EVI1 _ AML1
- Known as:
- EVI1 _ AML1
- Catalog number:
- Y214484
- Product Quantity:
- 200ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- EVI1 _ AML1
Related genes to: EVI1 _ AML1
- Gene:
- MECOM NIH gene
- Name:
- MDS1 and EVI1 complex locus
- Previous symbol:
- MDS1, EVI1
- Synonyms:
- MDS1-EVI1, PRDM3, KMT8E
- Chromosome:
- 3q26.2
- Locus Type:
- gene with protein product
- Date approved:
- 1990-07-10
- Date modifiied:
- 2019-04-23
- Gene:
- RUNX1 NIH gene
- Name:
- RUNX family transcription factor 1
- Previous symbol:
- AML1, CBFA2
- Synonyms:
- PEBP2A2, AMLCR1
- Chromosome:
- 21q22.12
- Locus Type:
- gene with protein product
- Date approved:
- 1991-08-20
- Date modifiied:
- 2019-04-23
- Gene:
- RUNX1T1 NIH gene
- Name:
- RUNX1 translocation partner 1
- Previous symbol:
- AML1T1, CBFA2T1
- Synonyms:
- CDR, ETO, MTG8, ZMYND2
- Chromosome:
- 8q21.3
- Locus Type:
- gene with protein product
- Date approved:
- 1993-12-16
- Date modifiied:
- 2016-10-05
Related products to: EVI1 _ AML1
Acute myeloid leukemia 1 protein,AML1,CBFA2,CBF-alpha-2,Core-binding factor subunit alpha-2,Homo sapiens,Human,Oncogene AML-1,PEA2-alpha B,PEBP2-alpha B,Polyomavirus enhancer-binding protein 2 alpha BAcute myeloid leukemia 1 protein,Aml1,Cbfa2,CBF-alpha-2,Core-binding factor subunit alpha-2,Mouse,Mus musculus,Oncogene AML-1,PEA2-alpha B,Pebp2ab,PEBP2-alpha B,Polyomavirus enhancer-binding protein 2Acute myeloid leukemia 1 protein,Aml1,Cbfa2,CBF-alpha-2,Core-binding factor subunit alpha-2,Oncogene AML-1,PEA2-alpha B,PEBP2-alpha B,Polyomavirus enhancer-binding protein 2 alpha B subunit,Rat,RattusAML1 Polyclonal Antibody, Reactivity: H M R, Gene ID: 861, Synonyms: RUNX1AML1 Polyclonal Antibody, Reactivity: H M, Gene ID: 861, Synonyms: RUNX1AML1 Polyclonal Antibody, Reactivity: H M, Gene ID: 861, Synonyms: RUNX1AML1 EMSA KitAML1 EMSA Probe SetAML1 (Ab-435) antibodyAML1 (Ab-435) antibodyAML1 (Ab-435) antibodyAML1 (Ab-435) antibodyAML1 (Ab-435) AntibodyAML1 (H297) pAb Host Rabbit Reactivity H,M,R Application WB IHC IFAML1 (phospho-Ser276) antibody Related articles to: EVI1 _ AML1
- RNA sequencing from 262 patients with paediatric acute myeloid leukaemia (AML) (JPLSG AML-12) was deconvoluted employing adult single-cell RNA-sequencing signatures and Zeng's method, which defined five cellular hierarchy subtypes: primitive, leukaemic stem/progenitor cell (LSPC)-Cycle, ProMono-like, granulocyte-monocyte progenitor (GMP)-like and intermediate. Principal component analysis revealed two main axes that distinguish paediatric from adult AML, with notable LSPC-Cycle and ProMono-like phenotype enrichment. LSPC-Cycle (>25% cycling stem-like cells) had proliferative and quiescent LSPCs, frequent French-American-British (FAB)-M7 and worst prognosis (overall survival odds ratio vs. GMP-like: 11.33). Morphology was related to the primitive (FAB-M0), GMP-like (M2/M4) and ProMono-like (M5) groups. Genomic patterns aligned with hierarchy: CBFA2T3::GLIS2, MYB::GATA1 and MECOM high expression in LSPC-Cycle; CBFB::MYH11, NUP98::NSD1 and NPM1 in the intermediate; and DEK::NUP214 and NUP98::KDM5A were concentrated in the primitive group. bZIP CEBPA and FLT3-ITD mutations clustered in the intermediate and primitive groups. Most of RUNX1::RUNX1T1 clustered in the intermediate group, whereas KMT2A::MLLT3 hierarchy differed with MECOM expression level. Paediatric AML comprised more primitive cells, rarely with mono-like/cDC-like dominance. LSPC-Cycle, FLT3-ITD and NUP98::KDM5A were considered independent prognostic factors in multivariate analysis. Findings indicate the prognostic relevance of cellular hierarchy and the importance of integrating hierarchy-specific molecular profiles for improved risk stratification and treatment formulation. - Source: PubMed
Publication date: 2026/02/03
Komori TomoyaKawai TomokoOkuno YusukeTsujimoto ShinichiKato ShotaKamitori TatsuyaSaida SatoshiIkeda JunjiOhki KentaroKato MotohiroTomizawa DaisukeTaga TakashiTakita JunkoHoribe KeizoAdachi SouichiHayashi YasuhideIto ShuichiShiba Norio - Myeloid sarcoma (MS) is a rare, extramedullary tumor consisting of myeloid blasts. Little is known about the genetic background of MS and the prognostic value of genetic abnormalities in MS. In particular, the broad variety of gene fusions that occur in MS is marginally covered by traditional testing methods due to lack of fresh tumor specimens. - Source: PubMed
Publication date: 2023/03/14
