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Qian Chu
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JCSE01 - Joint IASLC-CSCO-CAALC Session (ID 63)
- Event: WCLC 2019
- Type: Joint IASLC-CSCO-CAALC Session
- Track:
- Presentations: 1
- Moderators:Chunxue Bai, Tony Mok, Yi-Long Wu, Qing Zhou, Nan Wu
- Coordinates: 9/07/2019, 07:00 - 11:15, Toronto (1985)
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JCSE01.20 - Pilot Study on the Tumor Immune Microenvironment Between Non-Small Cell Lung Cancer (NSCLC) and Small Cell Lung Cancer (SCLC) (ID 3434)
07:00 - 11:15 | Presenting Author(s): Qian Chu
- Abstract
Abstract
Background
Tumor immune microenvironment plays an important role in immunotherapy and prognosis. However, the differences and the clinical significance between non-small cell lung cancer (NSCLC) and small cell lung cancer (SCLC) is still largely unknown.
Methods
Resected lung cancer FFPE specimens and matched peripheral blood mononuclear cells (PBMC) from six patients with NSCLC (three adenocarcinoma, three squamous cell carcinoma) and three patients with SCLC were collected. All of the nine patients underwent stage III disease. Tumor mutation burden (TMB) was evaluated by hybridization capture based next-generation sequencing with 1021 cancer associated genes. Tumor infiltrating lymphocytes (TILs) were assessed by immunohistochemistry using multiple immune markers and meanwhile the intratumoral T-cell repertoires were analyzed via high-throughput sequencing of TCR β-chain.
Results
Typical EGFR mutations in adenocarcinoma (2 in 3), NSCLC and RB1 mutations in SCLC (3 in 3) were observed. SCLC patients showed significantly higher TMB than NSCLC. Regarding to the tumor immune microenviroment, SCLC tumors exhibited lower infiltration of CD3+ and CD8+ TILs (P< 0.05). Furthermore, we found that SCLC patients tended to have lower TCR Shannon index (P= 0.167) and higher Clonality index (P= 0.095). Interestingly, patients with higher Shannon index exhibited better Overall Survival (OS) while Clonality was potentially associated with decreased OS. However, further study with more patients is needed to confirm the results.
Conclusion
Tumor immune microenvironment varies between NSCLC and SCLC patients. Specifically, less prevalent and lower diversity of TILs were observed in SCLCs. This might potentially influence survival outcomes.
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MA01 - Oligometastatic Disease (ID 114)
- Event: WCLC 2019
- Type: Mini Oral Session
- Track: Oligometastatic NSCLC
- Presentations: 1
- Now Available
- Moderators:Anne Marie Clasina Dingemans, Matthias Guckenberger
- Coordinates: 9/08/2019, 10:30 - 12:00, Copenhagen (1980)
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MA01.09 - Concomitant SBRT and EGFR-TKI Versus EGFR-TKI Alone for Oligometastatic NSCLC: A Multicenter, Randomized Phase II Study (Now Available) (ID 2214)
10:30 - 12:00 | Author(s): Qian Chu
- Abstract
- Presentation
Background
NSCLC patients harboring EGFR mutation generally develop resistance to EGFR TKI less than one year. Prior studies indicated that local consolidative therapy is associated with improved outcomes in patient with limited metastatic NSCLC. Radiotherapy is one of the ideal control methods for locally progressed patients, however, the optimal intervention time in order to slow the occurrence of EGFR-TKI resistance for advanced NSCLC patients with EGFR-sensitive mutations is still unclear. Our preliminary clinical and animal studies suggest that early combined radiotherapy prior to EGFR-TKI resistance can significantly improve the prognosis of patients. Our hypothesis is that the optimal intervention time of radiotherapy for EGFR mutation patients is 3 months after the beginning of EGFR-TKI.
Method
This is a prospective, multicenter, randomized controlled study to evaluate stereotactic body radiation therapy (SBRT) as a potential treatment for limited stage IV NSCLC (primary plus up to 3 metastatic sites) with sensitive EGFR mutation. The patients did achieve partial response or stable disease after three months treatment of the first-generation EGFR-TKI would be randomized to TKI combined SBRT (TS) or TKI alone. The primary endpoint was PFS (the time from the beginning of EGFR-TKI treatment to disease progression or death). The secondary endpoint was overall survival (OS) and safety. TKI wasn’t interrupted during the irradiation.
Result
A total of 61 patients were enrolled from Feb, 2017 to Jan, 2019. Median follow up was 22.3 months. Patients who TS (n: 30) had a significantly longer median PFS compared to those with TKI alone (n: 31) (PFS: 17.4 vs. 8.9 months P =0.042). T790M mutation was observed in 57.9% acquired resistance patients for TS group, and 39.3% for TKI alone group. Median PFS of T790M mutated patients was 17.4 months compared to 10.3 months of TKI alone group (P = 0.007). Multivariable analysis revealed that radiation fields were positively associated with PFS, 21.8 months for just primary tumor; 10.6 months for metastatic lesions and 18.3 months for primary and metastatic lesions (P= 0.006). OS data was not yet mature. None experienced >= grade 3 SBRT related toxicities.
Conclusion
A trend of improved long term PFS was noted in patients receiving SBRT for primary tumor combined EGFR TKI at the third month after the beginning of TKI. Moreover, this data suggested that benefit from radiation might be associated with delay the occurrence of T790M mutation. Further studies are required to investigate the molecular mechanisms underlying this association.
