Ask about this productRelated genes to: B7H1 antibody
- 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: B7H1 antibody
Related articles to: B7H1 antibody
- Immune checkpoint inhibitors (ICIs) have improved patient outcomes substantially in non-small cell lung cancer (NSCLC). Despite considerable effort, our understanding of the features that predict for immunotherapy response and resistance in patients remains incomplete. In this issue of the JCI, Isomoto and colleagues utilized a multiplex IHC platform to profile the spatial organization of the lung cancer tumor immune microenvironment, enabling the identification of spatial immune features that correlate with immunotherapy efficacy. This study enhances our knowledge of the spatial organization of features impacting ICI efficacy by identifying a three-variable spatial composite - including CD73 upregulation in EGFR-mutant NSCLC - that substantially outperforms PD-L1 expression in predicting immunotherapy efficacy. Moreover, it establishes spatial proteomic profiling as a platform for generating therapeutic hypotheses that are actionable and mechanistic in NSCLC. - Source: PubMed
Publication date: 2026/05/15
Zou TaoMinna John D - This case report describes an unusual clinical course of a patient with papillary thyroid carcinoma (PTC). The patient sequentially developed metastases to the cervical lymph nodes, lungs, pleura, and brain. Following tumor invasion into the latissimus dorsi muscle, a biopsy of this metastatic lesion revealed a BRAF V600E-mutant squamous cell carcinoma (SCC) phenotype indicating a high-grade dedifferentiation from the primary PTC. This metastatic focus also demonstrated upregulation of programmed cell death ligand 1 (PD-L1) expression. Subsequently, the patient exhibited a robust sensitivity to treatment with a programmed cell death protein 1 (PD-1) inhibitor and chemotherapy. This case highlights a highly aggressive evolutionary pattern of PTC and its associated potential for immunotherapy, providing valuable insights for the clinical management of thyroid cancer. - Source: PubMed
Publication date: 2026/04/29
Tian DanDeng ShuqinJin GaowaDa LenggaowaWang WenjuanWu YungaowaGao JialiXu TingWei KexinHan YalongZhao JunLi Quanfu - Second-generation epidermal growth factor receptor tyrosine kinase inhibitors (EGFR-TKIs) are key first-line therapies for advanced non-small cell lung cancer (NSCLC) with uncommon EGFR mutations, with risk stratification mainly based on EGFR mutation subtypes. Emerging evidence suggests programmed death-ligand 1 (PD-L1) expression may affect EGFR-TKI efficacy. This study compared associations of PD-L1 expression and EGFR mutation subtypes with outcomes in patients receiving first-line second-generation EGFR-TKI monotherapy. - Source: PubMed
Jin HongpingWang YueZhang YidanWu YiqingLiu TengfeiXu JianlinChu TianqingZhong HuaYang HuizhenZhong Runbo - Metastatic cutaneous melanoma (MCM) is primarily treated with BRAF/MEK inhibitors and immune checkpoint inhibitors (ICIs), but the long-term efficacy of these therapies is often limited by acquired resistance. Nicotinamide phosphoribosyltransferase (NAMPT), the rate-limiting enzyme in NAD biosynthesis, is frequently upregulated in MCM, supporting metabolic rewiring and targeted therapy resistance. Interferon-γ (IFN-γ) signaling plays a central role in melanoma biology, exerting both antitumor and immunoregulatory effects, linked with the onset of therapeutic resistance. Emerging evidence suggests that metabolic pathways may critically modulate IFN-γ responses; however, the functional interplay between NAD/NAMPT metabolism and IFN-γ signaling in melanoma cells remains poorly defined. - Source: PubMed
Publication date: 2026/05/14
Fiorilla IreneGhezzi BeatricePonzano AlessiaMoiso EnricoRiccardo FedericaTommasi NicolettaAvalle LidiaCarrà GiovannaUgolini FilippoCalussi EdoardoTodesco Alberto MariaDigiovanni SabrinaCasone FilippoRizza GiuliaPonzone LucaSzumera-Ciećkiewicz AnnaCavaletto MariaPorporato Paolo EttoreConti LauraRiganti ChiaraMassi DanielaCalautti EnzoAudrito Valentina - Despite numerous available treatment options, the overall prognosis for patients with unresectable hepatocellular carcinoma (uHCC) remains poor. This study aimed to evaluate the efficacy and safety of combining hepatic arterial infusion chemotherapy with FOLFOX (FOLFOX-HAIC), lenvatinib, and the PD-L1 inhibitor durvalumab in this population, with all uHCC patients receiving the triple-combination regimen as initial therapy. The primary objective was progression-free survival (PFS), and secondary outcomes included objective response rate (ORR), disease control rate (DCR), overall survival (OS), and safety. From August 2021 to September 2023, 40 uHCC patients were enrolled, with a median follow-up of 23.1 months (95% confidence interval [CI], 19.0-23.8); 3 deaths and 12 disease progressions were recorded. The median PFS was 15.8 months (95% CI, 8.3-23.3) with a 6-month PFS rate of 77.5% (95% CI, 63-90%), and 1- and 2-year OS rates were 97.5% and 94.0%, respectively. Per modified RECIST criteria, ORR was 75.0% (9 CR/pCR, 21 PR) and DCR was 95.0% (8 SD); median time to response (TTR) was 2.2 months and median duration of response (DOR) was 10.4 months. Seven patients (17.5%) underwent R0 conversion surgery, 3 (42.9%) achieving pCR. Safety was favorable: 85.0% had grade 1-2 adverse events, with grade 3 elevated alanine aminotransferase and thrombocytopenia each occurring in 2 patients (5.0%). No grade 4 adverse events were observed. Collectively, the triple-combination therapy of FOLFOX-HAIC, lenvatinib, and durvalumab exhibits promising therapeutic efficacy, favorable disease control, and a well-tolerated safety profile, providing a potential new treatment option for patients with uHCC. Trial number: NCT04961918. - Source: PubMed
Publication date: 2026/05/15
Li Shao-HuaZuo Zhi-JunLu Liang-HeXu Long-ZhouWang Qiao-XuanZhao Rong-CeMei JieLi Ji-BinZheng LieGuo Rong-PingWei Wei