Ask about this productRelated genes to: MAGEC2 Blocking Peptide
- Gene:
- MAGEC2 NIH gene
- Name:
- MAGE family member C2
- Previous symbol:
- MAGEE1
- Synonyms:
- CT10, MAGE-C2, HCA587
- Chromosome:
- Xq27.2
- Locus Type:
- gene with protein product
- Date approved:
- 2000-09-26
- Date modifiied:
- 2017-01-16
Related products to: MAGEC2 Blocking Peptide
Related articles to: MAGEC2 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 - X chromosome-wide association studies (XWAS) have successfully identified risk loci on the X chromosome associated with Parkinson's disease (PD) susceptibility. However, only three such studies have been completed to date. Here, we present the first XWAS using an African cohort, comprising 690 PD cases and 826 controls. We applied an established XWAS workflow to perform male- and female-stratified analyses, as well as a combined meta-analysis. The male-stratified analysis identified five significant variants, including one lead locus (rs200539602), while the female-stratified analysis revealed 29 significant variants and two lead loci (rs2499550 and rs58045540), where rs2499550 is an upstream variant of the protein-coding gene . The remaining female-stratified significant variants are expression quantitative trait loci for , , and , which are highly expressed in the brain and nerve tissues, making them strong candidates for further investigation. One previously reported PD XWAS locus (rs28602900) was also replicated at a significance threshold of 0.05. The meta-analysis identified five variants surpassing chromosome-wide significance, including two lead loci (rs140715059 and rs141026964), the latter has no significant expression quantitative trait locus information but lies closest to the protein-coding gene , which may warrant further follow-up. None of the meta-analysis signals replicated in prior neurodegenerative disease XWAS. Overall, this study provides novel insights into the contribution of the X chromosome to PD susceptibility and represents the first PD XWAS to include participants of African ancestry, highlighting the importance of extending genetic studies to diverse populations. - Source: PubMed
Publication date: 2025/12/26
Step KathrynWaldo EmilyLeal Thiago PeixotoMendes MarlaBardien SorayaMata Ignacio F - : The androgen receptor (AR) is a ligand-dependent transcription factor of the nuclear steroid receptor superfamily, implicated in the pathogenesis of various solid tumors. The gene, located on chromosome Xq11-12, is accompanied by several X-linked genes that modulate expression and function, including , , and members of the melanoma antigen gene (MAGE) family (, , , ). While the AR has been investigated in multiple tumor types, its role in adult-type diffuse gliomas remains largely unexplored. Here, we characterized AR protein expression and the promoter methylation status of the AR and associated regulatory genes in adult-type diffuse gliomas. : A retrospective analysis was conducted on 50 patients with adult-type diffuse gliomas, including IDH-mutant gliomas (grades 2-4) and IDH-wildtype glioblastomas (GBMs), classified according to the 2021 WHO criteria. AR nuclear expression was assessed by immunohistochemistry (IHC). Methylation-specific PCR and quantitative DNA methylation analyses were employed to evaluate promoter methylation of the AR and selected co-regulatory genes. : AR nuclear positivity correlated significantly with male sex ( = 0.04) and higher tumor grade, with the highest expression in IDH-wildtype GBMs ( = 0.04). In IDH-mutant gliomas, AR immunoreactivity was more prevalent in astrocytomas than in 1p/19q codeleted oligodendrogliomas ( = 0.02). AR expression was associated with unmethylated MGMT promoter status ( = 0.02). DNA methylation analysis revealed AR gene hypomethylation in tumors displaying nuclear AR positivity and in IDH-wildtype GBMs (Kruskal-Wallis < 0.05). Additionally, methylation patterns of AR co-regulators located on the X chromosome suggest epigenetic regulation of AR signaling in gliomas. : The findings reveal distinct AR pathway activation patterns in adult-type diffuse gliomas, particularly IDH-wildtype GBMs, suggesting that further exploration of antiandrogen therapies is warranted. - Source: PubMed
