Ask about this productRelated genes to: HOXA5 antibody
- Gene:
- HOXA5 NIH gene
- Name:
- homeobox A5
- Previous symbol:
- HOX1C, HOX1
- Synonyms:
- -
- Chromosome:
- 7p15.2
- Locus Type:
- gene with protein product
- Date approved:
- 1990-06-15
- Date modifiied:
- 2015-09-07
Related products to: HOXA5 antibody
Related articles to: HOXA5 antibody
- Glioblastoma (GBM) is the most aggressive primary brain tumor with a dismal prognosis. Ferroptosis is implicated in GBM pathogenesis. Heat shock protein B1 (HSPB1) is associated with tumor progression, yet its precise function and regulatory mechanism in GBM ferroptosis remain elusive. Differentially expressed genes were identified from the GSE151352 dataset. WGCNA was employed to identify GBM-associated modules, which were then intersected with genes from the FerrDb V2 database. HSPB1 expression and prognostic value were validated using TCGA and GEPIA databases, and clinical specimens. Functional assays (EdU, TUNEL, and Transwell) and ferroptosis indicators (lipid ROS, Fe, GSH) were assessed following HSPB1 modulation. Bioinformatics tools predicted METTL1-mediated m7G modification of HSPB1, and results were validated by RIP, dual-luciferase reporter assay, and mRNA stability assays. Transcriptional regulation of HSPB1 by HOXA5 was predicted and confirmed. A subcutaneous xenograft model was used to evaluate the METTL1-HSPB1 axis in vivo. Analysis revealed 2985 DEGs. WGCNA identified a GBM-correlated "red" module; intersection with ferroptosis genes pinpointed HSPB1. HSPB1 was significantly overexpressed in GBM, correlating with poor patient survival. HSPB1 knockdown suppressed GBM cell proliferation, migration, invasion, and induced ferroptosis. Mechanistically, METTL1 mediated m7G modification to HSPB1 mRNA to enhance its stability. Concurrently, HOXA5 bound to the HSPB1 promoter to activate its transcription. Silencing either METTL1 or HOXA5 downregulated HSPB1, inhibiting GBM malignant phenotypes. In vivo, the METTL1-HSPB1 axis promoted tumor growth. METTL1 stabilizes HSPB1 mRNA through m7G methylation, and HOXA5 transcriptionally activates HSPB1 expression. This regulation promotes GBM malignant progression. - Source: PubMed
Publication date: 2026/05/27
Li HongchaoChen YushengZhu YanyanKe ShanbaoWu Danting - Despite the proliferation of prognostic gene signatures for glioma, clinical translation remains stalled by poor reproducibility and overfitting. In this study, we address this stability crisis by developing a robust "Dual-Signature Framework" using stability selection-a rigorous resampling method-rather than standard regression. Analyzing RNA-seq data from 1351 patients across the TCGA (n = 694) and CGGA (n = 657) cohorts, we constructed two distinct models. The primary 20-gene "Data-Driven" signature achieved superior predictive accuracy (C-index: 0.7392), significantly outperforming 14 published benchmark models and the current best single-gene predictor (HOXA5). In parallel, we derived a 7-gene "Biology-Driven" signature (including HOXA5, CHI3L1, MMP14) that retained 98% of the predictive power (C-index: 0.7252) while prioritizing mechanistic interpretability. Both models successfully stratified patients into distinct risk groups with high statistical significance (Log-rank p < 0.001) in external validation. Comprehensive subgroup analyses across 19 clinical and molecular subgroups demonstrated robust performance (C-index range: 0.59-0.85), with extended calibration analysis confirming excellent probability estimation (Brier score 0.20 for 5-year predictions). By integrating stability-driven feature selection with biological pathway constraints, this study provides a reproducible, high-performance alternative to unstable "black box" models, offering a translation-ready tool for personalized glioma risk assessment. - Source: PubMed
Publication date: 2026/05/12
D'Costa Romeo MaclineIslam Md ShafiqulIslam Md Masudul - Chemoimmunotherapy for small cell lung cancer (SCLC) is initially effective; however, relapse is common. Patterns of progression may serve to prognosticate outcomes and identify biomarkers for relapsed SCLC. - Source: PubMed
Publication date: 2026/04/03
Kumar PareshSlaven James EZhou TianhaoTran MyaShields Misty D - Mediastinal gray zone lymphoma (MGZL) is a rare B-cell lymphoma characterized by overlapping clinicopathologic and molecular features of primary mediastinal B-cell lymphoma (PMBL) and classical Hodgkin lymphoma (CHL). Under current WHO-HEMA5 and International Consensus Classification (ICC) frameworks, MGZL is restricted to EBV-negative lymphomas arising in the mediastinum. This review summarizes current evidence on epidemiology, clinical presentation, pathology, molecular characteristics, diagnostic challenges, and therapeutic approaches to MGZL, with data derived from retrospective series, limited prospective cohorts, and recent molecular studies. MGZL predominantly affects young adults and commonly presents with bulky mediastinal disease. Diagnosis is challenging due to transitional morphology, pleomorphic Reed-Sternberg-like cells, and variable expression of B-cell and activation markers. Molecular studies demonstrate shared alterations with PMBL and CHL, including 9p24.1 (JAK2/PD-L1/PD-L2) gains, while additional reported features such as HOXA5 hypomethylation and MYC copy number gains support its biological distinctiveness, although evidence remains limited. Frontline treatment commonly involves intensive chemoimmunotherapy regimens such as DA-EPOCH-R; however, outcomes remain inferior to PMBL and CHL, with 5-year overall survival rates of approximately 40-60%. Relapsed or refractory disease frequently requires salvage chemotherapy and autologous stem cell transplantation. Immune-based therapies, including brentuximab vedotin and PD-1 inhibitors, have shown promising activity, particularly in combination. MGZL remains a diagnostically challenging and therapeutically complex lymphoma with inferior outcomes compared with related mediastinal lymphomas. Advances in molecular profiling and immunotherapy offer promising avenues toward more personalized treatment; however, prospective clinical trials and international collaboration are urgently needed to establish evidence-based management strategies for this rare entity. - Source: PubMed
Publication date: 2025/12/31
Zorlu TugbaSeyhan MertAbdullayeva NigarUlas TurgaySinan Dal Mehmet - Allergic asthma pathogenesis encompasses systemic immune, metabolic, and epithelial barrier dysfunction; however, minimally invasive tools to longitudinally explore these processes remain limited. - Source: PubMed
Publication date: 2026/01/06
Liu DanielKim MadelineDel Duca EsterBar JonathanLau MeganLargen JosephAgache IoanaGuttman-Yassky Emma