Yang YunfanShu YangTang YuanZhao ShaJia YongqianJi JieMa HongbingLin TingZheng KeXu HengWu Yu - The European LeukemiaNet (ELN) recently proposed a revised recommendation for the diagnosis and management of acute myeloid leukemia (AML) in adults, recognized as ELN-2022. However, validation in a large real-world cohort remains lacking. In this study, we aimed to validate the prognostic relevance of the ELN-2022 in a cohort of 809 de novo, non-M3, younger (ages 18-65 years) AML patients receiving standard chemotherapy. The risk categories of 106 (13.1%) patients were reclassified from that determined using ELN-2017 to that determined using ELN-2022. The ELN-2022 effectively helped distinguish patients as favorable, intermediate, and adverse risk groups in terms of remission rates and survival. Among patients who achieved first complete remission (CR1), allogeneic transplantation was beneficial for those in the intermediate risk group, but not for those in the favorable or adverse risk groups. We further refined the ELN-2022 system by re-categorizing AML patients with t(8;21)(q22;q22.1)/RUNX1::RUNX1T1 with KIT , JAK2 or FLT3-ITD mutations into the intermediate risk subset, AML patients with t(7;11)(p15;p15)/NUP98::HOXA9 and AML patients with co-mutated DNMT3A and FLT3-ITD into the adverse risk subsets, and AML patients with complex or monosomal karyotypes, inv (3)(q21.3q26.2) or t(3;3)(q21.3;q26.2)/GATA2,MECOM(EVI1) or TP53 mutation into the very adverse risk subset. The refined ELN-2022 system performed effectively to distinguish patients as favorable, intermediate, adverse, and very adverse risk groups. In conclusion, the ELN-2022 helped distinguish younger, intensively treated patients into three groups with distinct outcomes; the proposed refinement of ELN-2022 may further improve risk stratification among AML patients. Prospective validation of the new predictive model is necessary. - Source: PubMed
Publication date: 2023/03/13
Lo Min-YenTsai Xavier Cheng-HongLin Chien-ChinTien Feng-MingKuo Yuan-YehLee Wan-HsuanPeng Yen-LingLiu Ming-ChihTseng Mei-HsuanHsu Cheng-AnChen Jui-CheLin Liang-InSun Hsun-IChuang Yi-KuangKo Bor-ShengTang Jih-LuhYao MingChou Wen-ChienHou Hsin-AnTien Hwei-Fang - We investigated genome-wide DNA methylation patterns in 64 pediatric patients with acute myeloid leukemia (AML). Based on unsupervised clustering with the 567 most variably methylated cytosine guanine dinucleotide (CpG) sites, patients were categorized into 4 clusters associated with genetic alterations. Clusters 1 and 3 were characterized by the presence of known favorable prognostic factors, such as RUNX1-RUNX1T1 fusion and KMT2A rearrangement with low MECOM expression, and biallelic CEBPA mutations (all 8 patients), respectively. Clusters 2 and 4 comprised patients exhibiting molecular features associated with adverse outcomes, namely internal tandem duplication of FLT3 (FLT3-ITD), partial tandem duplication of KMT2A, and high PRDM16 expression. Depending on the methylation values of the 1243 CpG sites that were significantly different between FLT3-ITD+ and FLT3-ITD- AML, patients were categorized into 3 clusters: A, B, and C. The STAT5-binding motif was most frequently found close to the 1243 CpG sites. All 8 patients with FLT3-ITD in cluster A harbored high PRDM16 expression and experienced adverse events, whereas only 1 of 7 patients with FLT3-ITD in the other clusters experienced adverse events. PRDM16 expression levels were also related to DNA methylation patterns, which were drastically changed at the cutoff value of PRDM16/ABL1 = 0.10. The assay for transposase-accessible chromatin sequencing of AMLs supported enhanced chromatin accessibility around genomic regions, such as HOXB cluster genes, SCHIP1, and PRDM16, which were associated with DNA methylation changes in AMLs with FLT3-ITD and high PRDM16 expression. Our results suggest that DNA methylation levels at specific CpG sites are useful to support genetic alterations and gene expression patterns of patients with pediatric AML. - Source: PubMed
Yamato GenkiKawai TomokoShiba NorioIkeda JunjiHara YusukeOhki KentaroTsujimoto Shin-IchiKaburagi TaekoYoshida KenichiShiraishi YuichiMiyano SatoruKiyokawa NobutakaTomizawa DaisukeShimada AkiraSotomatsu ManabuArakawa HirokazuAdachi SouichiTaga TakashiHoribe KeizoOgawa SeishiHata KenichiroHayashi Yasuhide - Chromosome translocations involving the RUNX1 gene at 21q22 are recurring abnormalities in acute myeloid leukemia (AML) and myelodysplastic syndrome (MDS), that is, t(8;21) and t(3;21) and in B-cell acute lymphoblastic leukemia with t(12;21). These translocations result in the fusion of RUNX1 with RUNX1T1, MECOM, and ETV6, respectively, and are implicated in leukemogenesis. Here we describe 10 rare RUNX1 fusion gene partners, including six novel fusions, in myeloid neoplasia. Comprehensive molecular testing revealed the partner genes and features of these fusions in all the tested patients, and detected various recurring myeloid related gene mutations in eight patients. In two patients, RUNX1 mutations were identified. Most of these fusions were detected in patients with high-grade MDS and AML with a relatively short survival. Integration of conventional chromosome analysis, FISH testing and molecular genetic studies allow a comprehensive characterization of these rare RUNX1 fusions. Our study may help define myeloid neoplasms with rare and novel RUNX1 translocations and support appropriate patient management. - Source: PubMed
Publication date: 2020/10/21
Aypar UmutYao JinjuanLondono Dory MKhoobyar RoseScalise AngelaArcila Maria ERoshal MikhailXiao WenbinZhang Yanming