CD135 _ FLT3 (N_term)
- Known as:
- CD135 _ FLT3 (N_term)
- Catalog number:
- AP14352PU-N
- Product Quantity:
- 0.1 mg
- Category:
- -
- Supplier:
- ACR
- Gene target:
- CD135 _ FLT3 (N_term)
Related genes to: CD135 _ FLT3 (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: CD135 _ FLT3 (N_term)
Related articles to: CD135 _ FLT3 (N_term)
- Acute myeloid leukemia (AML) is a heterogeneous malignancy with a poor prognosis. Genetic and molecular profiling help guide treatment decisions, including the use of allogeneic hematopoietic stem cell transplantation (allo-HSCT), to reduce relapse risk. This study evaluated the impact of individual and co-mutational genetic profiles in AML patients in first complete remission after receiving allo-HSCT using data from the PETHEMA registry. A retrospective analysis assessed overall survival and relapse-free survival (RFS). Cox regression identified significant variables used to develop a risk score based on hazard ratios, incorporating age, AML type, transplant timing, and genetic/molecular alterations. A total of 717 patients (median age 56.5 years) were included, most classified as adverse risk by ELN2022 criteria. Both ELN2017 and ELN2022 risk classifications were validated. Multivariate analysis showed that DNMT3A, SF3B1, TP53, and WT1 mutations were linked to shorter RFS, whereas FLT3-ITD mutations correlated with prolonged RFS. These findings were integrated into a proposed prognostic score, which was validated. Therefore, this study highlights the prognostic importance of genetic mutations in AML patients undergoing allo-HSCT. These insights could inform pre-transplant strategies, including donor selection and conditioning regimens, as well as post-transplant maintenance therapy. - Source: PubMed
Publication date: 2026/05/07
Colmenares RafaelBarragán EvaRodríguez-Veiga RebecaTorres-Miñana LauraSánchez-García JoaquínTormo MarBernal TeresaMartínez-Sánchez PilarRodríguez-Arbolí EduardoGil CristinaSoria-Saldise ElenaSerrano JosefinaColorado MercedesGarcía-Fortes MaríaBilbao CristinaLópez-Lorenzo José LuisLarráyoz María JoséPérez-Santaolalla EstherLavilla-Rubira EsperanzaAlgarra LorenzoGarcía-Garay María CarmenChillón CarmenTorres-Ochando MelissaCouto CarmenGarcía-Boyero RaimundoAlmela ÁgataNoriega VíctorCallejas MartaBarrios ManuelCasado SoledadBalerdi AmaiaCabello AnaLabrador JorgeMateos María CarmenAmigo María LuzPérez-Encinas ManuelGarcía-Pérez María JoséCostilla LissetteBergua JuanCarreño-Tarragona GonzaloMartínez-López JoaquínAyala RosaMontesinos Pau - - Source: PubMed
Publication date: 2026/05/07
Crupi FrancescaCiolli GaiaPiccini MatteoScappini BarbaraFasano LauraQuinti ElisaPasquini AndreaCaroprese JessicaGianfaldoni GiacomoMotta GiovannaSanti RaffaellaMaccari ChiaraGuglielmelli PaolaVannucchi Alessandro MMannelli Francesco - ASXL1 mutations (ASXL1) are common in acute myeloid leukemia (AML) and have historically conferred an adverse prognosis with intensive chemotherapy. Given the increasing use of venetoclax (VEN)-based lower intensity therapy (LIT), the European LeukemiaNet introduced a four-gene genetic risk classifier in 2024 that categorizes ASXL1 as favorable risk in the absence of FLT3-ITD, RAS, and TP53 mutations. However, the prognostic significance of ASXL1 across different contemporary LIT+VEN backbones remains controversial. - Source: PubMed
Marvin-Peek JenniferDiNardo Courtney DLoghavi SanamRavandi FarhadBorthakur GautamDaver Naval GKadia Tapan MJabbour EliasDunbar AndrewTang GuilinShort Nicholas JHaddad Fadi GAbbas Hussein AKugler EitanMaiti AbhishekIssa Ghayas CTakahashi KoichiBhalla KapilPemmaraju NaveenAlvarado YesidShpall Elizabeth JPopat UdayRamdial JeremyChamplin Richard EKantarjian Hagop MGarcia-Manero GuillermoSenapati Jayastu - Mutations in the RAS gene family (NRAS, KRAS) are critical drivers of late-stage acute myeloid leukemia (AML) progression. They are frequently detected in relapsed/refractory AML and AML transformed from myelodysplastic syndrome (MDS). Occurring as late-stage genetic events, RAS mutations synergize with early drivers to promote leukemogenesis. While mutually exclusive with FLT3-ITD mutations, they coexist with KIT, RUNX1, CEBPA mutations and MLL rearrangements. Granulocyte-monocyte progenitors (GMPs) serve as the cellular origin for RAS-mutant leukemia stem cells (LSCs). Ultimately, RAS mutations drive monocytic differentiation of LSCs and venetoclax (VEN) resistance through BCL-2 family rewiring. Beyond AML, they are hallmark genetic lesions in juvenile myelomonocytic leukemia (JMML) and present in 15%-20% of pediatric acute lymphoblastic leukemia (ALL) cases. Here, we propose a comprehensive pathogenic model and targeted therapeutic framework focusing on RAS, MCL-1, BCL2L1 to overcome drug resistance and improve patient outcomes. - Source: PubMed
Publication date: 2026/04/11
Jiang CongfaWang HangxuanZhao JiaxinXu YuweiDuan Shiwei - Although next-generation sequencing (NGS) has allowed for the detection of mutations in acute myeloid leukemia (AML), the clinical relevance of variant allele frequency (VAF) for the majority of mutations is unknown. This study aimed to investigate whether the VAFs of AML-associated mutations could improve the prognostic classification in AML. - Source: PubMed
Publication date: 2026/05/05
Zhao LiCheng FengWei JinmingLiu RimingZhao QiZhang YanhongLi Yulan