Ask about this productRelated genes to: MAGEA10 antibody
- Gene:
- MAGEA10 NIH gene
- Name:
- MAGE family member A10
- Previous symbol:
- MAGE10
- Synonyms:
- MGC10599, CT1.10
- Chromosome:
- Xq28
- Locus Type:
- gene with protein product
- Date approved:
- 1994-04-04
- Date modifiied:
- 2015-11-13
Related products to: MAGEA10 antibody
Related articles to: MAGEA10 antibody
- T-cell receptor (TCR) repertoires are central to antitumor immunity, yet their dynamics in digestive system cancers remain poorly defined. We profiled TCR repertoires from 415 tumors in 145 patients with colorectal cancer (CRC, n = 96), gastric cancer (GC, n = 47), and hepatocellular carcinoma (LIHC, n = 2), integrating clinical and pathological features. Distinct repertoire architectures emerged: CRC was characterized by abundant TRB V-J combinations (e.g., TRBV10-2*00-TRBJ2-4*00), whereas GC showed higher abundance of TRG/TRD pairings (e.g., TRGV5P*00-TRGJP1*00, TRDV3*00-TRDJ1*00), reflecting tumor-specific immune surveillance. Conserved motifs ("CATWD," "YKKLF") across cancers indicate shared selective pressures, while antigen mapping revealed both common (KRAS, SF3B1, and BST2) and tumor-specific targets (MAGEA10, WT1 in CRC; PABPC1 in GC). In CRC, repertoire dynamics were tightly coupled to disease stage. Metastatic tumors (MT) displayed larger size, vascular invasion, and elevated serum markers, whereas primary tumors (PT) exhibited stronger immune infiltration with lymphocyte- and myeloid-driven responses. Tumor size was significantly and positively correlated with the number of TRD/TRG clonotypes shared between PT and MT. Shared clones were further classified into three categories, including stable, contracted, and expanded. Among these, expanded MT clones were dominated by the "NYGYTF" motif within the TRB chain (e.g., TRBV7-9*00-TRBJ1-2*00). The most abundant "NYGYTF"-containing clones recognized MLANA, a tumor-associated antigen linked to prognosis and therapeutic responsiveness, underscoring its potential role in CRC progression. Collectively, these findings delineate cancer- and stage-specific TCR repertoire alterations and antigen specificities, highlighting novel biomarkers and therapeutic targets to inform TCR-based diagnostics and personalized immunotherapies in CRC and GC. - Source: PubMed
Publication date: 2026/01/28
Li LeiLi JiaWang FangJiang RunzeWang HongLi XiangzeZhen Ya'nan - 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 - Tumor-associated macrophages (TAMs) promote immunosuppression, hindering immune checkpoint blockade and immunotherapy efficacy. To overcome this, we developed a novel multifunctional nanovaccine based on hepatitis B core virus-like particles (HBc VLP) to synergistically remodel the immunosuppressive tumor microenvironment through integrated TAM reprogramming and B7-H3 checkpoint blockade. - Source: PubMed
Publication date: 2025/10/17
Liang ShuntaoYin XiaoxuanChi YongjieWang KeyueMa LiYang ZhuXue XinWang ShouchengZhao KaiWang LianyanMa Juan - Histone acetylation is a critical modification that regulates gene expression by modulating chromatin structure and function. Histone acetyltransferases are essential for maintaining acetylation homeostasis, and the disruption of this balance can lead to aberrant gene expression and cancer development. Here, we describe that the cancer-specific protein MAGE-A10 increases cellular histone acetylation by stabilizing essential histone acetyltransferases KAT2A and KAT2B. The aberrant expression of MAGE-A10 in tumors prevents the degradation of KAT2A/2B through p62-mediated autophagy. Mechanistically, MAGE-A10 antagonizes the binding of KAT2A/2B with the E3 ubiquitin ligase complex CUL4A-DDB1, thereby decreasing the formation of their K63-linked ubiquitination. Furthermore, KAT2A enhances the transcription of the MAGE-A10 gene, forming a positive feedback loop that contributes to tumorigenesis. These findings provide insights into the molecular mechanisms hijacked in cancer that drive perturbed histone acetylation and suggest potential therapeutic strategies. - Source: PubMed
Publication date: 2025/10/07
Fu XuekunYang XuHuang JieHuang YuhongPotts Patrick RyanLiang Chao - Previous studies found that melanoma antigen genes (MAGE) were antigens expressed in various tumor cells but hardly expressed in normal tissues, and their unique expression pattern made them highly promising for cancer immunotherapy. MAGE-A10 was a member of the MAGE family, and although it was expressed in various tumors, its specific function remained unclear. In this study, we conducted a comprehensive pan-cancer analysis of MAGE-A10 expression, prognostic value, DNA methylation, genetic variation, function, immune infiltration, and drug sensitivity using multiple public databases. The results showed that MAGE-A10 was highly expressed in tumor tissues of most cancer types and was associated with poor prognosis. Additionally, MAGE-A10 was closely related to methylation levels, genetic variation, immune cell infiltration, immune therapy response, and chemotherapy resistance, possibly due to its role in regulating gene expression, cell differentiation, and immune response. Validation experiments in gastric cancer found that high expression of MAGE-A10 significantly affected patient prognosis. Gene set enrichment analysis (GSEA) indicated that high expression of MAGE-A10 was closely associated with the binding of histone deacetylases. Cell experiments showed that knocking down MAGE-A10 significantly reduced the proliferation, migration, and invasion capabilities of gastric cancer cells, which might be related to its regulation of the expression of cell adhesion molecule cadherins. In conclusion, this study indicated that MAGE-A10 was a potential tumor prognostic biomarker and immunotherapy target and played an important role in the proliferation, migration, and invasion of gastric cancer cells. - Source: PubMed
Publication date: 2025/09/01
Yin YichenWang BaozhenYang MingzheLiu WeidiWang AnqiLu ZhongtingChen JingLi Tao