Rabbit Anti-Human CD274
- Known as:
- Rabbit Antibody toHuman CD274
- Catalog number:
- 129-10136
- Product Quantity:
- 100
- Category:
- -
- Supplier:
- Ray Biotech
- Gene target:
- Rabbit Anti-Human CD274
Related genes to: Rabbit Anti-Human CD274
- Gene:
- CD274 NIH gene
- Name:
- CD274 molecule
- Previous symbol:
- PDCD1LG1
- Synonyms:
- B7-H, B7H1, PD-L1, PDL1, B7-H1
- Chromosome:
- 9p24.1
- Locus Type:
- gene with protein product
- Date approved:
- 2003-11-13
- Date modifiied:
- 2014-11-19
Related products to: Rabbit Anti-Human CD274
Related articles to: Rabbit Anti-Human CD274
- Chronic prostatitis/chronic pelvic pain syndrome (CP/CPPS) is a prevalent and debilitating condition with unclear etiology. Increasing evidence implicates immune dysregulation, yet the molecular mechanisms underlying impaired immune regulation remain poorly defined. This study investigated the role of altered immune responses within PBMC populations and DNA methylation in CP/CPPS pathogenesis. - Source: PubMed
Publication date: 2026/05/04
Thumbikat PraveenPattabiraman GouthamSharifzad FarzanehYang YongyongLiu ZhiqiangOsborn Catherine VMurphy Stephen FCao QiSchaeffer Anthony J - Bladder cancer (BLCA) is clinically heterogeneous, and conventional staging does not fully capture individual risk. Ribosome biogenesis (RiBi) is implicated in cancer, but its prognostic relevance in BLCA is not well defined. - Source: PubMed
Publication date: 2026/04/16
Luo GuangyueWang WeiboTai SupengYan LeiLuo HailangChang YifanYang LexingYan JunyiZhou JunLiang Chaozhao - PD-1/PD-L1 immune checkpoint inhibitors (ICIs) have demonstrated significant clinical efficacy in the treatment of bladder cancer. However, heterogeneous patient responses continue to limit the widespread adoption and overall effectiveness of these therapies. Consequently, identifying strategies to enhance treatment response has become a primary focus of current oncological research. This review summarizes the biological determinants of immune response in bladder cancer, including sex, gut microbiota, molecular subtypes, and the tumor microenvironment (TME). Furthermore, we evaluate key predictive biomarkers for ICI response, such as PD-L1 expression, tumor mutational burden (TMB), and circulating tumor DNA (ctDNA). Synergistic combination strategies-incorporating chemotherapy, radiotherapy, targeted therapy, and nanomedicine-are also detailed to provide novel insights into bladder cancer immunotherapy. Ultimately, the systematic elucidation of immune response mechanisms combined with technological innovation will facilitate the optimization of therapeutic strategies, leading to improved clinical outcomes for patients. - Source: PubMed
Publication date: 2026/04/17
Cheng YaxinDeng WenzhiLiu YunqingChen GuanjunCao Ke - The secretion of chemokines by cancer-associated fibroblasts (CAFs) is a critical driver of cancer progression. Nevertheless, the precise contribution of CAFs in the nasopharyngeal carcinoma (NPC) tumor microenvironment to disease progression is yet to be fully understood. In this study, C-X-C motif chemokine ligand 11 (CXCL11) was identified to be upregulated in tumor tissues of NPC patients and NPC cells compared to counterpart normal tissues and cell lines. The CAFs-secreted CXCL11 was found to enhance the proliferative, invasive, and migratory capacities of NPC cells. CAFs-derived CXCL11 upregulates CXCR3 expression to facilitate NPC cell proliferation, migration, and invasion. Through mechanism investigation, we confirmed that CXCL11/CXCR3 axis upregulated PD-L1 expression through p65-mediated transcription activation. Finally, experiments further validated the tumor-promoting role of CAFs-secreted CXCL11 in NPC. In conclusion, our findings reveal a novel mechanism wherein CAFs-secreted CXCL11 promotes NPC malignant progression by activating the CXCR3/PD-L1 signaling axis. - Source: PubMed
Publication date: 2026/05/04
Fang JieCheng HuijuanZhang PengWang Liang - : Metaplastic breast carcinoma (MBC) is a rare, aggressive malignancy that is often resistant to conventional chemotherapy and characterized by a triple-negative phenotype. While immune checkpoint inhibition shows promise, the prognostic significance and distribution of programmed death-ligand 1 (PD-L1) expression within the heterogeneous architecture of MBC remain poorly understood. This study aimed to evaluate PD-L1 expression and the density of tumor-infiltrating lymphocytes (TILs) to clarify their roles in patient stratification and overall survival (OS). : We retrospectively analyzed 48 MBC cases diagnosed between 2010 and 2025. PD-L1 expression was quantified using the Combined Positive Score (CPS) with the 22C3 antibody clone across diverse histological components. The density of stromal TIL density was assessed following internationally standardized guidelines. Clinical outcomes and clinicopathological parameters, including metastasis, lymphovascular invasion (LVI), and histological subtype, were correlated with biomarker status using Kaplan-Meier survival analysis and Cox proportional hazards regression models. : PD-L1 positivity (CPS ≥1) was identified in 72.9% of cases, one of the highest rates documented in literature. Notably, an inverse relationship was observed with PD-L1-negative tumors, which exhibited significantly higher rates of distant metastasis (46.2% vs. 17.1%; = 0.039). Multivariate analysis confirmed that low density of TILs (HR = 9.66; = 0.016), metastasis (HR = 4.40; = 0.023), and the presence of LVI (HR = 3.84; = 0.047) were strong independent predictors of mortality. While PD-L1 status alone did not directly dictate overall survival, mean overall survival was markedly reduced in the low TILs cohort (32.2 months) compared to the high TILs group (114.2 months). : The high prevalence of PD-L1 expression supports routine screening for immunotherapy eligibility in MBC. Our findings suggest that PD-L1-negative cases represent a high-risk biological subset driven by alternative immune evasion mechanisms. Integrating TIL density with conventional pathological parameters provides a more robust prognostic framework, enabling personalized therapeutic strategies for this challenging malignancy. - Source: PubMed
Publication date: 2026/04/10
Toyran TugbaBayram ErtuğrulAydınalp Camadan YaseminSahin BerksoyDalcı KubilayArslan Yusuf KemalErgin Melek