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Buge Oz
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P2.02 - Biology/Pathology (ID 616)
- Event: WCLC 2017
- Type: Poster Session with Presenters Present
- Track: Biology/Pathology
- Presentations: 1
- Moderators:
- Coordinates: 10/17/2017, 09:30 - 16:00, Exhibit Hall (Hall B + C)
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P2.02-073a - Does the PD-L1 Status and TIL Intensity Change in NSCLC and Syncronous Brain Metastases? (ID 10118)
09:30 - 09:30 | Presenting Author(s): Buge Oz
- Abstract
Background:
Programmed death-ligand 1(PD-L1) expression in Non-small Cell Lung Carcinoma (NSCLC) is tissue based predictive marker. However, the differential expression of PD-L1 in tumor microenvironment between synchronous primary tumor in lung and metastatic side, especially brain metastasis remains unclear. This study addresses whether there is concordance of PD-L1 status and tumor infiltrating lymphocytes (TIL) together with intensity of CD8 lymphocytes, between the synchronous primary tumor and brain metastasis.
Method:
PD-L1 expression was evaluated immunohistochemically in primary lung tumor and synchronous brain metastasis by using the Dako PD-L1 IHC 22C3 pharmDx kit (SK006) . TIL were scored via CD3 and CD8 positivity immunohistochemically. PD-L1 expression was also compared with TIL proportion and intensity of CD8 lymphocytes between paired tumor tissues. All brain metastatic tissues had been removed before any treatment therefore;the study allowed the comparison of lung carcinoma and their native brain metastasis (BM).PD-L1 scoring was categorized based on the proportion of membranous immuno-positive tumor cells using cutoff values 0-1%, 1-49% and 50%. CD3 and CD8 positivity in TIL was evaluated semi quantitatively. Spearman rank correlation test was used for statistical analysis.
Result:
Primary tumor tissues and synchronous brain metastases of 24 NSCLC cases were included the study. Histopathological suptype of the cases were17/24 (70.83 % ) adenocarcinomas and 2/24 squamous cell carcinoma (8.3%), 1/24 adeno-squamous Ca.(4.16%) and 4/24 large cell carcinomas and pleomorphic carcinomas (16.6%). Tumor subtypes were the same in both primary tumor and BM specimen. In primary tumors, PD-L1 positivity was observed in 25% (6/24), 37.5% (9/24) and 37.5% (9/24) using cutoff values 0-1% , 1-49% and 50% respectively. PD-L1expresion score and pattern showed significant correlation in paired BM (Spearman rho= .731,p ˂0.001). However the PD-L1 expression on TIL cells and proportion of TIL infiltration was not demonstrated same concordance (Spearman rho= .548, p=0.006). When CD8 lyhmpocyte intensity among the TIL cells was compared between primary tumor and BM, only 54.16% (13/24) of the pair tumors were compatible.
Conclusion:
This study demonstrates that the concordance of PD-L1 expression between primary NSCLC and BM is very high. Thus, evaluation of PD-L1 in either primary lung tumors or brain metastasis would be useful for choosing anti PD-1/PD-L1 immunotherapy in patient with NSCLC with BM. Due to the low compatibility of CD8 intensity in TIL cells, may not be sufficient enough as a therapeutic target to use for both primary and brain metastases. Further research on this subject is required to gain deeper insigth in to the mecanism/biology of CD8 lymhpocites intensity in TIL cells and PD-L1 expression in NSCLC.
