FLT3L_MOUSE Flt3 ligand ELISA tesk kit
- Known as:
- FLT3L_MOUSE Flt3 ligand Enzyme-linked immunosorbent assay test tesk reagent
- Catalog number:
- gen0862
- Product Quantity:
- 1
- Category:
- Peptides
- Supplier:
- EIAab
- Gene target:
- FLT3L_MOUSE Flt3 ligand ELISA tesk kit
Related genes to: FLT3L_MOUSE Flt3 ligand ELISA tesk kit
- 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: FLT3L_MOUSE Flt3 ligand ELISA tesk kit
Related articles to: FLT3L_MOUSE Flt3 ligand ELISA tesk kit
- FLT3-ITD occurs in approximately 20%-25% of cases of adult AML and is associated with increased relapse risk and shorter survival. FLT3-ITD status informs AML risk at diagnosis, but its dynamic changes during disease evolution are not well defined. We hypothesized that divergent FLT3-ITD clonal trajectories are shaped by preexisting molecular features detectable at diagnosis. We analyzed 319 intensively treated adults who were newly diagnosed with non-M3 de novo AML who experienced relapse and had paired FLT3-ITD mutation data at diagnosis and relapse. Patients were classified into four clonal evolution patterns: maintained FLT3-ITD negative (FLT3-ITD), FLT3-ITD loss (FLT3-ITD), FLT3-ITD acquisition (FLT3-ITD), and maintained FLT3-ITD positive (FLT3-ITD). The FLT3-ITD group was strongly associated with concurrent NPM1 and/or DNMT3A mutations, which were enriched compared with those in other groups (p < 0.001). ELN 2022 risk categories differed across clonal evolution patterns, with favorable-risk disease declining progressively from the FLT3-ITD to the FLT3-ITD group (44.3%-6.1%) while intermediate-risk disease rose correspondingly (21.2%-73.5%; both p < 0.001). With a median follow-up of 96.8 months, patients in the FLT3-ITD or FLT3-ITD group had significantly inferior relapse-free and overall survival compared with those in the FLT3-ITD group (p = 0.009 and p = 0.018, respectively, in univariate analyses; p = 0.001 and p = 0.006, respectively, in multivariate analyses adjusted for individual genetic risk features). Transcriptomics showed enrichment of inflammatory pathways in FLT3-ITD cases that persisted after adjustment for NPM1/DNMT3A co-mutations and FLT3-ITD allelic ratio, together with an inferred monocyte-rich profile. Overall, FLT3-ITD evolution is associated with distinct genomic and transcriptomic features present at diagnosis. TRIAL REGISTRATION: 202203013RSD. - Source: PubMed
Tsai Xavier Cheng-HongChang Yu-SungTien Feng-MingLo Min-YenKuo Yuan-YehTseng Mei-HsuanPeng Yen-LingYao Chi-YuanYao Szu-ChiLin Chien-ChinKo Bor-ShengYao MingTien Hwei-FangHou Hsin-AnChou Wen-Chien - - Source: PubMed
Publication date: 2026/09/21
Basendwah Abdulrahim MohammedMiyashita AkihiroFero HenriAlasmari MohammedAlabbas Fahad - While complex fusions involving three chromosomes are already uncommon in AML, the formation of two distinct fusion genes from an identical breakpoint is exceptionally rare. This paper reports the adult case of acute myeloid leukemia harboring dual fusion genes and , both originating from the same RUNX1 breakpoint (chr21:36206707, hg19). The 62-year-old male patient presented with primary refractory acute myeloid leukemia (AML), failed to achieve remission after induction chemotherapy, and had an overall survival of only 3 months. The translocation was cryptic and resulted in PRDM16 overexpression, which is associated with poor prognosis. Integrated molecular profiling revealed concurrent mutations in FLT3-ITD, U2AF1, and PTPN11, collectively indicating a very high disease risk. This case provides the first evidence for the novel mechanism of dual fusion gene formation from a single genomic breakpoint. - Source: PubMed
Publication date: 2026/09/16
Chen SiyuWu ShengwangZhang JingQiang XingLiu SihengYang WuchenPeng XianguiZhang XiRen JunZhang Cheng - Relapse remains the leading cause of treatment failure after allogeneic hematopoietic stem cell transplantation for acute myeloid leukemia and myelodysplastic syndromes. Post-transplant treatment may provide a third anti-leukemic effect after conditioning-related cytotoxicity has waned and before graft-versus-leukemia immunity is fully established. Prophylactic maintenance is initiated in high-risk patients despite undetectable measurable residual disease (MRD), whereas pre-emptive treatment is triggered by the detection of MRD or declining donor chimerism. Hypomethylating agents (HMAs) are biologically attractive and feasible with post-transplant-adapted dosing, but prophylactic azacitidine did not improve relapse-free or overall survival in a randomized trial. Newer decitabine-based, oral HMA, and venetoclax-containing strategies require confirmation. FMS-like tyrosine kinase 3 (FLT3) inhibitors have the strongest prospective evidence in a molecularly selected population. The QuANTUM-First trial supports quizartinib throughout induction, consolidation, and continuation, including after transplantation, whereas the MORPHO trial directly evaluated post-transplant gilteritinib and identified its clearest benefit in patients with detectable peri-transplant FLT3-internal tandem duplication (FLT3-ITD) MRD. This review traces the evolution of relapse prevention strategies and proposes a practical framework integrating baseline risk, serial MRD assessment, targetable biology, immune intervention, and post-transplant feasibility. - Source: PubMed
Publication date: 2026/09/19
Najima Yuho - - Source: PubMed
Wei Andrew H