Virtual Library
Start Your Search
X. Han
Author of
-
+
ORAL 17 - EGFR Mutant Lung Cancer (ID 116)
- Event: WCLC 2015
- Type: Oral Session
- Track: Treatment of Advanced Diseases - NSCLC
- Presentations: 1
- Moderators:P. Meldgaard, E. Felip
- Coordinates: 9/08/2015, 10:45 - 12:15, Four Seasons Ballroom F3+F4
-
+
ORAL17.01 - First-Line Icotinib Versus Cisplatine/Pemetrexed Plus Pemetrexed Maintenance in Advanced NSCLC Patients with EGFR Mutation (ID 742)
10:45 - 12:15 | Author(s): X. Han
- Abstract
- Presentation
Background:
Clinical studies with anti-EGFR agents demonstrate that EGFR TKIs play critical roles in the treatment of non-small cell lung cancer, especially in patients with positive EGFR mutation. Icotinib is an oral, selective EGFR TKIs. Phase 3 study showed that icotinib is non-inferior to gefitinib in treating unselected or EGFR-mutated advanced NSCLC patients as second-line therapy but better safety profile, which provide a rationale to examine icotinib in first-line setting. The objective of this study is to evaluate progression-free survival (PFS), overall survival (OS) and safety of icotinib in chemotherapy naïve NSCLC patients with EGFR mutation.
Methods:
In this phase 3, open-label, randomized study (CONVINCE, NCT01719536), 285 patients (pathologically confirmed NSCLC, positive 19/21 EGFR mutation, treatment naive) will be 1:1 randomized to receive oral icotinib (125 mg, three times daily) or cisplatine (intravenous [IV], 75 mg/m2, day 1) plus pemetrexed (IV, 500 mg/m2, day 1), patients achieving disease control after 4-cycle chemotherapy continue to receive single pemetrexed (IV, 500 mg/m2, day 1) as maintenance therapy until progression. Randomization will be stratified by performance status (0-1/2), smoking status (smoker/non-smoker), disease stage (IIIB/IV), and mutation type (19/21). A total of 228 events would provide 90% power to detect an HR for PFS of 1 at 2-sided significance level of 0.05. Response will be reviewed by both investigator and independent data monitoring committee using Response Evaluation Criteria In Solid Tumors (RECIST version 1.1). Progression Between January, 2013 and August, 2014, 285 patients were randomized and treated at 18 centers from 13 cities in China. The data cut-off was planned at October, 2015 when 228 PFS events were observed in full analysis set (80% maturity). Final results were expected on December, 2015.
Results:
Not applicable
Conclusion:
Not applicable.
Only Members that have purchased this event or have registered via an access code will be able to view this content. To view this presentation, please login, select "Add to Cart" and proceed to checkout. If you would like to become a member of IASLC, please click here.
-
+
P1.04 - Poster Session/ Biology, Pathology, and Molecular Testing (ID 233)
- Event: WCLC 2015
- Type: Poster
- Track: Biology, Pathology, and Molecular Testing
- Presentations: 1
- Moderators:
- Coordinates: 9/07/2015, 09:30 - 17:00, Exhibit Hall (Hall B+C)
-
+
P1.04-109 - Antitumor Efficacy of Histone Deacetylase Inhibitor or in Combination with EGFR-TKI in Non-Small Cell Lung Cancer Cell Lines (ID 3090)
09:30 - 17:00 | Author(s): X. Han
- Abstract
Background:
To investigate the antitumor efficacy of histone deacetylase inhibitor (HDACi) or in combination with epidermal growth factor receptor tyrosine kinase inhibitor (EGFR-TKI) in non-small cell lung cancer (NSCLC) cell lines.
Methods:
Ten NSCLC cell lines with varying mutation status were treated with chidamide (HDACi) and icotinib (TKI) alone or in combination. MTS assay was performed to determine IC~50~ of each drug or in combination. Cell cycle was analyzed by flow cytometry. Markers of epithelial-to-mesenchymal transition (E-cadherin), apoptosis (caspase-3, PARP) were determined by western blot.
