CELL INTELLIGENCE · 肿瘤细胞治疗研究
肿瘤细胞治疗研究
英文原题:PD-L1 expression in pancreaticobiliary adenosquamous carcinoma: a single-institution case series.
PD-L1 expression in pancreaticobiliary adenosquamous carcinoma: a single-institution case series.
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PB-ASCs 在炎症反应中显著富集,且 PD-L1 表达显著高于 PB-AC(P<0.001),提示免疫检查点抑制剂在管理 PB-ASC 患者中具有潜在的治疗作用。
程序性细胞死亡蛋白1(PD-1)/程序性细胞死亡配体1(PD-L1)通路是T细胞介导免疫反应的有效负性调节因子,在多种肿瘤中表达上调。胰胆管腺鳞癌(PB-ASC)是一种侵袭性癌症,与单纯胰胆管腺癌(PB-AC)相比预后更差。迄今为止,关于PB-ASC中PD-L1表达的已发表信息很少。本研究旨在探讨PB-ASC和PB-AC中PD-L1表达与TIL(肿瘤浸润淋巴细胞)之间的关系。
我们评估了15例PB-ASC(10例胰腺,5例胆囊)和34例对照PB-AC(22例胰腺导管,12例胆囊)中PD-L1的肿瘤表达,使用抗PD-L1(E1L3N)抗体。根据肿瘤组织中TIL(肿瘤浸润淋巴细胞)的分布,将所有肿瘤分为三种免疫表型:免疫炎症型(II)、免疫排斥型(IE)和免疫荒漠型(ID)。
PD-L1表达的频率在PB-ASC中显著高于PB-AC(10/15;66.7% vs 3/34;8.8%)。在PB-ASC中,PD-L1表达仅见于鳞状成分6例,仅见于腺状成分1例,同时见于鳞状和腺状成分3例。PB-ASC中PD-L1的表达与肿瘤免疫状态无关,而PB-AC中的表达仅见于具有II或IE表型的肿瘤。与PB-AC(22/34;65%;P=0.02)相比,ID表型在PB-ASC中相对少见(4/15;26.7%)。
The programmed cell death protein 1 (PD-1)/programmed cell death ligand 1 (PD-L1) pathway is a potent negative regulator of T-cell-mediated immune response that is upregulated in many neoplasms. Pancreaticobiliary adenosquamous carcinoma (PB-ASC) is an aggressive cancer that carries a poorer prognosis compared with pure pancreaticobiliary adenocarcinoma (PB-AC). To date, there is little published information regarding PD-L1 expression in PB-ASC. The aim of the study was to examine the relationship between PD-L1 expression and tumor-infiltrating lymphocytes in PB-ASC and PB-AC.
We evaluated 15 PB-ASCs (10 pancreatic, 5 gallbladder) and 34 control PB-ACs (22 pancreatic ductal, and 12 gallbladder) for tumor expression of PD-L1 using anti-PD-L1 (E1L3N) antibody. All tumors were classified into three immune phenotypes: immune inflamed (II), immune excluded (IE), and immune desert (ID) according to the distribution of tumor-infiltrating lymphocytes in tumor tissues.
The frequency of PD-L1 expression was significantly higher in PB-ASC (10/15; 66.7%) than in PB-AC (3/34; 8.8%). In PB-ASC, PD-L1 expression occurred exclusively in the squamous component in six cases, exclusively in the glandular component in one case, and in both the squamous and the glandular components in three cases. PD-L1 expression in PB-ASC was irrespective of the tumor immune status, whereas its expression in PB-AC was observed only in tumors with the II or IE phenotype. The ID phenotype was relatively rare (4/15; 26.7%) in PB-ASC compared with PB-AC (22/34; 65%; P=0.02).
PB-ASCs are notably enriched in inflammatory response and showed significantly higher PD-L1 expression than PB-AC (P<0.001), suggesting a potential therapeutic role for immune checkpoint inhibitors in managing patients with PB-ASC.
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