Publication date: 2025/09/28
Gatto LidiaAsioli SofiaMorandi LucaDi Oto EnricoDi Nunno VincenzoTosoni AliciaAprile MartaBartolini StefaniaGriva LuciaMelotti SofiaGentilini FrancescaPinto GiuseppeCasadei FrancescoFoschini Maria PiaTonon CaterinaLodi RaffaeleFranceschi Enrico - Cancer/testis antigen HCA587, also known as MAGE-C2, highly expressed in a wide range of malignant tumors with unique immunological characteristics, serves as a potential target for tumor immunotherapy. Synthetic long peptides from HCA587 (HCA587 SLP) were proved to be highly immunogenic and promising in the application of cancer vaccine composed of Freud's adjuvant (FA) and CpG 1826, whereas, scarce CD8 T cell response may limit their anti-tumor effects during previous research. In this study, notwithstanding the multiple potential of IFN-α in immune modulation, there was no evidence of IFN-α in enhancing the immune response elicited by HCA587 SLP vaccine (HCA587 SLP + FA + CpG 1826). Given the unpleasant side-effects of Freud's adjuvant, then we applied AddaVax as a substitute for Freud's adjuvant, and we demonstrated that HCA587 SLP, formulated with AddaVax and CpG 2395, could induce more robust immune response in comparison with combined use of AddaVax and CpG 1826 through ELISpot assay. Furthermore, both IFN-γ-secreting CD4 T cell and CD8 T cell responses could be elicited by HCA587 SLP in combination with AddaVax and CpG 2395, and CD8 T cell response was most obviously observed under the condition of 10-h inhibition of cytokine secretion by brefeldin A post 10-h stimulation with HCA587 SLP, suggesting that cross presentation of exogenous long peptides to CD8 T cells may require more time than direct presentation to CD4 T cells. This vaccine formulation also conferred protection against challenge with HCA587-expressing B16 melanoma presented by delayed tumor growth and prolonged survival compared. This formulation of HCA587 SLP vaccine holds promise for the treatment of patients with cancer in future clinical trials. - Source: PubMed
Publication date: 2025/05/06
Jiang ShanshanZhao ShuqiZhao QiaojiajieWang YinfangZhang WeihuaFeng YangmengZhang Lijie - Expression of the PD-1 protein by tumor cells is relatively common and has been shown to exert proliferation-inhibitory effects across various tumor types, including T-cell malignancies, non-small cell lung cancer, and colon cancer. However, harnessing this tumor suppressor pathway is challenging because PD-1 activation by PD-L1 also suppresses normal T-cell function. We hypothesized that cancer antigen-specific TCR-T cells engineered to express PD-L1 could selectively activate the PD-1 pathway in tumor cells while simultaneously preventing self-inhibition by knocking out intrinsic PD-1 expression in TCR-T cells. To test this hypothesis, we co-expressed a MAGE-C2-specific recombinant TCR and the PD-L1-encoding CD274 gene in normal human T cells in which the PDCD1 gene was knocked out. These engineered TCR-T cells targeted MAGE-C2-expressing malignant cells, activating PD-1 signaling to suppress tumor proliferation while maintaining suppressed PD-1 signaling in the TCR-T cells themselves. To evaluate the tumor-suppressive potential of this approach, we compared the efficacy of PDL1-MC2-TCR-T cells against subtypes lacking PD-L1 expression, PD-1 knockout, or both. Our findings demonstrated that this TCR-T model exhibited significantly enhanced cytotoxic efficacy compared to other subtypes in vitro, ex vivo, and in vivo. These results suggest that the targeted activation of intrinsic PD-1 signaling in T-cell malignancies inhibits tumor proliferation and, when combined with PD-1 inhibition in TCR-T cells, synergistically enhances their cancer-suppressing efficacy. This study provides a foundation for novel cancer treatment strategies. - Source: PubMed
Publication date: 2025/04/07
Zhao FangxinZhang XuanTang YingYang HongxinPan HaitingLi BeibeiAn RiwenGeyemuri WuYang ChaoWan FangWu Jianqiang