Results:
The results demonstrated that A549 (TKI-resistant, KRAS-mutated), HCC827 (TKI-sensitive, EGFR-mutated), HCC827IR (TKI-resistant, EGFR-mutated) was sensitive to chidamide, the IC~50~ of these three cell lines was less than 0.5nM and the IC~50~ of the other seven cell lines was more than 5μM. Chidamide increased the sensitivity of icotinib synergistically in EGFR and KRAS wild type cells (H292, Calu-3), KRAS mutant cells (A549, H460), and TKI resistant EGFR mutant cells (H1650, H1650GR, HCC827IR, H1975), but the synergistic effect was most meaningful in H1975 (EGFR L858R and T790M mutation). We also found that H460 and Calu-3 had no E-cadherin expression, H1975 had low level of E-cadherin expression, and the other seven cell lines had relatively high levels of E-cadherin expression. Moreover, with the increasing dosage of chidamide, E-cadherin expression was significantly increased in H1975 cell line, but was not changed in chidamide sensitive cell lines. In addition, chidamide alone or in combination with icotinib could induce H1975 cell cycle arrest at G1/S phase, and reduce the expression of casepase-3 and PARP.
Conclusion:
These results suggest that chidamide as a single agent exhibits antiproliferative effectives in NSCLC cells with EGFR and KRAS mutations. The combination of chidamide and icotinib may be a beneficial treatment strategy for NSCLC with EGFR-T790M mutation. But the role of chidamide in the antiproliferative or synergistic mechanisms should be further explored
-
+
P2.07 - Poster Session/ Small Cell Lung Cancer (ID 222)
- Event: WCLC 2015
- Type: Poster
- Track: Small Cell Lung Cancer
- Presentations: 1
- Moderators:
- Coordinates: 9/08/2015, 09:30 - 17:00, Exhibit Hall (Hall B+C)
-
+
P2.07-009 - Cisplatin Combined with Irinotecan or Etoposide for Untreated Extensive-Stage Small Cell Lung Cancer (ID 2258)
09:30 - 17:00 | Author(s): X. Han
- Abstract
Background:
This study aims to evaluate the efficacy and safety of irinotecan/cisplatin (IP) and etoposide/cisplatin (EP) in extensive-stage small cell lung cancer (ES-SCLC) and the distribution of UGT1A1. Simultaneously, the relationship between UGT1A1 genotypes and patient outcomes were assessed.
Methods:
Patients with untreated ES-SCLC were randomly assigned to receive either IP or EP, and blood specimens were collected to test the genotypes of UGT1A1*28 and UGT1A1*6. The association of efficacy and toxicity of IP regimen with UGT1A1 genotype was analyzed.
Results:
Of the 62 patients enrolled from three institutions, 30 patients were in the IP and 32 patients were in the EP arms, respectively. Disease control rates (DCR) with IP and EP were 83.3% and 71.9%, respectively (P=0.043). Median progression-free survival (PFS) for IP and EP were both 6 months. Median overall survival (OS) for IP and EP was 18.1 and 15.8 months respectively, without significant difference. Grade 3-4 thrombocytopenia was more common with EP (18.8% versus 6.7%, P=0.035), while the incidence of diarrhea was higher with IP (70% versus 15.6%, P=0.008). The incidence of grade1-4 late-onset diarrhea of wild-type, heterozygous and homozygous UGT1A1*28 were 65.0%，85.7% and 66.7% respectively (P=0.037). UGT1A1*28 polymorphisms, Eastern Cooperative Oncology Group (ECOG) performance status, chemotherapy cycles were the essential factors affecting grade1-4 late-onset diarrhea in a logistic regression analysis.Figure 1Figure 2
Conclusion:
The efficacy of IP regimen was similar to EP regimen for untreated ES-SCLC. UGT1A1 polymorphisms was associated with late-onset diarrhea, however it has no influence on efficacy.