Clinical Trial information: NCT03595644
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MA21 - Non EGFR/MET Targeted Therapies (ID 153)
- Event: WCLC 2019
- Type: Mini Oral Session
- Track: Targeted Therapy
- Presentations: 1
- Now Available
- Moderators:Benjamin Besse, Michael Thomas
- Coordinates: 9/10/2019, 14:30 - 16:00, Vienna (2016)
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MA21.02 - Genomic Origin and EGFR-TKI Efficacy of Pulmonary Adenosquamous Carcinoma (Now Available) (ID 578)
14:30 - 16:00 | Author(s): Qian Chu
- Abstract
- Presentation
Background
Lung adenosquamous carcinoma (ASC) is a heterogeneous disease that comprises of both adenocarcinoma (AC) and squamous cell carcinoma (SCC) components. Their genomic profile, evolutionary origin, and clinical management remain controversial. Objective of this study is to define the genomic origin of this heterogeneous tumor by independent genomic analyses of the AC and SCC components.
Method
Surgical ASCs were collected. AC component and SCC component were obtained separately by microdissection, and Lymph node (LN) metastases were gathered. Targeted sequence was performed for the two components using a 1021-gene panel, independently. Evolutionary relationship of the two components was analyzed. The independent cohorts of adenocarcinoma (n=170) and squamous cell carcinomas (n=62) were used for comparison. EGFR and concomitant mutations with response to EGFR-TKI were analyzed. Retrospective 517 ASCs underwent EGFR detections were collected from 11 centers. Objective response rate (ORR), disease control rate (DCR) and progression free survival (PFS) were analyzed in EGFR-positive patients received EGFR-TKIs.
Result
28 ASCs were collected. NGS was performed on AC component and SCC component samples, respectively. The most frequent alterations in 28 ASCs were EGFR mutation (79%), TP53 mutation (68%), MAP3K1 mutation (14%), EGFR amplification (32%), and MDM2 amplification (18%). 27 patients had trunk variations in the both components suggesting the monoclonal origin of ASCs. The prevalence of trunk mutations was correlated to those of AC, indicating that ASC might originate from AC. Only one patient did not carry any trunk variations between AC and SCC components, which were clearly and geographically distinguishable under the microscope. 22 had AC component or/and SCC component specific variations suggesting the common event of branch evolution. The 23 LNs of 13 patients mainly contained AC and ASC components (AC, SCC, and ASC: 11, 1, and 11, respectively), and each of the LNs carried the trunk mutations of the primary ASC. Like pure AC, the alterations of L858R and Exon 19 Dels of EGFR were common in the 28 ASCs. Unfortunately, these patients have not been treated with TKIs. Further, of 517 retrospective ASCs from 11 centers, 51.8% were EGFR-positive. For the 129 EGFR-positive ASCs who had received TKIs, the ORR and DCR were 56.6% and 89.1%, respectively. The median PFS was 10.1 months (95% CI: 9.0-11.2).
Conclusion
The AC and SCC components share a monoclonal origin, and a majority have branching evolution. ASC may represent a subtype of adenocarcinoma with EGFR mutation being the most common genomic anomaly and sharing similar efficacy to EGFR-TKIs.
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P1.17 - Treatment of Early Stage/Localized Disease (ID 188)
- Event: WCLC 2019
- Type: Poster Viewing in the Exhibit Hall
- Track: Treatment of Early Stage/Localized Disease
- Presentations: 1
- Moderators:
- Coordinates: 9/08/2019, 09:45 - 18:00, Exhibit Hall
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P1.17-05 - What Is the Optimal Number of Examined Lymph Node in Stage IA Non-Small Cell Lung Cancer? (ID 681)
09:45 - 18:00 | Author(s): Qian Chu
- Abstract
Background
1.To find out the optimal number of examined lymph nodes (ELNs) in stage IA non-small cell lung cancer (NSCLC). 2.To figure out whether there was a turning point beyond which ELNs might have adverse effects on survival.
Method
Using the Surveillance, Epidemiology, and End Results registry (SEER) database, we selected all NSCLC patients diagnosed with stage IA (T1N0M0) from 1995 to 2015. Cases from 1995 to 2005 were as analytical data set (group 1) and those from 2006-2015 as validation data set (group 2).The overall survival (OS) of patients with different ELNs was compared statistically by SPSS. The optimal cut point of ELNs was calculated by X-Tile and verified by univariable and multivariable analyses. Propensity score matching (PSM) was done by R software 3.5.2.
Result
In total, we extracted 57481 stage IA NSCLC patients (group 1, n = 20814; group 2, n = 36667). The PSM of Group 1 and Group 2 were balanced based on sex, age and race. In both groups, we divided patients into 3 subgroups, recorded as ELN = 0, 1≤ ELNs < n and ELNs≥ n. ELN = 0 had the highest risk of death in each subgroup (all p < 0.001). From n = 6 to n = 16, OS was significantly different between 1 ≤ ELNs < n, and ELNs ≥ n. But from n = 17 to n = 30, OS was the same between 1 ≤ ELNs < n and ELNs ≥ n. When dividing patients into ELNs = 0, 1-2, 3-5, 6-9, 10-29, ≥ 30,serial improvement in OS was seen with increasing ELNs, up to ELNs = 6-9, and beyond which there was little further incremental survival benefit. The survival curve of ELNs ≥ 30 even had an obvious trend to drop down.
Conclusion
For stage IA NSCLC, we suggested resecting 6-9 LNs was enough, and no more than 16 LNs. More than 16 ELNs did not improve survival and more than 30 ELNs might have a detrimental effect on survival.
