B7_H4 Antibody
- Known as:
- B7_H4 Antibody
- Catalog number:
- AF1134a
- Product Quantity:
- 0.1mg
- Category:
- -
- Supplier:
- Abgen
- Gene target:
- B7_H4 Antibody
Related genes to: B7_H4 Antibody
- Gene:
- VTCN1 NIH gene
- Name:
- V-set domain containing T cell activation inhibitor 1
- Previous symbol:
- -
- Synonyms:
- B7-H4, FLJ22418, B7S1, B7x, B7H4
- Chromosome:
- 1p13.1-p12
- Locus Type:
- gene with protein product
- Date approved:
- 2005-02-25
- Date modifiied:
- 2019-03-06
Related products to: B7_H4 Antibody
Related articles to: B7_H4 Antibody
- Cancer cells adopt multiple strategies to avoid detection and destruction by the immune system, including exploiting immune checkpoint pathways. B7x (B7-H4, B7S1, or ), a member of the B7/CD28 family, is frequently expressed in advanced bladder cancer, yet its role in bladder cancer progression and resistance to therapy remains poorly understood. Resistance to PD-1/PD-L1 immune checkpoint blockade immunotherapy significantly limits durable responses, with only 20%-25% of patients with muscle-invasive bladder cancer (MIBC) achieving long-term benefits. Here, we demonstrated that B7x mRNA and protein expression were associated with poor survival outcomes in MIBC patients and mouse models of bladder cancer, respectively. Stable expression of B7x in immune-competent bladder cancer mouse models resulted in enhanced tumor growth and splenomegaly, driven by the exclusion and suppression of tumor-infiltrating antitumor immune cells and the enrichment of pro-tumor and immunosuppressive cells. Consistently, in the IMvigor210 clinical trial, high B7x mRNA expression was correlated with poorer survival in MIBC patients treated with PD-L1 blockade. Notably, combination therapy targeting B7x alongside PD-1/PD-L1 or CTLA-4 blockade reduced tumor burden and overcame resistance to monotherapy. These findings establish B7x as a substantial driver of immune evasion in bladder cancer and highlight its potential as a therapeutic target to improve immune checkpoint blockade efficacy in MIBC. - Source: PubMed
Publication date: 2025/11/26
Pulanco Marc CZheng Xiang YuSankin AlexanderZheng DeyouZang Xingxing - - Source: PubMed
Publication date: 2026/04/19
Hu YunxiYang WenjiangGuo ShuangHuang Denghui - To elucidate the biological heterogeneity of gallbladder cancer (GBC) cells and refine post-operative risk stratification by investigating the expression and downstream signaling of the B7-family immune checkpoint molecules CD276 (B7-H3), VTCN1 (B7-H4), and HHLA2 (B7-H7) at single-cell resolution. - Source: PubMed
Publication date: 2026/04/18
Ma ChuhanHu HuixinLi YangZhong ChongliDong YunHaoChang ZhanhaoXu ShuoZhang YuyangHu HangqiLv ChaoTian Yu - Emerging data indicates that the lung microbiota contribute to the initiation and progression of lung cancer. Here, we investigate a wide range of immune checkpoint genes (ICGs) in the pulmonary microenvironment across lung carcinogenesis and explore the interplay between these immunoregulatory genes, the intratumoral microbiota, and inflammatory processes in the lungs. First, we estibalish that ICGs can considerably impact host immunity and efficacy of immunotherapy. Secondly, we identify , , and to significantly downregulate as tumors progress from early-stage to advanced-stage. In addition, the expression of , , and are significantly positively correlated with pulmonary inflammation. Finally, , , and levels positively correlate to immune- and inflammation-associated . Taken together, our study uncovers ICG signatures linked to tumor progression and sheds light on the complex network of microbiota-host immunity interactions within the lung microenvironment. This study lays the groundwork for future mechanistic studies and underscores the significance of microbiota-host immunity interactions for predicting and tracking the response to cancer treatment. - Source: PubMed
Publication date: 2026/04/01
Huang KunZhang ShuoLiu JinshuangYang ChengchengZeng GuangchunLi Bo - Intratumor heterogeneity (ITH) undermines transcriptome-based stratification in intrahepatic cholangiocarcinoma (iCCA). Here, we integrate multi-omics data from multi-region, single-region, and single-cell RNA sequencing cohorts to systematically characterize gene expression ITH. We uncover that immune and stromal heterogeneity are primary drivers of ITH, leading to misclassification of a median 27.8% of tumors by existing subtyping systems. To overcome this, we identify a low-intratumor-heterogeneity/high-intertumor-variability (LIHV) gene set and develop an ITH-insensitive classification system defining five subgroups: inflammatory (SI), metabolic (SII), atypical (SIII-1), immune-silent (SIII-2), and neurodegenerative (SIII-3). These subgroups exhibit distinct clinical outcomes, molecular features, immune landscapes, and therapeutic vulnerabilities. GPRC5A and VTCN1 serve as robust immunohistochemical biomarkers for SI and SIII tumors, while serum CEA and CA19-9 identify inflammatory iCCA. Therapeutically, HSP90 inhibition synergizes with anti-PD1 in inflammatory iCCA, whereas combined anti-PD1 and anti-TIM3 suppresses neurodegenerative iCCA. Collectively, our study provides a robust molecular framework and actionable therapeutic strategies for iCCA. - Source: PubMed
Publication date: 2026/03/30
Lin YoupeiPeng LihuaZhao HaichaoLin PenghuiChen LvGong ZunyunLin JianLiu DongbingYang XupengSong XiangzeZhang MaoJi ShuyiRao JunhuaLuo HuijuanCheng YifeiChen XiaofangSong GuoheHou HaoRao DongningZhang TianchengLiu WeirenZhang ShuXu GaoyangZhang JuanXiao LiyunLiang YanLiu YangChen YuhanCui ZhirouWang XiaoyingZhou JianGao QiangWu KuiFan Jia