CD135 _ FLT3
- Known as:
- CD135 _ FLT3
- Catalog number:
- GTX40173
- Product Quantity:
- 50 µg
- Category:
- -
- Supplier:
- ACR
- Gene target:
- CD135 _ FLT3
Related genes to: CD135 _ FLT3
- 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
AC220 AC220 is a uniquely potent and selective FLT3 inhibitor with IC50 of 0.56 +_- 0.3 nM and >10 mM for MC4-11 and A375, respectively. For research use only.anti-Flt3 CD135 (1A11)anti-Flt3 CD135 (1A11) type: Primary antibodies host: Mouseanti-Flt3 CD135 (3H1)anti-Flt3 CD135 (3H1) type: Primary antibodies host: Mouseanti-FLT3 CD135 (BV10A4H2)anti-FLT3 CD135 (BV10A4H2) type: Primary antibodies host: Mouseanti-FLT3 CD135 (Internal)anti-FLT3 (Ab-591)anti-FLT3 (Ab-591)anti-FLT3 (Ab-591)anti-FLT3 (Ab-591), Rabbit polyclonal to FLT3, Isotype IgG, Host Rabbitanti-FLT3 (Ab-591), Rabbit polyclonal to FLT3, Isotype IgG, Host RabbitAnti-FLT3 (BV10A4H2), Mouse Monoclonal to FLT3, Isotype IgG1, Host Mouseanti-FLT3 (Phospho-Tyr591) Related articles to: CD135 _ FLT3
- Acute myeloid leukemia (AML) is a molecularly heterogeneous malignancy where next-generation sequencing (NGS) has revolutionized risk stratification and treatment paradigms. However, the interplay between mutation cooperativity, clinical phenotypes, and biochemical markers of organ dysfunction remains poorly characterized. This study investigates how co-mutational patterns influence hematological/biochemical parameters and survival outcomes in AML. - Source: PubMed
Publication date: 2026/08/12
Xu ZhengrongZheng YingZheng YiYao YanyanGeng HailiLi XiaofanWang Shao-YuanPan Lili - Updated classifications incorporating myelodysplasia-related (MR) gene mutations reclassify many cases previously diagnosed as acute myeloid leukemia, not otherwise specified (AML, NOS). We evaluated the clinical significance of MR gene mutation burden, defined by mutation number and variant allele frequency (VAF), in AML, NOS. - Source: PubMed
Publication date: 2026/08/26
Lee TaegeunChu DaehyunKim MiyoungCho Young-UkHwang Sang-HyunLee Je-HwanChoi YunsukChoi Eun-JiIm Ho JoonKim HyeryJang Seongsoo - - Source: PubMed
Publication date: 2026/08/25
Yang Yi-TsungYao Chi-YuanYi Yong-HuaiKao Chein-JunKuo Yuan-YehLin Ming-EnHou Hsin-AnLin Chien-ChinChou Wen-ChienTien Hwei-Fang - Gene mutations and chromosome abnormalities are important components of prognostication in acute myeloid leukemia (AML). Here we assessed whether DNA methylation patterns in AML patients can augment risk assessments provided by genetic and other markers to better predict outcomes. Unsupervised DNA methylation patterns separating patients into 13 DNA methylation subtypes (epitypes) were used to classify 1,262 patients with de novo AML. Epitypes were predominantly comprised of a predominant genetic alteration; however, some patients within epitypes lacked cardinal alterations and were termed genetic alteration-like. Interestingly, patients displaying alteration-like DNA methylation patterns of CEBPAbZIP, FLT3-ITD, core-binding factor, KMT2A-rearrangements and other abnormalities displayed outcomes similar to patients with actual cardinal alterations. We further derived a DNA methylation signature enriched in patients with FLT3-ITD mutations that involved hypomethylation of STAT binding sites, termed the STAT hypomethylation signature (SHS). SHS positivity identified patients with inferior outcomes further adding to the prognostic significance of FLT3-ITD. Machine learning modeling revealed these DNA methylation signatures together significantly added to genetic, demographic and clinical markers to predict remission, relapse and overall survival. In summary, DNA methylation signatures capture patients who mimic cardinal genetic mutations providing additional prognostic information that may be used to in concert with standard genetic markers. - Source: PubMed
Publication date: 2026/08/25
Abdelbaky Salma BGiacopelli BrianKohlschmidt JessicaYamaguchi KyokoMrózek KrzysztofSher Ada ClearyWu Yue-ZhongOrwick ShelleyNicolet DeedraCoombes Kevin RBlachly James SPowell Bayard LKolitz Jonathan EBlum WilliamBaer Maria RCarroll Andrew JStone Richard MEisfeld Ann-KathrinByrd John COakes Christopher C - Relapse remains the leading cause of treatment failure and mortality in pediatric acute myeloid leukemia (pAML), yet the early molecular features underlying relapse susceptibility remain poorly understood. Here, we leveraged our previously generated single-cell chromatin accessibility dataset comprising 177,500 cells from 16 diagnostic pAML samples with long-term clinical outcome data, spanning t(8;21), inv(16), and FLT3-ITD subtypes and stratified into relapse (RPS) and non-relapsed (NRPS) cases. We show that RPS patients harbor relapse-associated chromatin accessibility signatures already detectable at diagnosis across multiple molecular subtypes. These patients display heightened innate immune and inflammatory activation and expansion of HSC/MPP-like leukemic progenitors with stem cell-like regulatory features. Motif enrichment analyses identify AP-1 family members, together with RUNX1, SPI1, and ETS factors, as central regulators shaping the relapse-associated epigenetic state. Elevated expression of these regulators predicts inferior survival across independent AML cohorts. Collectively, these findings suggest that early epigenetic priming of innate immune and inflammatory programs is associated with a relapse-prone state and highlight this core transcriptional network as a candidate biomarker framework in pAML. - Source: PubMed
Publication date: 2026/08/24
Cui BoyuLei MinghuiLiu LiweiShu MingxinYu FurongYang KaiPan YinSong Yunhong