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Shuai Zhu
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P07 - Early Stage/Localized Disease - Imaging and Biomarkers (ID 116)
- Event: WCLC 2020
- Type: Posters
- Track: Early Stage/Localized Disease
- Presentations: 1
- Moderators:
- Coordinates: 1/28/2021, 00:00 - 00:00, ePoster Hall
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P07.03 - The Impact of PD-L1 Expression on the Prognosis of Early-Stage Resected NSCLC: A Meta-Analysis of Literatures. (ID 1024)
00:00 - 00:00 | Presenting Author(s): Shuai Zhu
- Abstract
Introduction
Previous studies have demonstrated that programmed cell death-ligand 1 (PD-L1) serves as a poor prognostic biomarker for the survival in advanced-stage non-small-cell lung cancer (NSCLC) patients. However, the value of PD-L1 expression for the prognosis of early-stage NSCLC patients after complete resection remains controversial. Here, we conduct a meta-analysis to investigate the relationship between PD-L1 expression and prognosis in resected NSCLC.
Methods
Electronic databases, including PubMed, EMBASE, and the Cochrane Library, were searched up until June 30 2019, for studies evaluating the expression of PD-L1 and prognosis of the resected NSCLC. Hazard ratios (HRs) with 95% confidence interval (CI) of overall survival (OS) and disease-free survival (DFS) were pooled and analyzed. Heterogeneity and publication bias analyses were also performed.
Results
A total of 15 studies involving 3501 patients were enrolled. The pooled hazard ratio (HR) showed that PD-L1 expression was related to a much shorter DFS (HR =1.63, 95% CI: 1.26-2.12, P=0.022), as well a significantly worse OS (HR =1.68, 95% CI: 1.32-2.14, P=0.000). Furthermore, our analysis indicated that PD-L1 expression was significantly associated with gender (male vs. female: HR=1.25, 95% CI:1.02-1.52, p=0.028), tumor stage (III/IV vs. I/ II: HR= 2.39, 95% CI:1.85-3.08, p=0.000), lymph node metastasis (N+ vs N-: HR=3.54, 95%CI:2.56-4.88, p=0.000) and smoking status (Yes vs No: HR=1.37,95% CI:1.20-1.560, p=0.000).
Conclusion
The results of this meta-analysis suggest that PD-L1 expression predict an unfavorable prognosis in early-stage resected NSCLC. The role of individualized anti-PD-L1/PD-1immunotherapy in the adjuvant settings of resected NSCLC is worthy of being further investigated.
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P38 - Pathology - Pathology/Staging (ID 108)
- Event: WCLC 2020
- Type: Posters
- Track: Pathology, Molecular Pathology and Diagnostic Biomarkers
- Presentations: 1
- Moderators:
- Coordinates: 1/28/2021, 00:00 - 00:00, ePoster Hall
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P38.11 - Clinical and Molecular Characteristics of TSC1/2 Mutant Lung Cancer (ID 1154)
00:00 - 00:00 | Author(s): Shuai Zhu
- Abstract
Introduction
Tumor suppressor genes TSC1 and TSC2 inhibit cell growth through inactivation the function of mTORC1. Previous studies have demonstrated that loss of function mutation of either TSC1 or TSC2 gene result in formation of neoplasm in multiple tissues. However, the clinical significance of TSC1 and TSC2 in non-small-cell lung cancer (NSCLC) remains unknown. This study aimed to investigate the clinical and molecular characteristics of TSC1 and TSC2 mutation in NSCLC patients.
Methods
We retrieved the clinical and genomic information of 1144 NSCLC from the Pan-Lung cancer dataset through the cBioportal (www.cbioportal.org). The cohorts of TSC1 and TSC2 mutant patients were identified. We compared baseline characteristics of patients with the Fisher exact test for categorical data and the Mann-Whitney U test for continuous variables. Overall survival (OS) was estimated with Kaplan-Meier curves, and differences were compared with the log-rank test.
Results
Among 1144 patients, 27(2.36%) of them had TSC1 mutation and 40 (3.50%) had TSC2 mutation. Most patients with TSC1 and TSC2 mutations coexisted with other oncogenic gene alterations. TP53 was the most frequent concurrent gene (n=53), followed with ERBB family genes (n=24) and KRAS (n=15). Compared to squamous cell carcinoma, TSC1/2 mutation was slightly more common in adenocarcinoma (53.7% vs 46.3%). 61.2% TSC1/2 mutant patients were male and 88.1% patients had former/current smoking history. Kaplan–Meier analysis showed that the patients harboring TSC1 mutation had a median OS of 14.1 months, whereas patients with TSC2 mutation had a median OS 110.6 months. However, there was not a statistically difference (P=0.201).
Conclusion
TSC1/2 mutation may define a unique population of NSCLC, which often coexists with other oncogenic gene alterations such as TP53 mutation. The function of TSC1/2 mutation and the value of TSC1/2 as therapeutic target in NSCLC are under investigation.
