ETV6 antibody - N-terminal region (P100806_P050)
- Known as:
- ETV6 (anti-) - N-terminal region (P100806_P050)
- Catalog number:
- p100806_p050
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- ETV6 antibody - N-terminal region (P100806_P050)
Related genes to: ETV6 antibody - N-terminal region (P100806_P050)
- 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 - N-terminal region (P100806_P050)
Related articles to: ETV6 antibody - N-terminal region (P100806_P050)
- 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 - - Source: PubMed
Publication date: 2026/04/15
Wang'ondu Ruth WKairalla John AShago MaryAngiolillo AnneBreidenbach Heather MBurke Michael JCarroll Andrew JRabin Karen RSalzer WandaSchore Reuven JWang CindyHunger Stephen PTeachey David TrentRaetz Elizabeth ALoh Mignon LDavis Kara LRau Rachel E - The identification of molecular subgroups of pediatric B-cell acute lymphocytic leukemia (B-ALL) has proven to be a powerful tool in understanding disease pathogenesis and treatment stratification. Studies have suggested aberrant transcription factor function and epigenetic regulation can explain differences between B-ALL subtypes, however, the impact of 3D genome re-organization remains unclear. Here we used in situ Hi-C and RNA-seq to profile the chromatin architectural landscape in healthy B-cell progenitors and B-ALL patient samples harboring prognostically relevant structural variations, including ETV6::RUNX1, KMT2A::AFF1, and BCR::ABL. We showed that B-ALLs undergo subtype-specific changes that, in part, reflect the differentiation stage of the disease, and that they acquire aberrant chromatin configurations that allow expression of oncogenic drivers. One such driver, ERG, displayed increased interactivity and expression in ETV6::RUNX1 B-ALL, and evidence suggests it plays a role in regulating survival and differentiation. Overall, these results underscore the essential role of 3D nuclear organization in acute leukemia. - Source: PubMed
Publication date: 2026/04/14
Ghebrechristos Yohana EEvensen Nikki ACathelin Romane SLee SoobeomClark FinneganSaiz NestorClarke StanleyWitkowski Matthew TLin ZiyanNarang SonaliZhou HuaRaetz ElizabethTeachey David TLionnet TimothéeTsirigos AristotelisCarroll William LAifantis Iannis - Gene fusions generated by chromosomal rearrangements function as oncogenic drivers in human cancers. We previously showed that EWSR1-ETS oncofusions of Ewing sarcoma (EwS) directly induce surface expression of IL1 receptor accessory protein (IL1RAP), which along with limited expression in healthy tissues except placenta nominate IL1RAP as a promising EwS immunotherapy target. We therefore engineered antibody-drug conjugates (ADCs) with different cytotoxic payloads to target IL1RAP. ADCs potently blocked tumor growth and induced durable regression of EwS xenografts in mice, and diminished metastatic dissemination in vivo. Moreover, we show that other oncofusions also induce IL1RAP expression in diverse cancers, including NPM-ALK in anaplastic large cell lymphoma (ALCL), and ETV6-NTRK3 in multiple tumor types. IL1RAP expression rendered these malignancies similarly vulnerable to IL1RAP-targeting ADCs, which effectively blocked growth of ALCL xenografts and syngeneic ETV6-NTRK3+ sarcomas. Lack of detectable normal tissue toxicity, including in non-human primates, support the further clinical translation of IL1RAP-targeting ADCs. - Source: PubMed
Publication date: 2026/04/13
Zhang Hai-FengDe Dreuzy EdouardHuang Yue ZhouShin SeungminHuang Qing-FengDelaidelli AlbertoYang XiaqiuAdamiak VirginiaLytle AndrewArzoo AarzooLizardo Michael MLin QiaochuSanadi ShreyaRouleau MelanieLiu Lu-XinXu Li-YanLi En-MinLai RaymondPrimus ClémentineReda El Sayed SohaBourhis LucasGenin DelphineDemontrond LucasBouquet LucieDémolis LauraBarberot AmandineLameynardie StephaneDelabrière AlexisHua HaiqingYang JunjieIshima RiekoImle RolandBanito AnaSlack Graham WSavage Kerry JMaris John MBosse Kristopher RDimitrov Dimiter SSteidl ChristianLi WeiSainson Richard C ASorensen Poul H