ETV6 Mouse Monoclonal Antibody
- Known as:
- ETV6 Mouse Monoclonal Antibody
- Catalog number:
- BIN-002120-M01
- Product Quantity:
- 0.1mg
- Category:
- -
- Supplier:
- Zyagen
- Gene target:
- ETV6 Mouse Monoclonal Antibody
Related genes to: ETV6 Mouse Monoclonal Antibody
- 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 Mouse Monoclonal Antibody
Related articles to: ETV6 Mouse Monoclonal Antibody
- Measurable residual disease (MRD) is a key prognostic factor in pediatric acute lymphoblastic leukemia (ALL), but current gold-standard methods based on immunoglobulin/T-cell receptor (IG/TCR) rearrangements are complex and not informative in a subset of patients. Genomic breakpoints of oncogenic fusions (GFBs) are stable, biologically grounded markers that may overcome these limitations and improve MRD assessment. In a cohort of 403 patients with known or suspected fusions, a short-read, capture-based next-generation sequencing strategy coupled with an open-source pipeline identified patient-specific GFBs in 97% of cases. GFB-based MRD assays implemented by qPCR or ddPCR showed very high specificity and allowed lower detection thresholds, resulting in improved sensitivity relative to IG/TCR-based assays. Longitudinal monitoring in 104 patients across multiple pediatric ALL fusion subtypes demonstrated excellent overall concordance between methods in non-BCR::ABL ALL, while revealing fusion-dependent differences. GFB-based MRD was particularly informative in ETV6::RUNX1- and MEF2D-rearranged ALL, where IG/TCR tracking is frequently suboptimal or unreliable due to ongoing rearrangements or the absence of VDJ recombination, respectively. Altogether, this large-scale study establishes GFBs as robust, clinically implementable MRD markers and supports their integration into clinical strategies, provided that subtype-specific biology is considered when selecting markers and interpreting results. - Source: PubMed
Publication date: 2026/04/21
Houtman Arno HArfeuille ChloéStrullu MarionBaruchel AndréCavé HélèneCaye-Eude Aurélie - -like ALL is defined by a gene expression signature similar to that of -positive ALL and absence of all genetic subtype-defining aberrations, including the fusion. Within the International BFM Study Group, we assembled and analyzed a cohort of 100 patients (including 97 children) with -like ALL. We describe their diverse genetic landscape, centered around aberrations with frequent disruptions, as previously shown, but including various rare non-/non- gene fusions, and rearrangements of (r). We show that and aberrations do not occur exclusively in this subtype, which hampers its classification based solely on genomic data. We confirm our previous observation of a strong association of the CD27-positive/CD44low-negative immunophenotype with ::(-like) subtype. Compared to -positive ALL, patients with -like ALL are younger, have higher white blood cell counts at diagnosis, and have an inferior early treatment response. While overall survival is comparable, event-free survival is significantly lower in patients with -like ALL, with NCI risk, early treatment response, deletions, and mutations having prognostic relevance. Notably, Down syndrome is highly prevalent and associated with a worse outcome in -like ALL. In conclusion, we provide biological, demographic, and clinical characteristics of the largest -like cohort presented to date. - Source: PubMed
Publication date: 2026/04/17
Zaliova MarketaSchinnerl DagmarBoer Judith MCaye-Eude AurélieRehn JacquelineSchwab ClaireArfeuille ChloéAttarbaschi AndisheBergmann Anke KatharinaFiser Karelde Groot-Kruseman Hester AHaslinger SabrinaInthal AndreaJanotova IvetaLenk LennartMaurer-Granofszky MargaritaNebral KarinPoyer FionaSramkova LucieStary JanStrullu MarionStuchly JanSutton RosemaryVaskova MartinaWinkowska LucieCario GunnarCavé Hélèneden Boer Monique LHarrison ChristineStrehl SabineWhite DeborahTrka JanZuna Jan - We report the first documented case of chronic eosinophilic leukemia (CEL) with ETV6-SYK gene rearrangement manifesting as refractory bilateral nodular scleritis within a broader paraneoplastic autoimmune syndrome. A 25-year-old woman with pre-existing Hashimoto's thyroiditis developed progressive bilateral nodular scleritis with anterior uveitis that proved completely refractory to high-dose corticosteroids, methotrexate, and conventional disease-modifying antirheumatic drugs, along with papilledema and granulomatous rosacea, suggesting systemic inflammation. Comprehensive evaluation revealed persistent marked eosinophilia (peak 15,000/μL), prompting hematological investigation, including a bone marrow biopsy and cytogenetic analysis that confirmed CEL