TLX3 antibody - N-terminal region (ARP31925_P050)
- Known as:
- TLX3 (anti-) - N-terminal region (ARP31925_P050)
- Catalog number:
- arp31925_p050
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- TLX3 antibody - N-terminal region (ARP31925_P050)
Related genes to: TLX3 antibody - N-terminal region (ARP31925_P050)
- Gene:
- TLX3 NIH gene
- Name:
- T cell leukemia homeobox 3
- Previous symbol:
- HOX11L2
- Synonyms:
- RNX
- Chromosome:
- 5q35.1
- Locus Type:
- gene with protein product
- Date approved:
- 2001-12-17
- Date modifiied:
- 2017-12-06
Related products to: TLX3 antibody - N-terminal region (ARP31925_P050)
Related articles to: TLX3 antibody - N-terminal region (ARP31925_P050)
- T/myeloid mixed-phenotype acute leukemias (MPAL-T/M) is a type of rare and high-risk acute leukemia that carries both T- and myeloid- lineage markers. The diagnosis of MPAL requires integration of clinical, immunophenotypic, and genetic information. Optical Genome Mapping (OGM) technology is a particularly powerful tool to profile genome-wide variants and locate complex chromosomal rearrangements that may guide diagnosis and risk stratification in MPAL-T/M. - Source: PubMed
Publication date: 2026/02/22
Lum JoannaAnderson-Calleja JessicaVan Dine KimberlyManion EmilyXiao HongPerry Anamarija MBoyer DanielShao Lina - T-cell acute lymphoblastic leukemia (T-ALL) results from the malignant transformation of thymocytes blocked in their differentiation. Surface expression of the γδ T-cell receptor (γδTCR) is surprisingly frequent in T-ALLs, questioning the susceptibility of the γδ-lineage to leukemogenesis. Among 1233 T-ALL phenotyped in our center, 33% (n=403) expressed a TCR, of which 47% (n=191 (113 adults, 78 children)) were positive for γδTCR (γδTCR+). By integrating oncogenetic, immunogenetic, phenotypic and bulk transcriptomic data, we were able to delineate two distinct γδTCR+ T-ALL subtypes, with likely distinct physiological counterparts. The first (75% of cases) was characterized by ectopic expression of homeodomain-containing oncogenes (HD+), Vβ-Jβ rearrangements, phenotypic (including surface pre-TCRα chain) and transcriptional profiles reminiscent of cortical thymocytes, and was therefore termed cortical-like γδ T-ALLs. Transduction of murine T-cell progenitors and human CD34+ cells with HOXA9 or TLX3 (HD+ oncogenes) led to a differentiation bias toward γδTCR expressing thymocytes. The second (26%) was negative for these features, exhibited phenotypic and transcriptional profiles reminiscent of γδ thymocytes and was therefore termed bona fide γδ T-ALLs. These findings were validated in the COGAALL0434 cohort. Although bona fide γδ T-ALLs were enriched for early T-cell progenitor (ETP)-like and KMT2A-rearranged cases, they mostly eluded the phenotypic definition of ETP-ALLs. Similar to the ETP-like subtype, bona fide γδ T-ALLs were associated with a poor initial response to chemotherapy, but were sensitive to the BCL2-inhibitor venetoclax. Our results reveal developmental heterogeneity behind γδTCR expression in T-ALLs, and suggest that overrepresentation of this subtype reflects αβ-lineage commitment repression by HD+ oncogenes. - Source: PubMed
Publication date: 2026/01/27
Pinton AntoineCourtois LucienDelafoy ManonBonnet Mickaël FCieslak AgataLhermitte LudovickSimonin MathieuDourthe Marie-EmilieTouzart AuroreAndrieu Guillaume PDombret HervéBaruchel AndréSpicuglia SalvatorePayet-Bornet DominiqueBoissel NicolasMacintyre Elizabeth AAsnafi Vahid - Rearrangements involving BCL11B have emerged as important structural variants in acute leukemias with T lineage differentiation, yet their prevalence and biological significance remain incompletely defined. Using optical genome mapping (OGM), we identified BCL11B rearrangements in 25 of 2325 hematologic malignancies, restricted to T-lymphoblastic leukemia particularly early T precursor (ETP) subtype, mixed phenotype acute leukemia T/myeloid, and rare acute myeloid leukemia. Breakpoints at 14q32.2 were highly variable and largely cryptic by karyotyping. Twelve putative partner genes were detected, including four previously reported (TLX3, ARID1B, CDK6, and CCDC26) and 8 novel partners (FOXF1, TLX1, NUP98, LMO2, GAPDHP71, GRM4, TNFAIP3, and TRRAP). Evaluation of BCL11B expression showed that rearrangements involving partners