ETV6 Antibody (Center) Blocking Peptide
- Known as:
- ETV6 Antibody (Center) Blocking Peptide
- Catalog number:
- BP14496c
- Product Quantity:
- 2
- Category:
- -
- Supplier:
- Abgen
- Gene target:
- ETV6 Antibody (Center) Blocking Peptide
Related genes to: ETV6 Antibody (Center) Blocking Peptide
- Gene:
- ETV6 NIH gene
- Name:
- ETS variant 6
- Previous symbol:
- -
- Synonyms:
- TEL
- Chromosome:
- 12p13.2
- Locus Type:
- gene with protein product
- Date approved:
- 1995-11-28
- Date modifiied:
- 2019-04-23
Related products to: ETV6 Antibody (Center) Blocking Peptide
Related articles to: ETV6 Antibody (Center) Blocking Peptide
- The name of one of the authors in the article by Pedroza Romo et al. [(2026), Acta Cryst. D82, 516-532] is corrected. - Source: PubMed
Publication date: 2026/08/01
Pedroza Romo Maria JKeliiliki AlihikauaAverett Jacob CGonzalez Joseph FNoakes EthanWilson Elijah WSmith ConradAverett BlakeHansen DaltonNickles RileyBradford MilesSoleimani SaraSmith TobinNawarathnage SupeshalaSamarawickrama PrasadikaKelsch ArielBunn DerickStewart CameronAbiodun WisdomTsubaki EvanBrown SethDoukov Tzanko IMoody James D - We report an unusual case of juvenile myelomonocytic leukemia (JMML) in a 4-year-old male who had persistent monocytosis and intermittent anemia and thrombocytopenia beginning at 1 year of age. Given a history of recurrent skin infections, the patient initially received an evaluation for a primary immune disorder, but workup was inconclusive. Bone marrow examination was performed to further evaluate persistent and progressive cytopenias. The findings fulfilled the criteria for JMML with peripheral blood monocytosis ≥ 1×10/L, blast/promonocyte percentage of <20% in peripheral blood and bone marrow, clinical evidence of organ infiltration with hepatosplenomegaly, and absent fusion and gene rearrangements. Additionally, next generation sequencing (NGS) studies performed on the bone marrow aspirate revealed multiple acquired somatic mutations, including a G12D mutation, meeting criteria for the diagnosis of JMML in the context of this case. A novel R369W mutation in the setting of JMML was also detected, which may explain the striking megakaryocytic dysplasia in the bone marrow beyond what is typically seen in JMML. This case showed interesting features overlapping with Ras-associated autoimmune leukoproliferative disorder (RALD), including monocytosis and recurrent infections. Furthermore, this case demonstrated a need for more definitive criteria for distinguishing JMML from RALD. - Source: PubMed
Publication date: 2026/07/09
Brannock Kristina RKaumeyer BenjaminNicol Kathleen KChow Lionel M LRangarajan Hemalatha GKahwash Samir B - Patient A, a 1-year-and-6-month-old male, was admitted due to "fever for 2 days". Patient B, a 1-year-and-9-month-old male, the monozygotic twin brother of Patient A, was admitted due to "fever for 1 day and abnormal blood findings detected 1 h prior to admission". The twin siblings underwent bone marrow examinations and were consecutively diagnosed with acute lymphoblastic leukemia, both testing positive for the ETV6::RUNX1 fusion gene. They received chemotherapy according to the CCLG-ALL-2018 protocol for 2 years, and both achieved complete remission. Since the completion of treatment, they have remained in continuous complete remission for over 2 years of follow-up. This case report provides additional clinical evidence supporting "the in utero origin" and "two-hit" hypotheses in pediatric ALL. - Source: PubMed
Publication date: 2026/06/18
Li XiaohuaWang CuicuiLi JianchangLiu ChaoyueSun WeimeiZhang YanjunShi Jian - Lipoblastomatosis is a rare benign adipocytic tumour of infancy and early childhood, characterized by rapid growth. Diagnosis is challenging, owing to tumour heterogeneity and overlap with other pediatric soft-tissue neoplasms. PLAG1 rearrangement is the defining molecular hallmark, with an expanding list of fusion partners. We report a case of a 1-year-old child with a firm, nonmobile mass in the right thigh, which on CECT was deep-seated and heterogeneously enhanced. Gross evaluation of the excision specimen demonstrated an ill-circumscribed soft tissue mass. Histopathologically, the tumour showed myxoid nodules with primitive mesenchymal spindle-cell areas, and peripheral adipose tissue containing scattered lipoblasts, features suggestive of lipoblastomatosis. The IHC study showed S100 and CD34 positivity in adipocytes, and desmin and myogenin positivity in spindle-cell components. Molecular testing by NGS revealed a COL1A2::PLAG1 gene fusion, thus further establishing the diagnosis. Differentials such as myxoid liposarcoma, fibrous hamartoma of infancy, and infantile fibrosarcoma also harbour distinct genetic drivers, including EWSR1::DDIT3, EGFR exon 20 alterations, and ETV6::NTRK3, respectively. This case highlights the diagnostic workup of soft-tissue tumours and underscores the importance of integrating histopathology, IHC, and molecular testing. Identification of PLAG1 rearrangement is crucial for confirming the diagnosis. With the growing number of molecularly defined soft-tissue tumours of diagnostic and prognostic significance, incorporating molecular analysis is essential in the evaluation of soft-tissue lesions. - Source: PubMed
Publication date: 2026/06/26
K MadanM MalathiPereira Loretta AnnShetty Rohan - Many diseases evolve through complex, nonlinear trajectories shaped by interacting genetic, cellular, and environmental factors over time. Such dynamics are difficult to represent using static risk models, particularly in biologically heterogeneous conditions such as pediatric acute lymphoblastic leukemia (ALL). Here, we present a large concept model (LCM) as a mechanistic, hypothesis-generating framework for simulating longitudinal disease trajectories using pediatric ALL relapse dynamics as a proof-of-concept exemplar. We developed a causal longitudinal modeling framework implemented within the aiHumanoid v11.0 platform to characterize post-remission relapse dynamics. Seven clinically relevant ETV6::RUNX1-based genotypic profiles were simulated from remission baseline (T0) through 2 post-remission intervals (T1 = 3 months; T2 = 6 months). Longitudinal remission-to-relapse changes were evaluated across genotype- and age-defined virtual cohorts using descriptive nonparametric effect-size-oriented measures. Relapse dynamics were summarized using 2 composite system-level metrics: the relapse risk score and relapse pressure index. The model generated distinct genotype- and age-associated trajectory patterns across relapse-relevant biological domains and produced composite measures reflecting modeled relapse pressure within the simulation environment. Greater relapse-associated biological divergence was observed in selected genotype-age strata, particularly in domains related to clonal evolution, treatment resistance, and minimal residual disease. This ALL-focused proof of concept demonstrates the architectural and analytic potential of mechanistic trajectory simulation for hypothesis generation, longitudinal systems modeling, and future integration with real-world longitudinal datasets. - Source: PubMed
Publication date: 2026/06/30
Danter Wayne R