CBFA2T3 antibody - N-terminal region (ARP33993_P050)
- Known as:
- CBFA2T3 (anti-) - N-terminal region (ARP33993_P050)
- Catalog number:
- arp33993_p050
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- CBFA2T3 antibody - N-terminal region (ARP33993_P050)
Related genes to: CBFA2T3 antibody - N-terminal region (ARP33993_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
Related products to: CBFA2T3 antibody - N-terminal region (ARP33993_P050)
Related articles to: CBFA2T3 antibody - N-terminal region (ARP33993_P050)
- CBFA2T3::GLIS2-positive myeloid neoplasms occur predominantly in infants and can closely mimic pediatric small round cell sarcomas. We describe a 14-month-old boy who presented with left leg pain, an abnormal gait, and a destructive left ischial mass. Tissue biopsy was initially interpreted as an undifferentiated Ewing-like sarcoma. Bone marrow aspiration contained approximately 2% unclassified large cells, while trephine biopsy demonstrated focal tumor infiltration. Marrow tumor cells showed strong CD56 and weak CD61 expression and were positive for WT1, CD43, ERG, CD117, and BCL2. Lysozyme, MPO, TdT, and CD71 were negative. Diagnostic bone marrow flow cytometry was not performed. Molecular studies on pelvic lesion tissue showed negative results on EWSR1 break-apart fluorescence hybridization (FISH). Broad RNA fusion testing detected CBFA2T3::GLIS2, joining CBFA2T3 exon 11 to GLIS2 exon 3, without a covered Ewing or Ewing-like sarcoma-defining fusion. After one cycle of cyclophosphamide, doxorubicin, and vincristine under the provisional sarcoma diagnosis, treatment was redirected to a 10-day course of cytarabine, etoposide, and daunorubicin. Severe myelosuppression was managed with anti-infective and supportive therapy. Subsequent marrow morphology, trephine biopsy, and flow cytometry showed no evident residual tumor. Follow-up MRI demonstrated marked reduction of the pelvic mass, although residual osseous abnormalities persisted. The patient subsequently continued treatment elsewhere. Available records documented additional targeted therapy and maternal haploidentical hematopoietic stem cell transplantation (HSCT). The first reported post-transplant molecular assessment detected no CBFA2T3::GLIS2 fusion transcript. Detailed post-transfer treatment parameters and long-term outcomes were unavailable. This case highlights the value of integrated tissue and marrow assessment and broad RNA fusion testing in EWSR1-negative infantile small round cell tumors. - Source: PubMed
Publication date: 2026/09/17
Chen SimanChen JianxiaYao Qiang - Acute myeloid leukemia (AML) remains a major therapeutic challenge despite remarkable advances in genomic characterization. Although molecular profiling has transformed disease classification and risk stratification, treatment for most patients continues to rely on cytotoxic chemotherapy regimens developed more than 50 years ago. Numerous attempts to improve outcomes through treatment intensification, alternative chemotherapy approaches, and targeted agents have produced incremental benefits for selected patient populations, but have failed to fundamentally alter outcomes for many high-risk AML subtypes. A major obstacle to the broader application of immunotherapy in AML has been the absence of targets that clearly distinguish leukemic cells from normal hematopoietic tissues. Consequently, most immune-based therapies have focused on AML-associated antigens such as CD33, CD123, and CLEC12A, resulting in a narrow therapeutic window and significant hematopoietic toxicity. Recent advances in large-scale transcriptomic profiling, integrated genomic analyses, and immunopeptidomics have enabled systematic identification of AML-restricted biomarkers linked to leukemia-defining oncogenic programs. Rather than seeking a universal AML antigen, these approaches have uncovered subtype-specific targets, including FOLR1 in CBFA2T3::GLIS2 AML, CLEC2A in KMT2A-rearranged AML, mesothelin or CD7 in selected high-risk AML subsets, and intracellular targets such as WT1, PRAME, NPM1 neoantigens, and fusion-derived peptides. These discoveries have created opportunities for immunotherapeutic approaches capable of selectively targeting leukemic cells, while preserving normal hematopoiesis. This Spotlight Review discusses the evolution of AML biomarker discovery from prognostic classification to therapeutic target identification and highlights emerging AML-restricted biomarkers that may enable a new generation of biologically-precise immunotherapies for molecularly defined AML subsets. - Source: PubMed
