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J. Chen
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P2.01 - Poster Session with Presenters Present (ID 461)
- Event: WCLC 2016
- Type: Poster Presenters Present
- Track: Biology/Pathology
- Presentations: 1
- Moderators:
- Coordinates: 12/06/2016, 14:30 - 15:45, Hall B (Poster Area)
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P2.01-025 - MiR-146b Functions as a Suppressor miRNA and Prognosis Predictor in Non-Small Cell Lung Cancer (ID 6396)
14:30 - 14:30 | Author(s): J. Chen
- Abstract
Background:
Non-small cell lung cancer (NSCLC) is the leading cause of cancer-related death worldwide; however, science has not yet been able to substantially improve the prognosis of lung cancer patients. Accumulating evidence suggests that microRNAs (miRNAs) are key players in the regulation of tumor development and metastasis. Expression of six miRNAs previously shown to play roles in tumor development (miR-146b, miR-128b, miR-21, miR-221, miR-34a, and Let-7a) in other tumor types
Methods:
Expression of six miRNAs previously shown to play roles in tumor development (miR-146b, miR-128b, miR-21, miR-221, miR-34a, and Let-7a) in other tumor types was examined using real-time RT-PCR in 78 specimens of NSCLC.
Results:
The results revealed that patients with low expression of miR-146b had significant shorter median and mean survival time than those with high miR-146b expression (33.00 and 30.44 months versus 42.0 and 36.90 months, respectively; log-rank test P=0.048), thus low miR-146b expression level was associated with poor prognosis in NSCLC patients. Univariate Cox hazard regression analysis demonstrated that miR-146b expression levels tended to be a significant prognostic indicator of NSCLC (adjusted hazard ratio=0.482, 95% CI: 1.409- 29.593, P=0.016). Multivariate Cox proportional hazard regression analysis showed that miR-146b expression levels were an independent prognostic factor for NSCLC patients (hazard ratio=0.259, 95% CI: 0.083-0.809, P=0.020). Furthermore, the effects of miR-146b on NSCLC cell growth and invasion in vitro were investigated. Our findings demonstrate that ectopic expression of miR-146b suppresses proliferation and colony formation ability of lung cancer H1299 cells in vitro. In addition, miR-146b induced G0/G1 phase arrest in H1299 cells and over-expression of miR-146b inhibited lung cancer cell migration and invasion in vitro.
Conclusion:
Our findings demonstrate that miR-146b functions as a suppressor miRNA and prognosis predictor in NSCLC.
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P2.02 - Poster Session with Presenters Present (ID 462)
- Event: WCLC 2016
- Type: Poster Presenters Present
- Track: Locally Advanced NSCLC
- Presentations: 1
- Moderators:
- Coordinates: 12/06/2016, 14:30 - 15:45, Hall B (Poster Area)
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P2.02-042 - Surgical Management of Squamous Cell Carcinoma of the Lung: Survival and Functional Outcomes (ID 6398)
14:30 - 14:30 | Author(s): J. Chen
- Abstract
Background:
Squamous cell carcinoma (SCC) of the lung is a unique clinical and histologic category of non-small cell lung cancer (NSCLC) and accounts for about 30% of all lung cancer. Surgical intervention is the principal treatment for SCC. The purpose of this study was to evaluate the survival rates for surgical treatment of squamous NSCLC and the prognostic patient factors.
Methods:
We retrospectively evaluated the files of 170 patients with squamous NSCLC who were treated at the department of lung cancer surgery, Tianjin Medical University General Hospital, between January 2008 and December 2011. Univariate (Cox regression analysis) and multivariate (likelihood ratio) analyses were carried out for overall survival (OS) and the median survival duration. A P-value of < 0.05 was defined as significant.
Results:
The median OS was 29 months, the 1-year OS was 78.2%, and the 5-year OS was 15.3%. On univariate analysis, the Eastern Cooperative Oncology Group Performance Status (ECOG-PS) score; tumor (T) stage; node (N) stage; type of surgery; type of lymphadenectomy; and the presence of residual carcinoma at the incised margin, intravascular cancer, and pleural effusion were significantly related to patient survival (P < 0.05). On multivariate analysis, the smoking index (P = 0.002), ECOG-PS (P = 0.000), T stage (P = 0.005), and N stage (P = 0.000) were independent prognostic factors.
Conclusion:
The OS of patients with squamous lung carcinoma was low. The survival rates gradually decreased as patients’ ECOG-PS declined. The patients without lymph-node involvement (N0) had longer survival than those with N1 and N2 lymph-node involvement. Both OS and disease-free survival are worse in SCC of the lung than for NSCLC in general. At present, we still depend on surgical intervention for squamous NSCLC; there is an unmet need for novel effective therapies.
