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J. Zhang
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P1.03 - Chemotherapy/Targeted Therapy (ID 689)
- Event: WCLC 2017
- Type: Poster Session with Presenters Present
- Track: Chemotherapy/Targeted Therapy
- Presentations: 1
- Moderators:
- Coordinates: 10/16/2017, 09:30 - 16:00, Exhibit Hall (Hall B + C)
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P1.03-052 - Comparing EGFR-TKI with EGFR-TKI plus Chemotherapy as 1st Line Treatment in Advanced NSCLC Patients with Both Mutated EGFR and Bim Polymorphism (ID 10516)
09:30 - 09:30 | Author(s): J. Zhang
- Abstract
Background:
Not all advanced non-small cell lung cancer (NSCLC) patients with epidermal growth factor receptor (EGFR) activating mutations could get benefit from 1[st] line treatment of EGFR tyrosine kinase inhibitors (TKIs). Our previous study indicated that B-cell chronic lymphocytic leukemia/lymphoma-like 11 (Bim) deletion polymorphism was about 10% and was significantly associated with a poor clinical response to EGFR-TKIs in EGFR mutation-positive NSCLC. This retrospective study compared efficacy and tolerability of the EGFR-TKI alone versus EGFR-TKI plus chemotherapy as the 1[st] line treatment in advanced NSCLC patients with both activated EGFR mutation and Bim polymorphism.
Method:
Main included criterias were patients older than 18 years, histologically confirmed stage IIIB or IV NSCLC, EGFR mutation-positive (exon 19 deletion or 21 L858R mutation) and Bim polymorphism. Patients received gefitinib 250mg orally a day or gefitinib together with up to 4 cycles of pemetrexed/gemcitabine and platinum until disease progression or unacceptable toxic effects. The primary endpoint was progression-free survival (PFS); the second endpoint included objective response rate (ORR), overall survival (OS) and toxicity.
Result:
From June 2014 to September 2016, 65 patients were enrolled into this trial. 36 of them received gefitinib, and 29 received gefitinib plus pemetrexed/gemcitabine and platinum. Median PFS was significantly longer in EGFR-TKI plus chemotherapy-treated patients than in EGFR-TKI (7.2 [95% CI 5.35-9.05] vs 4.6 [4.01-5.19] months; p=0.008). The ORR was significantly lower in EGFR-TKI than in EGFR-TKI plus chemotherapy-treated patients (38.9% vs. 65.5% p=0.046). EGFR-TKI plus chemotherapy was associated with more grade 3 or 4 hematological toxic effects than EGFR-TKI (8 neutropenia, 4 thrombocytopenia vs. no any event). Figure 1
Conclusion:
Compared with EGFR-TKI, EGFR-TKI plus chemotherapy conferred a significant higher ORR and longer PFS in advanced NSCLC patients with both activated EGFR mutation and Bim polymorphism. An open-label, multicenter, randomized, phase 2 study is ongoing to validate these results in our institute ( NCT03002844).
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P3.15 - SCLC/Neuroendocrine Tumors (ID 731)
- Event: WCLC 2017
- Type: Poster Session with Presenters Present
- Track: SCLC/Neuroendocrine Tumors
- Presentations: 1
- Moderators:
- Coordinates: 10/18/2017, 09:30 - 16:00, Exhibit Hall (Hall B + C)
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P3.15-015 - LCNEC Tumor Location, Divided into Central and Peripheral Type, Has Distinct Clinicopathologic Feature, Genomic Characteristics and Survival (ID 8397)
09:30 - 09:30 | Author(s): J. Zhang
- Abstract
Background:
Pulmonary large cell neuroendocrine carcinoma (LCNEC) represents a rare entity in lung cancer. Due to poor understanding of its biologic characters, optimal treatment strategy for patient with LCNEC remains undetermined. Recent data reveals that LCNEC can be divided into SCLC and NSCLC type based on distinct genomic signatures. It has been considered that SCLC is a central-type lung cancer and LCNEC usually locates in peripheral or midzone of lung. In the present study, we examined that whether there are significant differences between central tumors and peripheral tumors of LCNEC, in terms of clinicopathologic features, survival, and genomic profiles.
Method:
A total of 126 cases (113 cases with surgical samples) of pulmonary LCNEC were included in the present study. The tumors with invasion of the segmental and/or lobar bronchus were classified as central LCNEC and those without as peripheral LCNEC. EGFR mutations, ALK translocations, ROS1 translocations, Kras mutations, RET translocations and BRAF mutations were detected. Overall survival (OS) was determined from the date of operation until reported death or last follow-up visit. OS was analyzed by the Kaplan-Meier plots and the log-rank test was used to calculate the significance between groups. The prognostic factors for OS were analyzed using univariate and multivariate COX analyses.
Result:
Central tumors were associated with smoking history (p=0.047), higher T stage (p<0.001), N stage (p=0.001), TNM stage (p=0.014), and larger tumor size (p<0.001) compared with peripheral tumors. Although neuroendocrine marker expression of CD56, CGA, and SYN was not significantly different according tumor location, central tumors had higher expression of NSE (p=0.003). Moreover, peripheral tumors had higher incidence of EGFR mutations (18.8 vs. 0%, p=0.023) and similar incidence of Kras mutations (10.4 vs. 8.0%, p=1.000). Tumors harboring EGFR mutations were all pure LCNEC. No ALK translocations, ROS1 translocations, RET translocations and BRAF mutations were identified. The median OS was 3.71 years. TNM stage (p=0.039) and N stage (p=0.068) were associated with survival. Interestingly, central tumors had poorer survival compared with peripheral tumors, in terms of median OS (1.51 vs. 4.04 years), 1-year OS rate (54.0 vs. 83.9%), 2-year OS rate (37.0 vs. 75.9%), 3-year OS rate (31.7 vs. 59.9%). After multivariate analyses, tumor location was still an independent prognostic factor for OS (HR, 2.675, 95% CI, 1.384-5.171, p=0.003).
Conclusion:
Primary tumor location of LCNEC, divided into central and peripheral type, has distinct clinicopathologic feature, genomic characteristics and survival, which may help classify and manage patients with LCNEC.