Publication date: 2026/09/24
Meshinchi SoheilLocatelli Franco - This study aimed to investigate the clinical characteristics of primary pure erythroid leukemia (PEL) in children, particularly PEL with NFIA::CBFA2T3 or NFIA::RUNX1T1 fusions. We retrospectively analyzed clinical data from three children with PEL who were treated at the Capital Center for Children's Health, Capital Medical University, between September 2017 and September 2021, and reviewed the literature. All three patients had cytogenetic alterations: case 1 had t (1;16) (p32;q24), case 2 had an NFIA::CBFA2T3 fusion, and case 3 had an NFIA::RUNX1T1 fusion. All three patients responded poorly to standard intensive chemotherapy for acute myeloid leukemia (AML) and to regimens containing hypomethylating agents. Cases 1 and 3 died after continued disease progression. Case 2 underwent intensive chemotherapy followed by umbilical cord blood stem cell transplantation, relapsed 2 months after transplantation, and died soon thereafter. These findings suggest that primary PEL in children is characterized by an insidious onset, rapid progression, and poor response to commonly used AML chemotherapy regimens, and that patients may benefit from hematopoietic stem cell transplantation after achieving complete remission. - Source: PubMed
Zhong D XLi J JZhang LZhang Z XLi J HHu M ZLiu R - - Source: PubMed
Huang JiayuWu TingZhu HongmingLi JianfengZhu YongmeiWeng XiangqinHuang TingJiang ChuanheLu HaiyangZhang YunxiangHu Xiaoxia - Repetitive mild traumatic brain injury (RMTBI) and Alzheimer's disease (AD) share some pathological features, such as tau pathology, inflammation, and neurodegeneration. Tissue injury and aging are linked to cellular DNA methylation alterations in the circulation, which can result in altered gene expression, making it a promising therapeutic target for dysfunctional gene expression. It is unknown whether DNA methylation and potentially related gene expression pathophysiological mechanisms are shared between athletes exposed to RMTBI and AD. The aim was to explore the blood DNA methylomes and transcriptomes from a cohort of professional fighters (PFs) with RMTBI and AD to understand if there are significant differences in the DNA methylome that could potentially impact the transcriptome and thus contribute to pathophysiology in RMTBI. Given that RMTBI and AD share pathological features, it was hypothesized that RMTBI could also share DNA methylome and transcriptome features with AD. The methylomes (Infinium Human Methylation EPIC BeadChip) and transcriptomes (Illumina NovaSeq 6000) from active PFs (aPFs) or retired PFs (rPFs) were compared with AD and cognitively normal (CN) control groups. Several differentially methylated positions (DMPs) in the genome were linked to differentially expressed RNA transcripts that were unique to group comparison. Of these, identified in the young CN versus aPF comparison, as well as and , identified in the rPF versus AD comparison, had significant differentially methylated RNA expression. Interestingly, a DNA methylation site located in the region was also associated with brain volume in an RMTBI subcohort. Distinct DNA methylation and corresponding gene expression alterations observed in the RMTBI cohort, compared with the AD cohort, suggests no shared DNA methylation pathophysiological contributors to AD and RMTBI pathobiology. This information is novel and suggests that DNA methylation could play an important, unique role in RMTBI underlying pathobiology. - Source: PubMed
Publication date: 2026/08/23
Weber GraceKhrestian MariaFormica ShaneTuason ElizabethRao StephenPillai JaganRitter AaronBernick CharlesLeverenz James BBekris Lynn M