Co-expression of PD-1 and PD-L1 predicts poor outcome in nasopharyngeal carcinoma

PD-L1 鼻咽癌 免疫组织化学 医学 免疫系统 肿瘤微环境 内科学 肿瘤科 血液学 放化疗 癌症研究 肿瘤浸润淋巴细胞 癌症 病理 免疫疗法 放射治疗 免疫学
作者
Jianwei Zhang,Wenfeng Fang,Tao Qin,Yunpeng Yang,Shaodong Hong,Wenhua Liang,Yuxiang Ma,Hongyun Zhao,Yan Huang,Cong Xue,Pei‐Yu Huang,Zhihuang Hu,Yuanyuan Zhao,Li Zhang
出处
期刊:Medical Oncology [Springer Science+Business Media]
卷期号:32 (3) 被引量:122
标识
DOI:10.1007/s12032-015-0501-6
摘要

Tumor immune evasion is a hallmark of cancer. The programmed death-1/programmed death-ligand 1 (PD-1/PD-L1) pathway has been suggested to play an important role in T cell tolerance and tumor immune escape. In this study, we aimed to evaluate the correlation between the expression of PD-1/PD-L1 and the post-treatment outcome in patients with nasopharyngeal carcinoma (NPC). Formalin-fixed, paraffin-embedded tissue biopsies from 139 patients with histological diagnosis of NPC treated with conventional chemoradiotherapy were studied. By using immunohistochemistry staining, expressions of PD-1 on tumor-infiltrating lymphocyte and PD-L1 on tumor tissue were detected. The staining results were evaluated with H-score. The correlation between PD-1/PD-L1 expression and clinical characteristics and post-treatment outcome were analyzed. PD-1(+) immune cell were present in 52 of these 139 tumors (37.4%). PD-L1 expression was detected in 132 patients (95.0%), which located on tumor tissue. High expression of PD-L1 (median H-score >35) in tumor tissue significantly correlated with a poor prognosis of disease-free survival (P = 0.009). Co-expression of PD-1 and PD-L1 in NPC at diagnosis correlated with the poorest prognosis of disease-free survival (P = 0.038). PD-1/PD-L1 co-expression reflected the selective suppression of cytotoxic lymphocytes in the tumor microenvironment and predicted recurrence and metastasis of NPC after conventional therapies. Blocking this pathway in patients with co-expression of PD-1/PD-L1 provides a potential therapy target for NPC.
最长约 10秒,即可获得该文献文件

科研通智能强力驱动
Strongly Powered by AbleSci AI
科研通是完全免费的文献互助平台,具备全网最快的应助速度,最高的求助完成率。 对每一个文献求助,科研通都将尽心尽力,给求助人一个满意的交代。
实时播报
moon发布了新的文献求助10
2秒前
夕立完成签到,获得积分10
7秒前
隐形曼青应助李海洋采纳,获得10
9秒前
15秒前
16秒前
英姑应助一YI采纳,获得10
16秒前
燕晓啸完成签到 ,获得积分0
17秒前
17秒前
18秒前
英姑应助guozizi采纳,获得20
20秒前
淡淡友卉发布了新的文献求助10
20秒前
dennisysz发布了新的文献求助10
22秒前
qf123456发布了新的文献求助10
23秒前
Liuuhhua完成签到,获得积分10
23秒前
崔振魁完成签到,获得积分10
24秒前
Yam呀完成签到 ,获得积分10
25秒前
淡淡友卉完成签到,获得积分10
29秒前
32秒前
脑洞疼应助大媛媛采纳,获得10
34秒前
37秒前
Jasper应助科研通管家采纳,获得30
40秒前
传奇3应助科研通管家采纳,获得10
40秒前
打打应助科研通管家采纳,获得30
40秒前
情怀应助科研通管家采纳,获得10
41秒前
科研通AI5应助科研通管家采纳,获得10
41秒前
科研通AI5应助科研通管家采纳,获得30
41秒前
慕青应助科研通管家采纳,获得10
41秒前
FashionBoy应助科研通管家采纳,获得10
41秒前
科研通AI5应助科研通管家采纳,获得10
41秒前
41秒前
上官若男应助科研通管家采纳,获得10
41秒前
Neo完成签到,获得积分10
41秒前
牟翎完成签到,获得积分10
42秒前
42秒前
42秒前
微光完成签到,获得积分10
43秒前
大喜子发布了新的文献求助10
46秒前
微光发布了新的文献求助10
46秒前
hanatae完成签到,获得积分10
46秒前
动漫大师发布了新的文献求助10
46秒前
高分求助中
【此为提示信息,请勿应助】请按要求发布求助,避免被关 20000
ISCN 2024 – An International System for Human Cytogenomic Nomenclature (2024) 3000
Continuum Thermodynamics and Material Modelling 2000
Encyclopedia of Geology (2nd Edition) 2000
105th Edition CRC Handbook of Chemistry and Physics 1600
Maneuvering of a Damaged Navy Combatant 650
the MD Anderson Surgical Oncology Manual, Seventh Edition 300
热门求助领域 (近24小时)
化学 材料科学 医学 生物 工程类 有机化学 物理 生物化学 纳米技术 计算机科学 化学工程 内科学 复合材料 物理化学 电极 遗传学 量子力学 基因 冶金 催化作用
热门帖子
关注 科研通微信公众号,转发送积分 3777470
求助须知:如何正确求助?哪些是违规求助? 3322820
关于积分的说明 10211936
捐赠科研通 3038215
什么是DOI,文献DOI怎么找? 1667191
邀请新用户注册赠送积分活动 798010
科研通“疑难数据库(出版商)”最低求助积分说明 758133