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P2.03a - Poster Session with Presenters Present (ID 464)
- Event: WCLC 2016
- Type: Poster Presenters Present
- Track: Advanced NSCLC
- Presentations: 1
- Moderators:
- Coordinates: 12/06/2016, 14:30 - 15:45, Hall B (Poster Area)
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P2.03a-001 - A Randomized Phase III Clinical Trial of Anlotinib Hydrochloride in Patients with Advanced Non-Small Cell Lung Cancer (NSCLC) (ID 4722)
14:30 - 14:30 | Author(s): J. Chen
- Abstract
Background:
Anlotinib hydrochloride, a novel multi-targeted tyrosine kinase inhibitor (TKI) was found to exhibit excellent inhibitory efficiency on a variety of receptor tyrosine kinases (RTK) involved in tumor progression, especially the vascular endothelial growth factor receptor (VEGFR), fibroblast growth factor receptor (FGFR), platelet-derived growth factor receptor (PDGFR) and stem cell-factor receptor (c-Kit). This ongoing trial aimed at evaluating the efficacy and safety of anlotinib hydrochloride comparing with placebo in advanced NSCLC patients who had received at least two previous chemotherapy and EGFR/ALK targeted therapy regimens.
Methods:
This Phase III, randomized, double-blind, placebo-controlled study (NCT 02388919) is ongoing in 31 centers in China under the supervision of Independent Data Monitoring Committee (IDMC). Pathological stage IIIB/IV adult advanced NSCLC patients (Pts) who had failed with at least two previous chemotherapy and EGFR/ALK targeted therapy regimens were eligible. The status of EGFR and ALK genes should be clear in all enrolled pts. Pts with sensitive EGFR or ALK mutations must had received and appeared intolerance to pervious targeted therapies. Pts were randomized (2:1) to receive Anlotinib hydrochloride or placebo once daily (12 mg) from day 1 to 14 of a 21-day cycle until progression. Dose reduction to 8 or 10 mg/day could be applied when grade 3 or 4 treatment-related toxicities were observed. The minimal sample size was estimated to 450 patients. The primary endpoint is overall survival (OS) and second endpoints are progression-free survival (PFS), overall response rate (ORR), disease control rate (DCR) and quality of life (QoL). Quality of life was assessed via EORTC QLQ-C30, safety is determined using standard NCI-CTCAE v4.02, and responses are evaluated according to RECIST v1.1.
Results:
This study started in February 2015, up to early July 2016, a total of 420 pts have been enrolled (93.3 % of 450 pts). Among enrolled pts, about 80 % were diagnosed as adenocarcinoma, EGFR mutation or ALK rearrangement was found in 1/3 of the pts. The overall analyses will start after 300 OS events.
Conclusion:
Anti-angiogenesis is the main mechanism of Anlotinib hydrochloride for preventing the tumor progression. Results of randomized, placebo-controlled Phase II trial (NCT01924195) has been reported in WCLC 2015, however, advantages in PFS (4.8 vs. 1.2 months) and OS (9.3 vs. 6.3 months) were observed in Anlotinib arm from the renewed data. Based on these exciting data, we are looking forward for the results of the Phase III trial
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P3.02c - Poster Session with Presenters Present (ID 472)
- Event: WCLC 2016
- Type: Poster Presenters Present
- Track: Advanced NSCLC
- Presentations: 1
- Moderators:
- Coordinates: 12/07/2016, 14:30 - 15:45, Hall B (Poster Area)
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P3.02c-021 - PD 0332991, a Selective Cyclin D Kinase 4/6 Inhibitor, Sensitizes Lung Cancer Cells to Killing by EGFR TKIs (ID 6394)
14:30 - 14:30 | Author(s): J. Chen
- Abstract
Background:
The acquired resistance of EGFR-TKIs in non-small cell lung cancer (NSCLC) is a big challenge in the targeted therapy. It is necessary to investigate whether CDK4/6 inhibitor PD 0332991 could contribute to reverse the drug resistance of EGFR TKI resistant human lung cancer cell in vitro and in vivo and to explore the underlying mechanisms.
Methods:
Cell viability, proliferation, cell cycle and apoptosis were measured by MTT assay, EDU assay, cell cycle and apoptosis assay, respectively. The underlying mechanisms were assessed by real-time PCR, western-blot and microarray analysis. Tumor xenograft animal study was performed to verify the effect of PD 0332991 in vivo. Lung adenocarcinoma patients with acquired resistance to EGFR-TKIs were given a tentative treatment of PD 0332991.
Results:
Our study showed that PD 0332991 could potentiate significantly the gefitinib induced growth inhibition of both EGFR-TKI sensitive PC-9 and EGFR-TKI resistant PC-9/AB2 cells, through down-regulating the proliferation, inducing cell apoptosis and G0/G1 cell cycle arrest. In the mice experiments in vivo, we found the mice treated by PD 0332991 and gefitinib showed a fastest tumor regression, and a most delayed relapse pattern. The tumor from the mice treated by the combination showed a significantly down-regulated proliferation, an up-regulated apoptosis and a less angiogenesis confirmed by Ki67, TUNEL and CD34 staining, respectively. In addition, we reported an adenocarcinoma patient with gefitinib resistance had a remarkable clinical remission after administrated with PD 0332991.
Conclusion:
Our research showed, for the first time, that PD 0332991 could contribute EGFR-TKI resistant NSCLC cells to overcome the acquired resistance in vivo and in vitro. This might provide a novel treatment strategy for the patients with EGFR-TKI resistance.
