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Y. Cheng
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Poster Session (ID 8)
- Event: ACLC 2018
- Type: Poster Session
- Track:
- Presentations: 4
- Moderators:
- Coordinates: 11/07/2018, 00:00 - 00:00, Poster Hall
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P028 - A Novel Method for Detecting Surface PD-L1 on Circulating Tumor Cells in Peripheral Blood of Patients with SCLC (ID 135)
00:00 - 00:00 | Author(s): Y. Cheng
- Abstract
Background:
Previous studies have demonstrated that circulating tumor cell (CTC) might work as an alternative to biopsy tissues in the diagnoses of small cell lung cancer (SCLC). Programmed death ligand 1 (PD-L1) is one of the most commonly used biomarkers in immune targeted therapies. However, the expression of PD-L1 in CTC is still unknown. This study aimed to establish an approach to measure PD-L1 in peripheral CTCs from SCLC patients.
Method:
Control cells were screened by monoclonal culture and confirmed by immunohistochemistry (IHC) staining and flow cytometry. PD-L1 expression in CTCs and tumor tissue samples from SCLC patients was measured by CellSearch system while the usage of PD-L1 antibody was optimized.
Results:
The purity of PD-L1 positive H446 cells had been improved from 70% to 95% by clonal selection, and PD-L1 negative PC3 cells showed lower than 5% purity. In CellSearch system, positive control cells had 98% PD-L1 expression while negative control had less than 3% expression. In two SCLC patients with CTC positive expression, PD-L1 expression was found with 100% (1/1) and 40% (2/5) positive rate.
Conclusion:
CellSearch system was used to establish a novel approach for measuring surface PD-L1 expression on CTC, and showed supporting evidences in SCLC patients, thus providing novel insights for automatic assay of PD-L1 in peripheral samples. -
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P029 - Circulating MDSCs Derived from Small Cell Lung Cancer Patients Secrete TGF - Beta 1 and Play Roles in Angiogenesis (ID 151)
00:00 - 00:00 | Author(s): Y. Cheng
- Abstract
Background:
Studies showed that small cell lung cancer (SCLC) induced CD33+cells production in vitro and the CD33+ cells present typical features of myeloid-derived suppressor cells (MDSCs). We previously reported CD33+CD11b+HLA-DR-MDSCs level was elevated in peripheral blood of SCLC patients and has a prognostic value for SCLC patients. In this study we further explored the mechanisms of SCLC-derived MDSCs involved in angiogenesis.
Method:
Peripheral blood specimens from SCLC patients and healthy volunteer were collected and CD11b+/CD33+cells were separated using magnetic bead. Giemsa stain was used in morphological identification of the cells. CD11b+/CD33+cells were cultured in vitro for 72 hrs, then TGF-?1 in cell pellets and supernatant was detected using RT-PCR and western blot, or ELISA respectively. Endothelial tube formation was performed through culturing HUVEC cells on Matrigel using the supernatant as medium. The supernatant was added into HUVEC cells cultured on Matrigel to test angiogenesis effects.
Results:
RT-PCR data showed that CD33+ and CD11b+MDSCs from SCLC expressed higher level of TGF-?1 than those from healthy control, 0.349 vs 0.174 (P=0.000632) and 0.191 vs 0.105 (P=0.000867), respectively, and the expression of TGF-?1 in CD33+MDSCs was higher than that in CD11b+cells (P=0.0382). In addition, the western blot results showed that CD33+MDSCs from SCLC expressed higher TGF-?1 than that in control (0.391 vs 0.164?P=0.000491), however, the similar effects were not seen in CD11b+ cells. TGF-?1 expression in supernatant was higher in SCLC-derived CD33+ or CD11b+MDSCs than those in healthy control, 0.620 vs 0.324 (P=0.0155) and 0.482 vs 0.307 (P=0.0413), respectively), and the TGF-?1 level was higher in CD33+MDSCs than that in CD11b+MDSCs (P=0.00668). A significant decrease in tube formation and TGF-?1 level was found in SCLC patients after treatment compared to those before treatment.