currently considered "BCL11B-activated", such as ARID1B, CCDC26, and CDK6, did not uniformly associate with BCL11B overexpression. Conversely, cases with TLX3::BCL11B, previously thought to upregulate TLX3, demonstrated strong BCL11B expression (3 of 4 cases). Clinically, newly diagnosed patients, most treated with venetoclax based regimens, achieved high remission rates. Our data delineate the structural diversity of BCL11B rearrangements identified by OGM and show that BCL11B activation cannot be reliably inferred from partner gene identity alone. BCL11B immunohistochemistry as a practical surrogate for assessing BCL11B activation is recommended in routine practice. - Source: PubMed
Publication date: 2026/01/23
Tang GuilinWang Sa AJen Wei YingMedeiros L JeffreyWang WeiFang HongHu ShiminJain NitinJabbour Elias JosephZou Ying SXu Jie - TAL1 is one of the most frequently dysregulated oncogenes in T-cell Acute Lymphoblastic Leukaemia (T-ALL). However, the precise frequency and prognostic impact associated with its dysregulation remains unclear and is confounded by TAL1's diverse dysregulation mechanisms. TAL1 dysregulation is detected by TAL1 transcript quantification, though this technique may be subject to interference by TAL1 transcripts deriving from residual haematological cells that physiologically express high levels of the gene. We hypothesised TAL1 DNA methylation could provide a more reliable biomarker than TAL1 transcript quantification alone. We extensively studied TAL1 dysregulation in a large adult and paediatric T-ALL cohort (n = 401) and designed a TAL1 specific MS-MLPA assay to determine methylation levels. Whereas monoallelic TAL1 + T-ALL had homogeneous gene expression profiles, never expressed other driver oncogenes and were TAL1 hypomethylated (methylation ratio <0.4), biallelic TAL1 + T-ALL were enriched in expression of other driver oncogenes (TLX1, TLX3, HOXA), and had heterogeneous transcriptomes and TAL1 methylation levels. In PDX analysis, monoallelic TAL1 expression was stable, contrary to biallelic expression which mostly derived from residual non-malignant haematopoietic cells. Importantly, we report 5 novel TAL1 dysregulation mechanisms using long-read nanopore and OGM analysis, and show that TAL1 hypomethylation identifies TAL1 dysregulation, and is associated with worse prognosis. - Source: PubMed
Publication date: 2025/08/08
Smith CharlotteCharbonnier GuillaumeSimonin MathieuBalducci EstelleSteimle ThomasAndrieu Guillaume PCieslak AgataCourgeon MarianneLeLorc'h MarcMayakonda AnandPlass ChristophLe Nezet AurélieLatiri MehdiIfrah NorbertDombret HervéHuguet FrançoiseBaruchel AndréMacintyre ElizabethPetit ArnaudBoissel NicolasAsnafi VahidTouzart Aurore - Shared genetic developmental programs in which specific transcription factors affect similar cell fate decisions in distinct tissues are common. In the developing dorsal neural tube and cerebellum, PTF1A is essential for specification of GABAergic inhibitory neurons and suppression of alternative glutamatergic excitatory neuronal fates. Previous studies in the mouse dorsal neural tube identified the transcriptional repressor PRDM13 as a transcriptional target of PTF1A that functions to suppress the alternate cell fates to ensure precision in neuronal cell identity. The presence of PRDM13 in PTF1A + cerebellar progenitors suggests a similar role for PRDM13 in cerebellar neuronal specification. Cerebellar agenesis in humans with missense mutations in PRDM13, and perturbations in cerebellar development in Prdm13 mutant mice and zebrafish, confirm PRDM13 requirement in this tissue. Here we add to these findings showing additional mutant alleles in mouse Prdm13 phenocopy the perturbation in cerebellar cell fates seen with the absence of PTF1A, including loss of PAX2+ interneuron and Purkinje cell inhibitory neuronal lineages, increases in TLX3+ excitatory neuronal lineages, increased apoptosis, and reduced cerebellar size. Additional defects are seen in the placement of TBR1+ cerebellar cells. Thus, using Prdm13 mutant mice, we support conclusions that PRDM13 functions to specify balanced numbers of inhibitory and excitatory neuronal progenitors in the developing cerebellum. - Source: PubMed
Publication date: 2025/07/26
Ma Z ZackHale Michael AMona BishakhaUruena AnaJohnson Jane E