Anti_Human, mab CTLA_4 Source Mouse
- Known as:
- Anti_Human, mab CTLA_4 Source Mouse
- Catalog number:
- 101-M345
- Product Quantity:
- 100 µg
- Category:
- -
- Supplier:
- Reliatech
- Gene target:
- Anti_Human mab CTLA_4 Source Mouse
Related genes to: Anti_Human, mab CTLA_4 Source Mouse
- Gene:
- CTLA4 NIH gene
- Name:
- cytotoxic T-lymphocyte associated protein 4
- Previous symbol:
- CELIAC3, IDDM12
- Synonyms:
- CD152, CD, GSE, CTLA-4
- Chromosome:
- 2q33.2
- Locus Type:
- gene with protein product
- Date approved:
- 1989-05-25
- Date modifiied:
- 2019-04-23
Related products to: Anti_Human, mab CTLA_4 Source Mouse
Related articles to: Anti_Human, mab CTLA_4 Source Mouse
- Colon cancer (CC), a malignancy with high global incidence and mortality, remains a major public health burden. As a pivotal aspect of tumor metabolic reprogramming, fatty acid metabolism has drawn significant research interest. This study was designed to elucidate the relationship between fatty acid metabolism-related gene expression and prognosis in patients with CC. - Source: PubMed
Publication date: 2026/03/15
Zhou ShulingChen MinDong ZhikunYang YongShi XiaoruiKang HuanShi ChangbeiWang Xuan - Programmed death-1 (PD-1) inhibitors are anticancer drugs that function as immune checkpoint blockers, targeting PD-1 proteins on the surface of cells to restore immune system activity against tumors. While cutaneous adverse events associated with immune checkpoint inhibitor therapy are well documented, this case highlights the reactive histopathologic changes that can occur in benign nevi during treatment. Here, we present the case of a 51-year-old Hispanic female with a history of melanoma on the chest who was seen in clinic for routine follow-up. Three suspicious pigmented lesions located on the right upper back, abdomen, and left shoulder were biopsied for further analysis. Histopathologic examination indicated an intradermal melanocytic nevus with irritation and inflammation, an inflamed, mildly dysplastic compound melanocytic nevus, and a compound melanocytic nevus with marked inflammation and no atypia. Additional clinical history revealed that the patient was receiving treatment for advanced melanoma with immune checkpoint inhibitors. Increased awareness of these features in melanocytic lesions associated with PD-1 and cytotoxic T-lymphocyte-associated protein 4 (CTLA-4) inhibitors may help with accurate diagnosis. - Source: PubMed
Publication date: 2026/03/17
Sohail NehaaSohail AyaanDurrani SanaaBilbaoa JorgeAbbud Cesar ASimpson BrendaReyes Barron Cynthia - - Source: PubMed
Publication date: 2026/03/28
Fadili HajarFahi MohammedAllaoui AbireSnoussi MalakOusti FadwaGhazi BouchraMoudatir MinaAadam ZahraEchchilali KhadijaZrara AbdelhamidBousfiha Ahmed AzizEl Bakkouri Jalila - 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
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Publication date: 2026/04/20
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