Polyclonal Rabbit AML1 (Ab-435) Antibody
- Known as:
- Polyclonal Rabbit AML1 (Antibody-435) Antibody
- Catalog number:
- KA0204
- Product Quantity:
- 100ul
- Category:
- -
- Supplier:
- KareBay
- Gene target:
- Polyclonal Rabbit AML1 (Ab-435) Antibody
Related genes to: Polyclonal Rabbit AML1 (Ab-435) Antibody
- 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: Polyclonal Rabbit AML1 (Ab-435) Antibody
Related articles to: Polyclonal Rabbit AML1 (Ab-435) Antibody
- - Source: PubMed
Publication date: 2026/04/29
Chang Yu-HanChang Guang-HuiGao Hai-TaoFu QiangZhao Xiao-SuQin Ya-ZhenJiang QianJiang HaoXu Lan-PingWang YuZhang Xiao-HuiHuang Xiao-JunTang Fei-Fei - Acute myeloid leukemia (AML) is a highly lethal hematologic malignancy, and reliable prognostic biomarkers remain urgently needed. We investigated the expression and clinical relevance of the actin cytoskeleton regulator N-WASP in AML. Analysis of TCGA data revealed significantly reduced N-WASP expression in AML compared with normal tissues, and low expression was associated with adverse clinical features, including FAB-M1/M4 subtypes, DNMT3A mutations, and cytogenetic abnormalities such as t(8;21)/RUNX1::RUNX1T1 and del(7q). Patients with low N-WASP expression exhibited shorter overall survival, and multivariate Cox regression identified N-WASP reduction as an independent risk factor, alongside advanced age and FLT3, DNMT3A and TP53 mutations. Co-expression and enrichment analysis highlighted FNIP1, CLIP1, RICTOR and BRAF as N-WASP-associated regulators converging on mTOR signaling. Experimental validation via RT-qPCR and western blotting in AML bone marrow samples and cell lines confirmed the downregulation of N-WASP and key co-expressed genes. Collectively, these results demonstrate that N-WASP is suppressed in AML and is closely associated with disease risk and clinical outcome. N-WASP may serve as a novel prognostic biomarker and potential therapeutic target warranting further investigation. - Source: PubMed
Publication date: 2026/04/22
Liu CuiSun JianLuo YanHuang PeiChen Yan - The 2022 European LeukaemiaNet acute myeloid leukemia (AML) classification allocates AML with t(8;21) RUNX1::RUNX1T1 fusion and AML with inv(16) or t(16;16) CBFB::MYH11 fusion (collectively, core-binding factor AML), AML with NPM1 without FLT3-ITD mutation and AML with CEBPA bZIP in-frame mutation into the favorable-risk strata based on initial molecular diagnostics. Generally, these entities have a relatively low risk of relapse (< 30%-40%) and many patients (> 50%-60%) survive long-term with intensive chemotherapy alone. However, there is growing literature that patterns of co-mutation, and more importantly, postremission measurable residual disease (MRD) status, modify these risks dynamically; necessitating an adaptive approach to optimize patient outcomes. In this review, we summarize evidence on how molecular and MRD features could assist clinicians in identifying high-risk patients within these favorable-risk subgroups, and where escalation of therapy, including with allogeneic transplantation in first remission, may be beneficial. - Source: PubMed
Publication date: 2026/03/20
Tedjaseputra AdityaRussell NigelDillon Richard - - Source: PubMed
Publication date: 2026/04/10
Jagadish GayathriKulkarni Jayashree DKumari PrasannaKorlimarla Aruna - Relapsed/refractory RUNX1::RUNX1T1-positive acute myeloid leukemia remains a therapeutic challenge due to high relapse rates post-allogeneic hematopoietic stem cell transplantation. Preclinical evidence suggests that RUNX1::RUNX1T1 fusion proteins sensitize cells to poly ADP-ribose polymerase inhibitors by suppressing homologous recombination repair. This study explores the safety and efficacy of a novel conditioning regimen incorporating olaparib (a PARPi) for relapsed/refractory RUNX1::RUNX1T1+ AML patients undergoing allo-HSCT. - Source: PubMed
Publication date: 2026/03/25
Xue SongMa WeiChen ManSun Hui-PengCao Xing-Yu