Ask about this productRelated genes to: MAGEA6 Blocking Peptide
- Gene:
- MAGEA6 NIH gene
- Name:
- MAGE family member A6
- Previous symbol:
- MAGE6
- Synonyms:
- CT1.6, MAGE3B, MAGE-3b
- Chromosome:
- Xq28
- Locus Type:
- gene with protein product
- Date approved:
- 1994-04-04
- Date modifiied:
- 2017-05-12
Related products to: MAGEA6 Blocking Peptide
Related articles to: MAGEA6 Blocking Peptide
- Oral squamous cell carcinoma (OSCC) commonly arises from oral potentially malignant disorders (OPMDs), yet reliable molecular biomarkers that predict malignant transformation remain scarce. Because epithelial carcinogenesis follows similar multistep trajectories across multiple organs, pan-cancer transcriptional analyses may reveal conserved pathways relevant to early oral tumorigenesis. This study aimed to identify shared transcriptional signatures across carcinomas and evaluate their applicability to precancerous-to-carcinoma progression. Bulk RNA-seq data from five carcinomas (lung, colon, breast, prostate, and head and neck squamous cell carcinoma, HNSCC) were obtained from TCGA to identify shared differentially expressed genes (DEGs) (|logFC| ≥ 2; FDR < 0.05). Functional enrichment, clustering, and gene-pathway network analyses characterized conserved biological processes. Independent GEO datasets containing premalignant and malignant samples, including OPMD and OSCC cohorts, were examined to assess early-stage relevance. A conserved 45-gene signature was identified, enriched for transcriptional regulation, chromatin organization, and RNA polymerase II-mediated processes. Regulatory hubs, including ZIC5, MYBL2, ONECUT2, POU4F1, and PDX1, and strong upregulation of cancer-testis antigens (MAGEA3, MAGEA6, MAGEC2) were notable. Integration with premalignant datasets revealed 13 genes consistently dysregulated across early lesions, involving pathways such as cell differentiation, apoptosis, and lipid transport. Several genes remained altered from normal tissue through OPMD to OSCC, supporting their potential as stable biomarkers. This study identifies conserved transcriptional programs shared across epithelial cancers and detectable in OPMDs. These findings highlight promising biomarker and regulatory candidates for improving early detection and risk stratification of oral precancer, addressing a critical unmet need in OSCC prevention and clinical management. - Source: PubMed
Publication date: 2026/04/13
Kazemi Kimia SadatMiyazawa MartaHanemann João Adolfo CostaIonta MarisaOliveira Pollyanna Francielli deLeask AndrewFranca Cristiane MirandaSperandio Felipe Fornias - Somatotropinomas are a subtype of pituitary adenomas that have a particular predilection to invade the cavernous sinus. The objective of this systematic review was to examine the evidence regarding the molecular basis for cavernous sinus invasion in somatotropinomas. This review was conducted in accordance with the 2020 PRISMA guidelines on the 13th of April 2025. Inclusion criteria were reports of associations between somatotropinoma molecular changes and cavernous sinus invasion in adult patients. Title/abstract screening and full text screening were performed, with studies assessed for risk of bias using the Newcastle-Ottawa scale. A total of 43 studies were identified, studying 1824 patients (724 invasive tumours). Overall, 33 studies identified molecules that were upregulated in invasive tumours, and 20 studies identified molecules that were downregulated. Few studies incorporated modern proteomic or transcriptomic techniques. Risk of bias was low with a mean Newcastle-Ottawa Scale score of 7.0 (± 0.6). Molecules associated with invasion were related to epithelial-mesenchymal transition (E-cadherin, ESRP1, Fascin 1 and MMP-9), cellular proliferation (PTTG,AIP, TCERG1, EIF2β, E2F1,Notch 2, STAT3, ARRB1, TGFB1, SMAD3, SOX9, SGK1, MAGEA6 DLL3, EGFL7 and pEGFR), hormonal signalling (GNAS, DRD5, DRD1, sst5TMD4, SSTR2 and SSTR5) and tumour angiogenesis (VEGF and Drp1). These molecular variations present a possible explanation for the proclivity of somatotropinomas for the cavernous sinus. Identified molecules represent options for novel targeted therapies or biomarkers that could inform prognostication. Modern proteomic and transcriptomic techniques and larger somatotropinoma datasets are required to further elucidate the molecular pathways responsible for cavernous sinus invasion in somatotropinomas. - Source: PubMed