harboring the ETV6-SYK fusion oncogene. Recognition of this molecular target enabled precision therapy with fostamatinib, a spleen tyrosine kinase (Syk) inhibitor, combined with adalimumab, a tumor necrosis factor-alpha (TNF-α) inhibitor, resulting in complete and sustained remission of all inflammatory manifestations over 18 months of follow-up. This case underscores the critical importance of maintaining high clinical suspicion for paraneoplastic autoimmune syndromes in patients with treatment-refractory inflammatory conditions, particularly when accompanied by atypical systemic or unexplained laboratory findings, and demonstrates that molecularly targeted precision medicine approaches can transform treatment outcomes in complex paraneoplastic rheumatic disorders. - Source: PubMed
Publication date: 2026/03/17
Ji Byung CAung ThandaCastellino JanelleKahlon Kanwarpal STsui EdmundGlasgow Ben J - Acute lymphoblastic leukemia (ALL), the most common malignancy in children and adolescents, arises from a heterogeneous and multifactorial etiology involving genetic and environmental factors. Studies of seasonal variation in ALL diagnosis have yielded inconsistent results, likely reflecting differences in study design and population characteristics. Here, we evaluated seasonal variation across ALL immunophenotypes, including two common genetic subtypes. - Source: PubMed
Publication date: 2026/04/16
Bychkov GlebBang BenedicteEngsner NiklasTettamanti GiorgioHeyman Mats MarshallNordenvall Anna SkarinHerold NikolasTaylan FulyaPontén EmeliAlbert JanJörnsten RebeckaStrannegård ClaesNordgren Ann - To evaluate the clinical value of minimal residual disease (MRD)-guided risk stratification in different subtypes of pediatric B-cell acute lymphoblastic leukemia (B-ALL). In this retrospective cohort study, a total of 666 newly diagnosed B-ALL children admitted to the Children's Hospital, Zhejiang University School of Medicine between October 2018 and June 2023 were enrolled. Risk stratification (low, intermediate, and high risk) and treatment were conducted according to the Zhejiang Children's Hospital acute lymphoblastic leukemia (ZJCH-ALL)-2019 protocol. Based on the cytogenetic and molecular biological characteristics of leukemia cells, patients were categorized into three groups: ETV6::RUNX1 fusion gene-positive group, hyperdiploid group, and non-ETV6::RUNX1 and non-hyperdiploid B-ALL (NENH-B-ALL) group. The adjustments in risk stratification based on MRD levels across these groups were analyzed. The value of MRD-based risk adjustment strategies in different B-ALL subgroups was assessed using Kaplan-Meier survival analysis and the Cox proportional hazards model. Among the 666 patients, there were 379 males and 287 females, with the age of onset 4.7 (3.2, 7.6) years. The ETV6::RUNX1-positive, hyperdiploid, and NENH-B-ALL groups comprised 168 (25.2%), 199 (29.9%) and 293 (44.0%) patients, respectively; additionally, 6 patients exhibited both hyperdiploidy and ETV6::RUNX1 positivity. Risk stratification was adjusted based on MRD levels on day 15 and day 29 in 153 (23.0%) and 5 (0.8%) patients, respectively. The 5-year overall survival (OS) and event-free survival (EFS) rates for all 666 patients were (95.9±0.8)% and (92.1±1.2)%, respectively. Notably, EFS was significantly superior in the ETV6::RUNX1-positive and hyperdiploid groups compared to NENH-B-ALL group ((97.6±1.2)% and (96.5±1.4)% (85.6±2.4)%, <0.001). In the ETV6::RUNX1-positive group, the 5-year EFS rates for the low, intermediate, and high-risk groups were 100%, (98.5±1.5)%, and (80.0±10.7)%, respectively (<0.001). In the hyperdiploid group, the 5-year EFS rates were (96.7±1.9)%, 100%, and (87.7±6.7)% (<0.001). In the NENH-B-ALL group, the 5-year EFS rates were (97.2±1.9)%, (85.8±3.6)%, and (74.4±5.4)% (<0.001). Multivariate analysis identified age ≥10 years (=3.37, 95% 1.81-6.27), initial white blood cell count ≥50×10/L (=2.31, 95% 1.24-4.32), MRD ≥0.1% on day 15 (=1.88, 95% 1.01-3.49), MRD ≥0.01% on day 29 (=2.72, 95% 1.19-6.21), and NENH-B-ALL subtypes (=1.66, 95% 1.16-2.39) as independent adverse prognostic factors (all <0.05). In patients with ETV6::RUNX1 positivity or hyperdiploidy, MRD is less effective in distinguishing between low-risk and intermediate-risk groups but can precisely identify the high-risk group with significantly poorer prognosis. Conversely, in NENH-B-ALL, MRD effectively stratifies patients into low, intermediate, and high-risk categories, demonstrating superior discriminatory power in prognostic stratification. - Source: PubMed
Publication date: 2026/04/16
Liang JXu X JXu W QTang Y MZhang J YSong HLiao CShen D YShen H PZhao F YGuo X PJin F FChen H P