) after adjustment for age, white blood cell count, other gene mutations, midostaurin treatment, and allogeneic hematopoietic stem cell transplantation. At 2 years, cumulative incidence of relapse reached 42.5% (95% CI 37.0-47.9) in patients with macroclones, 45.1% (38.3-51.6) in patients with microclones, and 29.4% (26.6-32.3) in patients without FLT3-ITD. In NPM1-mutated AML, both microclones and macroclones were associated with higher levels of measurable residual disease (MRD) and increased relapse risk, without independent impact on overall survival after adjustment for MRD. Analysis of paired samples further revealed that 41.8% of relapses in patients with FLT3-ITD microclones at diagnosis were associated with a macroclone at relapse. These findings challenge current risk stratification models and support the integration of NGS-based FLT3-ITD detection into the diagnostic and prognostic workflow for AML. Prospective trials addressing the management of patients with FLT3-ITD microclones are warranted, as is their consideration in future ELN guidelines. - Source: PubMed
Publication date: 2026/05/21
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