Publication date: 2026/04/16
Ovenden Christopher DillonCandy NicholasBacchi StephenSorvina AlexandraCastle-Kirszbaum MendelPoonnoose SantoshVrodos NikitasJukes AlistairSantoreneos StephenTorpy David JPsaltis AlkisDe Sousa Sunita - This study aims to identify novel biomarkers for the early diagnosis of lung adenocarcinoma (LUAD), with the goal of facilitating early intervention to improve patient prognosis. - Source: PubMed
Publication date: 2026/01/05
Huang ShuyuGan YuhanZhong RuifangWang SiyingKang YanliChen JinhuaChen FalinChen LiangyuanYou Jianbin - The immune microenvironment is critical in gastric cancer (GC), yet epithelial-specific genes linked to immune infiltration remain poorly defined. We integrated single-cell RNA-seq (GSE112302) and TCGA-STAD data to identify epithelial-related differentially expressed genes (DEGs). MAGEA3 and MAGEA6 were selected to classify immune subtypes. Immune infiltration was analyzed using ESTIMATE, CIBERSORT, ssGSEA, and Xcell. WGCNA and survival analysis identified prognostic immune-related genes. MAGEA3/6-high tumors showed low immune infiltration, defining an immune-cold subtype, while MAGEA3/6-low tumors were immune-hot. Further analysis confirmed that BCL11B and PAEP expression levels were significantly associated with immune cell infiltration and immune regulatory activity. MAGEA3/6 expression defines immune subtypes in GC and highlights potential targets for immunotherapy. - Source: PubMed
Publication date: 2025/12/26
Li LinenChen HaoZhou FengShi Yanqing - Based on mRNA Expression Profiles of 57 Patient-Derived Colorectal Cancer Stem-Like Cell (CRC-SC) Lines Compared With Normal Colonic Epithelial Stem-Like Cells (NCE-SCs), we Identified Five CRC Subtypes. The First Subtype of CRC-SCs Showed Markedly Increased Expression of MUC12, PIGR, PLA2G2A, SLC4A4, and ZG16, Which Were Barely Detectable in the Other Subtypes. Importantly, Their Expression Correlated With Favorable Outcomes in Both the Discovery Cohort and Independent Two Test Cohorts From Public Databases. The Remaining Four Subtypes Showed High Expression of DEFA6, BST2, MAGEA6, or IGF2 Compared With NCE-SCs. Although the Expression of Each Gene Individually Influenced Patient Outcomes, Additional Co-Expressed Genes Within Each Subtype Were Also Associated With Prognosis. Furthermore, Integrating the Five Subtype-Specific Signatures Produced a Practical Prognostic Indicator, Designated as the General Colorectal Cancer Signature (GCS), and Provided Individualized Predictive Signatures for Each Patient. The Clinical Significance of GCS Was Further Validated in a Novel Orthotopic Xenograft Mouse Model, Which Recapitulated Patient Outcomes: CRC-SCs With Low GCS Scores Developed Distinct Liver and Lung Metastases, Whereas Those With High Scores Did Not. Apparent Associations Were Observed Between Activating RAS/RAF Mutations and BST2 Expression, and Between the Absence of SMAD4 Mutation and IGF2 Expression, but These Had no Significant Impact on Patient Survival, Suggesting That Driver Gene Mutations May Not Directly Influence GCS. Collectively, Our Findings Provide a Comprehensive Overview of Clinically Relevant Molecular Subtypes of CRC-SCs, Representing the Current Landscape of CRC Molecular Expression Subtypes. They Also Enable Rapid, Low-Cost Outcome Prediction and Suggest Potential Targets for Therapeutics Development. - Source: PubMed
Publication date: 2025/10/31
Kakizaki FumihikoMiyoshi HiroyukiYamamoto TakehitoMorimoto TomonoriMatsubara HiroyukiKitano ShoichiYamaura TadayoshiMaekawa HisatsuguBrown J BSato Tosiya ShunObama KazutakaSakai YoshiharuKawada KenjiTaketo Makoto Mark