Conclusion:
The TGF-?1 was highly expressed in both CD11b+ or CD33+MDSCs from SCLC in both transcription and translation levels, along with level change after treatment implying TGF-? signaling pathway may participate in MDSC-mediated angiogenesis in SCLC. Moreover, the expression level of TGF-?1 was discrepant in different phenotypes of MDSCs demonstrating the plastic phenotype of MDSCs in SCLC. -
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P107 - The Study of Relationship Between Tumor Burden (TMB) and Molecular Typing of Non-Small Cell Lung Cancer (NSCLC) (ID 127)
00:00 - 00:00 | Author(s): Y. Cheng
- Abstract
Background:
Tumor mutation burden (TMB) is one of the strongest biomarker to stratify patients suitable for immunotherapy. However, the relationship between TMB and other typical genetic profile in lung adenocarcinoma is not clear. This study aimed to explore the genetic characteristics of non-small cell lung cancer (NSCLC) relationship between TMB and typical genetic profile in NSCLC patients.
Method:
Tumor tissue from 11 NSCLC patients in Jilin Cancer Hospital from July 2018 to August 2018 were tested by next generation sequencing (>500 target gene panel). 10 mutations/1 M basepairs as cut-off value, patients were divided into high tumor butden (TMB-High) and low tumor burden (TMB-Low). TMB relationship with lung cancer core genes (EGFR, ALK, ROS1, KRAS, BRAF, MET, RET and ERBB2), tumor suppressor genes, proto-oncogenes, and MSI was statistically analyzed.
Results:
Among the 11 NSCLC patients, 45% (5/11) of patients were TMB-low and 55% (6/11) of patients were TMB- high. 100% (11/11) of patients were microsatellite Stable (MSS) and there were no MSI patients. In TMB-low patients, there were 14 mutations in 9 tumor suppressor genes and 1 mutation in 1 proto-oncogene; 40% (2/5) of these patients had TP53 mutations; 60% (3/5) of these patients had 5 mutations in 4 lung cancer core genes (EGFR, MET, KRAS and ROS1). In TMB-high patients, there were 29 mutations in 17 tumor suppressor genes, 8 mutations in 4 proto-oncogenes; 100% (6/6) of these patients had TP53 mutations.; 83% (5/6) of these patients had 9 mutations in 4 lung cancer core genes.
Conclusion:
Compared with TMB-high, TMB-low patients have less number of tumor suppressor genes, proto-oncogene mutations, TP53 mutations and lung cancer core gene mutations In addition, TMB may not be associated with MSI. This study could further understand the genetic characteristics of NSCLC and provide new theoretical basis for immunotherapy for NSCLC. -
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P109 - Combined Chemotherapy Versus Topotecan Monotherapy as Second-Line Treatment for Patients with Sensitive Relapsed SCLC (ID 160)
00:00 - 00:00 | Author(s): Y. Cheng
- Abstract
Background:
Cisplatin, etoposide and irinotecan are primary drugs in the treatment of small cell lung cancer. We did this retrospective study to investigate whether combined chemotherapy with cisplatin, etoposide, and irinotecan was better than topotecan alone as second-line chemotherapy in patients with sensitive relapsed SCLC.
Method:
Between 1stSep, 2014 and 30thSep, 2017?We collected the patients information in Jilin Province Cancer Hospital. All patients with SCLC responded in first-line treatment and showed radiological evidence of disease relapse or progression at least 90 days after completion of the first-line treatment. 36 patients received combination chemotherapy with cisplatin plus etoposide plus irinotecan and 42 patients received topotecan alone. Combination chemotherapy consisted of five 2-week courses of intravenous cisplatin 25 mg/m 2 on days 1 and 8, intravenous etoposide 60 mg/m 2 on days 1
