Journal Thoracic Oncology

Abstracts Journal of Thoracic Oncology • Volume 12 Issue S1 January 2017
28-8pharmDx
≥ 1% positive ≥ 5% positive ≥ 10 % positive
OA 87 (80–94) 95 (91–99) 90 (83–95)
APA 86 (77–94) 94 (86–99) 84 (71–93)
ANA 88 (80–94) 96 (92–99) 92 (87–97)
PPA 81 (69–92) 91 (79–100) 79 (63–93)
NPA 93 (85–100) 98 (94–100) 95 (88–100)
There was high agreement between the cytological and histological scores,
applying to both pharmDx kits and all cutoffs (Table), not changing by
exclusion of cytological cell blocks containing 1%, >5%, >10% and hereafter in
10% increments. The pathologist was blinded to previous evaluations of pair
members. Overall Agreement (OA) and Average Positive (APA) and Negative
Agreement (ANA) were calculated Results: Agreement statistics for 28-8
pharmDx and 22C3 pharmDx with different cutoffs for PD-L1 positivity in
cytology and histology specimens, % (95% CI)
PD-L1 IHC 22C3
pharmDx and
PD-L1 IHC 28-8
pharmDx on
cytological cell
blocks
≥ 1% ≥ 5% ≥ 10 % ≥ 50%
OA 94 (90–99) 98 (94–100) 97 (92–100) 93 (87-98)
APA 93 (87-97) 97 (91-100) 94 (85-100) 80 (61-94)
ANA 95 (90-99) 98 (95-100) 98 (94-100) 96 (92-99)
PD-L1 IHC 22C3
pharmDx and
PD-L1 IHC 28-8
pharmDx on
histological
material
≥ 1% ≥ 5% ≥ 10 % ≥ 50%
OA 97 (92-100) 99 (97-100) 95 (91-99) 93 (86-97)
APA 96 (92-100) 98 (95-100) 93 (84-98) 80 (62-94)
ANA 97 (92-100) 99 (97-100) 97 (93-99) 96 (92-99)
High OA, APA and ANA were found for agreement between 22C3pharmDx
and 28-8pharmDx on cytological clot material, as well as on histological
tissue for all cutoffs. The APA at cutoff 50% positivity was the lowest (80%);
the CIs were however wide due to small number of positive samples at this
cutoff. Pearson r 2 were 0.96-0.97 Conclusion: High correlation between
PD-L1 IHC 22C3 pharmDx and PD-L1 IHC 28-8 pharmDx was observed on both
cytological and histological specimens, suggesting that these assays may be
used interchangeably in testing of lung tumors for PD-L1 expression. However,
more data is needed to alter current guidelines.
Keywords: PD-L1, NSCLC, Cytology/histology, agreement
POSTER SESSION 2 – P2.01: BIOLOGY/PATHOLOGY
IMMUNE MECHANISMS IN THORACIC CANCER AND TARGETED THERAPY –
TUESDAY, DECEMBER 6, 2016
P2.01-050 CLINICOPATHOLOGICAL CHARACTERISTICS OF PD-L1
EXPRESSION IN LUNG ADENOCARCINOMA
Shafei Wu, Xiaohua Shi, Jian Sun, Yuanyuan Liu, Zhiyong Liang, Xuan Zeng
Pathology, Peking Union Medical College Hospital, Beijing/China
Background: Lung adenocarcinoma (AD) is a common variant lung cancer,
accounting for about 70% of non-small cell lung cancer. PD1/PD-L1 is a
promising immune therapy target which has achieved promising results in the
late stage NSCLC patients in the ongoing clinical trials. Because of different
accompanying diagnostic antibodies employed in different clinical trials
and limited data regarding PD-L1 expression in the small number of patients
enrolled in clinical trials, there is an urgent need to examine the expression of
PD-L1 in lung cancer samples in order to enrich patients who will benefit from
the immune targeted therapy. Our goal was to detect PD-L1 expression and
analyze its expression with the clinicopathological characteristics. Methods:
Protein expression of PD-L1 was examined by immunohistochemistry method
using the VENTANA PD-L1 (SP263) rabbit monoclonal antibody. Messenger
RNA level of PD-L1 was evaluated by in situ hybridization method. Tissue
microarrays (TMAs) containing formalin fixed paraffin embedded (FFPE) lung
adenocarcinoma cases were used in this study. Results: This study included
133 cases of lung AD totally. PD-L1 expression rate in lung ASC was 16.5% at
the mRNA level and 13.5% at the protein level, which the kappa coefficient of
the two examination methods was 0.824 (P=0.000, highly correlated). PD-L1
expression in lung AD was found to be highly expressed in female patients and
smokers (P=0.019 and 0.002), while no association was identified between
PD-L1 expression and age, tumor size, clinical stage, positive pleural invasion,
histological type (lepidic or non-lepidic type), lymph node metastasis or
therapy methods. Overexpression of PD-L1 was a significantly indicator of
shorter recurrence free survival (RFS) time and overall survival duration
(P=0.000 and 0.000). Multivariate analysis revealed that PD-L1 expression
was an independent risk factor for poor RFS and overall survival (P=0.004
and 0.006). Conclusion: PD-L1 overexpression is more frequently observed in
smokers in lung adenocarcinoma. PD-L1 expression is an indicator of worse
prognosis in surgically resected lung adenocarcinoma patients.
Keywords: PD-L1 SP263 mRNA lung cancer
POSTER SESSION 2 – P2.01: BIOLOGY/PATHOLOGY
IMMUNE MECHANISMS IN THORACIC CANCER AND TARGETED THERAPY –
TUESDAY, DECEMBER 6, 2016
P2.01-051 MYELOID-DERIVED SUPPRESSOR CELL EXPRESSION
WITHIN THE MICROENVIRONMENT OF LUNG ADENOCARCINOMA
Yasuto Jin 1 , Hiroyuki Shimada 1 , Shuta Yamauchi 1 , Osamu Matsubara 1 ,
Kazuteru Yamanaka 1 , Naohiko Inase 2
1 Hiratsuka Kyosai Hospital, Hiratsuka/Japan, 2 Tokyo Medical and Dental University,
Tokyo/Japan
Background: Myeloid-derived suppressor cells (MDSCs) are implicated in
immune suppression of cancer and chronic inflammation. Although PD-1/
PD-L1 checkpoint inhibitors show clinical efficacy as immunotherapy
for lung cancer, the mechanisms by which lung cancers are refractory to
immunotherapy remain to be fully understood. MDCSs are thought to
contribute to T-cell exhaustion and have been proposed to play a role in tumor
progression. In human lung cancer, the relationship between MDSCs and
clinico-pathological factors, and the relevance of MDSCs to its diagnosis and
treatment is yet to be elucidated. Methods: Tissue specimens were obtained
from 30 surgically treated patients with stage I to IV NSCLC. Correlation
between immunohistochemical staining for CD33, CD14, CD11b, CD8 and
PD-L1 (SP263), and clinico-pathological factors were ebaluated. For PD-L1,
membranous staining of any intensity of in more than 25% of tumor cells
was considered positive. Histologic subtypes were compared with the degree
Copyright © 2016 by the International Association for the Study of Lung Cancer
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