RUNX1 antibody - middle region (P100814_P050)
- Known as:
- RUNX1 (anti-) - middle region (P100814_P050)
- Catalog number:
- p100814_p050
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- RUNX1 antibody - middle region (P100814_P050)
Related genes to: RUNX1 antibody - middle region (P100814_P050)
- Gene:
- CBFA2T3 NIH gene
- Name:
- CBFA2/RUNX1 translocation partner 3
- Previous symbol:
- -
- Synonyms:
- MTGR2, ZMYND4, MTG16, RUNX1T3, ETO2
- Chromosome:
- 16q24.3
- Locus Type:
- gene with protein product
- Date approved:
- 1998-08-13
- Date modifiied:
- 2016-10-05
- 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
Related products to: RUNX1 antibody - middle region (P100814_P050)
Related articles to: RUNX1 antibody - middle region (P100814_P050)
- 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 - The t(16;21)(q24;q22) translocation creates the :: (also known as , ) fusion gene, representing a rare but clinically significant subtype of myeloid neoplasms. This comprehensive study presents detailed clinical, immunophenotypic, cytogenetic, and molecular data from 10 new cases while integrating findings from 35 previously reported cases. Patients showed a median age of 48 years with notable female predominance. Immunophenotypic analysis consistently demonstrated a distinctive hybrid myeloid/B-lymphoid phenotype characterized by CD19 co-expression with myeloid markers. Cytogenetic evaluation revealed additional chromosomal abnormalities in 75.6% of cases, with trisomy 8 being most frequent (42.2%). Next-generation sequencing identified recurrent mutations in (50%), , , and (each 25%). Clinically, this fusion strongly correlated with therapy-related myeloid neoplasms and demonstrated significantly worse survival outcomes compared to :: AML, highlighting its distinct clinicopathological features and adverse prognostic implications. - Source: PubMed
Publication date: 2025/12/22
Guo DongmeiWang CuiYao JingyaChen LongNie YanboLiu EnbinTian XinHou XiaojuYang ShaobinLin Yani - The leukemia fusion gene CBFB-MYH11 requires RUNX1 for leukemogenesis, but the underlying mechanism is unclear. By in vitro studies, we found that CBFβ-SMMHC, the chimeric protein encoded by CBFB-MYH11, could enhance the binding affinity between RUNX1 and its target DNA. Increased RUNX1-DNA binding was also observed in myeloid progenitor cells from mice expressing CBFβ-SMMHC. Moreover, only CBFβ-SMMHC variants able to enhance the DNA binding affinity by RUNX1 could induce leukemia in mouse models. Marked transcriptomic changes, affecting genes associated with inflammatory response and target genes of CBFA2T3, were observed in mice expressing leukemogenic CBFβ-SMMHC variants. Finally, we show that CBFβ-SMMHC could not induce leukemia in mice with a Runx1-R188Q mutation, which reduces RUNX1 DNA binding but does not affect its interaction with CBFβ-SMMHC or its sequestration to cytoplasm by CBFβ-SMMHC. Our data suggest that, in addition to binding RUNX1 to regulate gene expression, enhancing RUNX1 binding affinity to its target DNA is an important mechanism by which CBFβ-SMMHC contributes to leukemogenesis, highlighting RUNX1-DNA interaction as a potential therapeutic target in inv(16) acute myeloid leukemia. - Source: PubMed
Publication date: 2025/08/05
Zhen TaoCao YaqiangDou TongyiChen YunLopez GuadalupeMenezes Ana CatarinaWu XufengHammer John ACheng JunGarrett LisaAnderson StacieKirby MarthaWincovitch StephenSisay BayuElkahloun Abdel GWu DiCastilla Lucio HYang WeiJiang JiansenZhao KejiLiu P Paul - - Source: PubMed
Wang Wei JLoghavi Sanam - The past 25 years of clinical trials have produced few improvements in pediatric AML (pAML) outcomes. This is acutely evident in patients with t(16;21)(p11;q22), yielding . Patients with -positive AML relapse quickly and do not respond to transplantation. Major histocompatibility complex (MHC) class I & II receptors and costimulatory molecules are absent at diagnosis in positive AML, mirroring the phenotype and outcomes of post-transplant relapse. We show that this is driven by overexpression of and in multiple clinical cohorts. While AML is the most extreme example, this phenotype is shared by lethal driven AML, and patients with have significantly worse outcomes when EZH2 overexpression co-occurs. The FDA-approved EZH2 inhibitor tazemetostat reverses this phenotype, re-establishes MHC presentation, and elicits immune effector cell-mediated elimination. EZH2 inhibitors may provide the first targeted therapeutic frontline option for AML patients with , with the potential for broader frontline immunostimulatory benefits. - Source: PubMed
Publication date: 2025/09/18
Buteyn Nathaniel JLaMantia Samantha JBurke Connor GSartori Vincent JDeering-Gardner EveDeBruine Zachary JKamarudin DahlyaChandler Darrell PMonovich Alexander CPerez Monika WYi Joanna SRies Rhonda EAlonzo Todd ARyan Russell JhMeshinchi SoheilTriche Timothy J