CD135 _ FLT3 Control Peptide
- Known as:
- CD135 _ FLT3 Control Peptide
- Catalog number:
- AP14352CP-N
- Product Quantity:
- 0.1 mg
- Category:
- -
- Supplier:
- ACR
- Gene target:
- CD135 _ FLT3 Control Peptide
Related genes to: CD135 _ FLT3 Control Peptide
- 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 Control Peptide
Related articles to: CD135 _ FLT3 Control Peptide
- 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 - Leukemic stem cells (LSCs) are the cellular reservoir most strongly implicated in relapse of acute myeloid leukemia, yet their operational detection by multiparameter flow cytometry remains challenging because of immunophenotypic overlap with normal progenitors and variability across assays. Including CD45RA in the CD34⁺CD38⁻ gating strategy substantially improves discrimination between malignant and normal stem/progenitor populations and thus enables more precise LSC enumeration in a single-tube format. Given the clinical importance of accurately quantifying the LSC compartment, we evaluated a refined single-tube flow cytometry assay that incorporates CD45RA within the CD34 + CD38- gate to increase specificity for the leukemic stem compartment. - Source: PubMed
Publication date: 2026/05/02
Navidinia Amir AbbasRostami ShahrbanooKarami NajibeShemshadinia MohammadrezaPatekhor Habibeh SabriHajaliaskari AkramMohammadi SaeedRostami TaherehBarkhordar MaryamVaezi MohammadJanbabaei GhasemChahardouli Bahram - Acute myeloid leukemia (AML) blasts often have high CD135 (FLT3 receptor) expression, but its clinical impact is unclear. We analyzed CD135 expression, and the clinical characteristics and outcomes of 214 patients with de novo AML diagnosed between October 2022 and May 2024. Subsequently, we collected data on additional 78 patients, diagnosed with AML at four medical centers from June to December 2024, for external validation. The high-CD135-expression group had significantly lower CD34 surface expression (p = 0.003) and higher CD33 expression (p = 0.014) on AML blasts. The high-CD135-expression group also showed a higher frequency of NPM1 (p < 0.001) and DNMT3A (p = 0.032) mutations, but was not significantly associated with CD135 expression (p = 0.229). The patients in the high-CD135-expression group had lower initial induction therapy response rates than those in the low-CD135-expression group (p < 0.001). High CD135 expression was independently associated with poorer OS and PFS. In the subgroup of patients with high CD135 expression and FLT3-ITD mutations, those who received TKI combined with chemotherapy had significantly better OS (p = 0.007). Then we developed a prognostic nomogram incorporating CD135 expression. This model performed well both in the development cohort (area under the curve [AUC] = 0.817) and multicenter validation cohort (AUC = 0.722). CD135 expression on AML blasts is a pivotal marker that integrates molecular pathogenesis with clinical outcomes, highlighting its dual role as a prognostic indicator and therapeutic target in precision clinical approaches for AM. - Source: PubMed
Publication date: 2026/05/02
Nie JinhongGao LuShao YingchunYang LiCao JunjieXu JingeWang YuhangZhang YuqiCui TongZhou ShiyuanZhu WenjuanZhu MingqingMa XiaoWu DepeiWu Xiaojin