Virtual Library
Start Your Search
Y. Chen
Author of
-
+
P1.07 - Immunology and Immunotherapy (ID 693)
- Event: WCLC 2017
- Type: Poster Session with Presenters Present
- Track: Immunology and Immunotherapy
- Presentations: 1
- Moderators:
- Coordinates: 10/16/2017, 09:30 - 16:00, Exhibit Hall (Hall B + C)
-
+
P1.07-005 - A Systematic and Genome-Wide Correlation Analysis of PD-L1 Expression and Common NSCLC Driver Genes (ID 7537)
09:30 - 09:30 | Author(s): Y. Chen
- Abstract
Background:
Programmed cell death ligand 1(PD-L1) targeted immunotherapy is emerging as a promising therapeutic strategy for non-small-cell lung cancer (NSCLC). However, the association of PD-L1 and EGFR, KRAS, and ALK and other driver genes in NSCLC are not well known. To explore the potential association, we systematically integrated published articles and analyzed RNA-seq dataset from The Cancer Genome Atlas project (TCGA) in order to comprehensively investigate the association between PD-L1 and the mutation and expression of these common driver mutations.
Method:
The relevant articles published in English were searched by using the database of PubMed, Web of science and Embase up to September 2016. The effect sizes were estimated by odds ratio with a correspondent 95% confident interval (CI), which were pooled by random effect or fixed effect models. Subgroup and sensitivity analysis were performed and the Begg’s test was used to analysis the potential publication bias. We further applied the Pearson correlation analysis to investigate the association of PD-L1 and the expression of driver genes. Wilcoxon rank sum was used to evaluate the expression difference of PD-L1 among population.
Result:
A total of 9934 lung cancer cases were collected from 34 published studies. Patients with EGFR wild type (OR 0.68, 95% CI 0.48 to 0.96; P = 0.03), KRAS mutation positivity (OR 1.27, 95% CI 1.02 to 1.58; P=0.03) or non-adenocarcinoma histology (OR 0.68, 95% CI 0.47 to 0.98; P =0.04) were associated with high PD-L1 expression rate. However, PD-L1 expression was not associated with the status of ALK. Complementary to the findings of the meta-analysis, results from the TCGA project indicated that the expression of PD-L1 was significantly higher for patients with squamous cell carcinoma than adanocarcinoma (p=0.023) while the expression of common driver genes including EGFR, KRAS, ALK, MET, ROS1, PIK3CA, RET, HER2, NRAS and BRAF do not correlate with PD-L1 expression in NSCLC.
Conclusion:
High expression of PD-L1 was associated with the presence of EGFR wild-type, KRAS mutations or non-adenocarcinoma histology in NSCLC patients. Our results provide evidences for screening candidates for anti-PD-1/PD-L1 treatments.