PD-L1, FGFR1, PIK3CA, PTEN, and p16 expression in pulmonary emphysema and chronic obstructive pulmonary disease with resected lung squamous cell carcinoma.
Aged
Aged, 80 and over
B7-H1 Antigen
/ immunology
Carcinoma, Squamous Cell
/ complications
Class I Phosphatidylinositol 3-Kinases
/ immunology
Cyclin-Dependent Kinase Inhibitor p16
/ immunology
Female
Humans
Immunohistochemistry
Lung Neoplasms
/ complications
Lymphocytes, Tumor-Infiltrating
/ immunology
Male
Middle Aged
PTEN Phosphohydrolase
/ immunology
Pulmonary Disease, Chronic Obstructive
/ diagnosis
Pulmonary Emphysema
/ diagnosis
Receptor, Fibroblast Growth Factor, Type 1
/ immunology
Retrospective Studies
Severity of Illness Index
COPD
Emphysema
Lung squamous cell carcinoma
PD-L1
Journal
BMC pulmonary medicine
ISSN: 1471-2466
Titre abrégé: BMC Pulm Med
Pays: England
ID NLM: 100968563
Informations de publication
Date de publication:
03 Sep 2019
03 Sep 2019
Historique:
received:
15
10
2018
accepted:
02
08
2019
entrez:
5
9
2019
pubmed:
5
9
2019
medline:
26
3
2020
Statut:
epublish
Résumé
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.
Sections du résumé
BACKGROUND
BACKGROUND
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.
METHODS
METHODS
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.
RESULTS
RESULTS
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.
CONCLUSIONS
CONCLUSIONS
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.
Identifiants
pubmed: 31481045
doi: 10.1186/s12890-019-0913-8
pii: 10.1186/s12890-019-0913-8
pmc: PMC6724334
doi:
Substances chimiques
B7-H1 Antigen
0
CD274 protein, human
0
CDKN2A protein, human
0
Cyclin-Dependent Kinase Inhibitor p16
0
Class I Phosphatidylinositol 3-Kinases
EC 2.7.1.137
PIK3CA protein, human
EC 2.7.1.137
FGFR1 protein, human
EC 2.7.10.1
Receptor, Fibroblast Growth Factor, Type 1
EC 2.7.10.1
PTEN Phosphohydrolase
EC 3.1.3.67
PTEN protein, human
EC 3.1.3.67
Types de publication
Comparative Study
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
169Subventions
Organisme : KAKENHI
ID : 26462139
Références
Thorax. 2004 Aug;59(8):679-81
pubmed: 15282388
Am J Respir Cell Mol Biol. 2004 Dec;31(6):601-10
pubmed: 15374838
Am J Respir Crit Care Med. 2007 Aug 1;176(3):285-90
pubmed: 17478615
Thorax. 2007 Nov;62(11):932-7
pubmed: 17573447
Chest. 2007 Dec;132(6):1932-8
pubmed: 18079226
Am J Respir Crit Care Med. 2008 Oct 1;178(7):738-44
pubmed: 18565949
Clin Cancer Res. 2008 Oct 15;14(20):6618-24
pubmed: 18927303
Thorax. 2010 Jan;65(1):14-20
pubmed: 19729360
N Engl J Med. 2010 Jun 24;362(25):2380-8
pubmed: 20573926
Am J Respir Crit Care Med. 2011 Apr 1;183(7):891-7
pubmed: 20935112
Respiration. 2011;81(4):265-84
pubmed: 21430413
Lung Cancer. 2012 Apr;76(1):61-6
pubmed: 21945657
Eur Respir J. 2012 May;39(5):1230-40
pubmed: 22088970
Clin Cancer Res. 2012 Feb 15;18(4):1167-76
pubmed: 22228640
PLoS One. 2012;7(7):e42227
pubmed: 22848747
Lung. 2012 Dec;190(6):613-20
pubmed: 22965854
J Thorac Oncol. 2012 Oct;7(10):1513-21
pubmed: 22982652
Nat Rev Cancer. 2013 Apr;13(4):233-45
pubmed: 23467302
Respirology. 2014 Jan;19(1):98-104
pubmed: 24033868
Br J Cancer. 2014 Jun 10;110(12):2914-22
pubmed: 24853178
N Engl J Med. 2014 Nov 20;371(21):1963-71
pubmed: 25264305
N Engl J Med. 2015 Oct 22;373(17):1627-39
pubmed: 26412456
Am J Respir Crit Care Med. 2016 Mar 15;193(6):642-51
pubmed: 26517304
Ann Am Thorac Soc. 2015 Nov;12 Suppl 2:S169-75
pubmed: 26595735
Lancet. 2016 Apr 30;387(10030):1837-46
pubmed: 26970723
Mod Pathol. 2016 Jul;29(7):735-42
pubmed: 27080983
N Engl J Med. 2016 Nov 10;375(19):1823-1833
pubmed: 27718847
Clin Lung Cancer. 2017 Sep;18(5):504-511.e1
pubmed: 28038981
Eur Respir J. 2017 Jun 22;49(6):
pubmed: 28642306
Lung Cancer. 2017 Oct;112:96-101
pubmed: 29191607
Clin Radiol. 1982 Jul;33(4):379-87
pubmed: 7083738
BMJ. 1997 Oct 18;315(7114):980-8
pubmed: 9365295