TLX3 Polyclonal Antibody, ALEXA FLUOR 594 Conjugated
- Known as:
- TLX3 Polyclonal Antibody, ALEXA FLUOR 594 Conjugated
- Catalog number:
- bs-6240r-a594
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Bioss
- Gene target:
- TLX3 Polyclonal Antibody ALEXA FLUOR 594 Conjugated
Related genes to: TLX3 Polyclonal Antibody, ALEXA FLUOR 594 Conjugated
- 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 Polyclonal Antibody, ALEXA FLUOR 594 Conjugated
Related articles to: TLX3 Polyclonal Antibody, ALEXA FLUOR 594 Conjugated
- - Source: PubMed
Publication date: 2026/09/11
Yao QiangChen XiaoyongLuo MeizhuLin ZhenhuFu Xiaoying - Radiation-induced brain injury (RIBI) is a serious complication of cranial radiotherapy, yet its molecular mechanisms remain unclear. This study aimed to identify novel therapeutic targets for RIBI through integrated dual-omics analysis. - Source: PubMed
Publication date: 2026/08/29
Li XuejiaoShu KunHe XiaoZhou MinDing Zhongxiang - Adult T-lymphoblastic leukemia often harbors cryptic structural variants that remain undetected by standard cytogenetic and targeted molecular testing, limiting precise risk stratification and therapeutic planning. This case is notable for the use of optical genome mapping (OGM) to uncover multiple disease-defining and likely oncogenic genomic alterations in an adult patient with newly diagnosed T-lymphoblastic leukemia. The report highlights how comprehensive structural variant profiling can refine prognosis and identify clinically meaningful aberrations that would otherwise be missed in routine practice. - Source: PubMed
Publication date: 2026/05/24
Maxfield Amanda MBickford Michelle ATonseth Kyle ABao JingMurad FarzanaWilson Devon NWainman Lauren MHill John MDonnelly Liam LKaur PrabhjotTafe Laura JKarrs Jeremiah XKhan Wahab A - BACKGROUND: 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. CASE PRESENTATION: We report two MPAL-T/M cases with comprehensive clinical, immunophenotype, and genetic results. A shared chromosomal rearrangement between chromosomes 14q32 and 16q24, t(14;16)(q32;q24), was detected in both leukemias. The t(14;16) has breakpoints 500-900 kb downstream to the BCL11B gene on chromosome 14, and within or near LINC01081 on chromosome 16, juxtaposing BCL11B enhancer to a novel gene on chromosome 16. In addition, both leukemias were positive for WT1 mutations and negative for FLT3-ITD. CONCLUSION: These cases represent the first report of recurrent translocation, t(14;16), in MPAL-T/M. The t(14;16) with these breakpoints is consistent with the juxtaposition of BCL11B enhancer to a novel gene on chromosome 16, similar to BCL11B::TLX3 in T-ALL. This report highlights the clinical relevance of OGM in identifying critical gene rearrangement that creates enhancer hijacking in the diagnosis of MPAL-T/M. These discoveries, along with further chromatin topology and gene expression studies, may provide a new window into the underlying biology of these aggressive leukemias. - 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-ALLs phenotyped in our center, 33% (n = 403) expressed a TCR, of which 47% (n = 191; 113 adults, 78 children) were positive for γδTCR (γδTCR+). Using a comprehensive analysis, we were able to delineate 2 distinct γδTCR+ T-ALL subtypes, with distinct physiological counterparts. The first (75% of cases) was characterized by ectopic expression of homeodomain-containing oncogenes (HD+), Vβ-Jβ rearrangements, and 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 subtype (25%) exhibited phenotypic and transcriptional profiles reminiscent of γδ thymocytes, and was 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. These trials were registered at www.clinicaltrials.gov as NCT00222027 (GRAALL2003), NCT00327678 (GRAALL2005), NCT03709719 (GRAALL2014), and NCT00408005 (Children's Oncology Group AALL0434 trial). - Source: PubMed
Pinton AntoineCourtois LucienDelafoy ManonBonnet MickaëlCieslak AgataLhermitte LudovicSimonin MathieuDourthe Marie-EmilieTouzart AuroreAndrieu Guillaume PDombret HervéBaruchel AndréSpicuglia SalvatorePayet-Bornet DominiqueBoissel NicolasMacintyre ElizabethAsnafi Vahid