Department of Respiratory Medicine, Tokyo Women's Medical University, Tokyo, Japan.
Departments of Thoracic Surgery, Tokyo Women's Medical University Yachiyo Medical Center, Chiba, Japan.
BMC Pulm Med. 2019 Sep 3;19(1):169. doi: 10.1186/s12890-019-0913-8.
Emphysema and chronic obstructive pulmonary disease (COPD) are well known independent risk factors for lung cancer. However, the developmental mechanisms between emphysema/COPD and lung cancer remain unknown. The purpose of this study was to evaluate PD-L1, FGFR1, PIK3CA, PTEN, and p16 expression in squamous cell carcinoma (SCC) associated with emphysema/COPD.
A total of 59 patients with squamous cell lung carcinoma (SCC) resected between 2008 and 2012 were retrospectively reviewed. Emphysema was assessed according to the Goddard score. Total severity was divided into none-mild (0-7), moderate (8-15), and severe (≥ 16). Local severity around the existing tumor was divided into no emphysema (0) and presence of emphysema (1-4). COPD severity was based on the Global Initiative for Chronic Obstructive Lung Disease (GOLD) criteria. PD-L1, FGFR1, PIK3CA, PTEN, and p16 expression were evaluated by immunohistochemistry (IHC). Expression level was classified as tumor cells (TC) 3 (≥ 50%), TC2 (5-49%), TC1 (1-4%), or TC0 (< 1%), and as tumor-infiltrating immune cells (IC) 3 (≥ 50%), IC2 (5-49%), IC1 (1-4%), or IC0 (< 1%) for PD-L1. Expression level was compared between none-mild/moderate-severe total emphysema, no/presence of local emphysema, no COPD/COPD, and GOLD 1/GOLD 2, 3.
PD-L1 expression was significantly correlated with severity of emphysema in TC0, 1, 2 vs. TC3 (P = 0.012). PD-L1 was significantly higher inversely in none-mild emphysema compared to moderate-severe (95% CI, 0.061-5.852, P = 0.045). There were no other significant associations between PD-L1, FGFR1, PIK3CA, PTEN, and p16 expression and total/local severity of emphysema or presence of COPD/GOLD stage.
PD-L1 expression in SCC was correlated with severity of emphysema in TC0, 1, 2 vs. TC3 and more frequent in none-mild emphysema than moderate-severe emphysema.
肺气肿和慢性阻塞性肺疾病（COPD）是众所周知的肺癌独立危险因素。然而，肺气肿/COPD 和肺癌之间的发展机制尚不清楚。本研究旨在评估与肺气肿/COPD 相关的鳞状细胞癌（SCC）中 PD-L1、FGFR1、PIK3CA、PTEN 和 p16 的表达。
回顾性分析 2008 年至 2012 年间切除的 59 例鳞状细胞肺癌（SCC）患者。根据 Goddard 评分评估肺气肿。总严重程度分为无轻度（0-7）、中度（8-15）和重度（≥16）。现有肿瘤周围的局部严重程度分为无肺气肿（0）和存在肺气肿（1-4）。COPD 严重程度基于全球慢性阻塞性肺疾病倡议（GOLD）标准。通过免疫组织化学（IHC）评估 PD-L1、FGFR1、PIK3CA、PTEN 和 p16 的表达。表达水平分为肿瘤细胞（TC）3（≥50%）、TC2（5-49%）、TC1（1-4%）或 TC0（<1%）和肿瘤浸润免疫细胞（IC）3（≥50%）、IC2（5-49%）、IC1（1-4%）或 IC0（<1%）用于 PD-L1。在无轻度/中度重度肺气肿、无/存在局部肺气肿、无 COPD/COPD 和 GOLD 1/GOLD 2、3 之间比较 PD-L1 的表达水平。
PD-L1 表达在 TC0、1、2 与 TC3 之间与肺气肿严重程度显著相关（P=0.012）。与中度至重度肺气肿相比，无轻度肺气肿中 PD-L1 显著降低（95%CI，0.061-5.852，P=0.045）。PD-L1、FGFR1、PIK3CA、PTEN 和 p16 表达与肺气肿总/局部严重程度或 COPD/GOLD 分期之间无其他显著相关性。
SCC 中 PD-L1 的表达与 TC0、1、2 与 TC3 之间的肺气肿严重程度相关，与中度至重度肺气肿相比，无轻度肺气肿中 PD-L1 更为常见。
