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Mong-Wei Lin
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P1.01 - Advanced NSCLC (ID 158)
- Event: WCLC 2019
- Type: Poster Viewing in the Exhibit Hall
- Track: Advanced NSCLC
- Presentations: 1
- Moderators:
- Coordinates: 9/08/2019, 09:45 - 18:00, Exhibit Hall
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P1.01-132 - Clinicopathological and Genomic Comparisons Between Different Histologic Components in Combined Small Cell and Non-Small Cell Lung Cancer (ID 1559)
09:45 - 18:00 | Presenting Author(s): Mong-Wei Lin
- Abstract
Background
Histologic transformation from adenocarcinoma to small cell lung cancer (SCLC) is one of the mechanisms of acquired resistance after epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor (TKI) treatment. Furthermore, de novo combined SCLC/non-small cell lung cancer (NSCLC) have occasionally been reported; however, their mutational statuses and clinicopathological features have not yet been elucidated. In this study, we aimed to profile the genetic backgrounds of these 2 different histologic components by investigating patients with de novo combined SCLC/NSCLC as well as those with lung adenocarcinoma who experienced SCLC transformation after TKI treatment.
Method
Four patients with de novo combined SCLC/NSCLC were investigated, as were 4 other patients with lung adenocarcinoma who experienced SCLC transformation after TKI treatment. The different histologic components of the tumors in each patient were tested for thyroid transcription factor-1, p40, synaptophysin, chromogranin A, p53, retinoblastoma protein (Rb), and achaete-scute homolog 1 (ASCL1) via immunohistochemistry, and were macroscopically dissected for mutational analysis using next-generation sequencing with the Oncomine Focus Assay and Comprehensive Assay panel.
Result
Our study comprised two groups of patients: the first group were patients with de novo combined SCLC/NSCLC and the second group were lung adenocarcinoma with SCLC transformation after TKI treatment. De novo combined SCLC/NSCLC patients have poor prognoses and poor responses to EGFR TKI. In both groups, identical EGFR/TP53/RB1 mutations and p53/Rb expression patterns were observed in both SCLC and NSCLC components. A high frequency of activating mutations involving PI3K/AKT1 signaling pathway was observed in de novo combined SCLC/NSCLC and also in the SCLC component of the second group after TKI treatment. Nuclear ASCL1 expression was present in SCLC but absent or barely present in adenocarcinoma in 7 cases.
Conclusion
Our data imply that inactivation of TP53/RB1 function is a possible early event in the histogenesis of synchronous and metachronous SCLC/NSCLC. Moreover, the non-adenocarcinoma (SCLC) component might arise from the adenocarcinoma (NSCLC) component through a mechanism that involves the activation of the ASCL1 and PI3K/AKT1 signaling pathways.
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P2.09 - Pathology (ID 174)
- Event: WCLC 2019
- Type: Poster Viewing in the Exhibit Hall
- Track: Pathology
- Presentations: 1
- Moderators:
- Coordinates: 9/09/2019, 10:15 - 18:15, Exhibit Hall
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P2.09-29 - Correlation of Tumor Spread Through Air Spaces and Clinicopathological Characteristics in Surgically Resected Lung Adenocarcinomas (ID 1547)
10:15 - 18:15 | Presenting Author(s): Mong-Wei Lin
- Abstract
Background
Tumor spread through air spaces (STAS) has recently been reported as a novel invasive pattern in lung adenocarcinoma, but the correlation between other clinicopathological and genetic profiles has not been well studied. The aim of this study was to investigate these correlations in patients with surgically resected lung adenocarcinoma.
Method
Five hundred consecutive patients with lung adenocarcinoma who underwent curative lung tumor resection and with available STAS profile were reviewed retrospectively from January to December 2016. The correlations of STAS presence and clinicopathological and genetic characteristics were analyzed.
Result
One hundred thirty-four patients (26.8%) had positive STAS. The pathological stage of these patients was adenocarcinoma in situ, IA, IB, II, and III in 25 (5%), 343 (68.6%), 63 (12.6%), 29 (5.8%), and 40 (8%), respectively. Multivariate analysis showed that the presence of STAS was significantly correlated to higher T (p=0.001) and N (p=0.032) stages, moderate/poor differentiation (p=0.001), and the presence of lymphovascular invasion (p=0.001). Although positive epidermal growth factor receptor mutation and non-lepidic histologic subtypes were correlated with the presence of STAS in the univariate analysis, they were not significantly correlated with the presence of STAS in the multivariate analysis (p=0.676 and 0.286, respectively).
Conclusion
STAS was significantly correlated with several invasive clinicopathological characteristics, including higher T and N stages, moderate/poor differentiation, and the presence of lymphovascular invasion in surgically resected lung adenocarcinoma. The correlation may lead to poor clinical outcomes in patients with positive STAS. Based on our results and current evidence, the presence of STAS may be considered as a staging profile in future staging system.
