CircMED13L_012 promotes lung adenocarcinoma progression by upregulation of MAPK8 mediated by miR-433-3p.

BACKGROUND: Metastasis and disease refractoriness remain as major challenges for non-small cell lung cancer (NSCLC) treatment and understanding the underlying molecular mechanisms is of scientific and clinical value. Therefore, in this study, we aimed to explore the effects of circMED13L_012 on the proliferation, migration, invasion and drug-resistance of NSCLC tumor cells. METHODS: In this study, we utilized clinical samples and NSCLC cell lines to explore the association between circMED13L_012 expressions and tumor cell metastasis and chemo resistance. CCK8 and transwell assay were conducted to explore the impact of circMED13_012 on NSCLC tumor proliferation and migrative capabilities. Dual-luciferase reporter gene assay was conducted to validate the circMED13L_012 interaction network. RESULTS: Our results demonstrated that circMED13L_012 exhibited significantly elevated average level in our clinical samples of NSCLC, compared with normal tissues. circMED13L_012 level was positively correlated with disease stage and metastatic status. Increased circMED13L_012 expression was associated with the enhanced migration, proliferation and chemo resistance of NSCLC cell lines. Further experiments indicated that circMED13L_012 promoted malignant behavior of NSCLC tumor cells by targeting MAPK8 through modulation miR-433-3p expression. CONCLUSIONS: Our study for the first time demonstrated that circMED13L_012-miR-433-3p-MAPK8 axis played important role for NSCLC pathogenesis, which could be potential therapeutic target for the development of future NSCLC treatment.

Correlation Analysis of the TP53 Mutation With Clinical Characteristics in the Prognosis of Non-Small Cell Lung Cancer.

Background: Non-small cell lung cancer (NSCLC) with TP53 mutations has a worse prognosis. It was generally more resistant to chemotherapy and radiation. Our aim was to investigate the correlation between the TP53 co-mutated gene and clinical features, and prognostic value in patients with NSCLC. Methods: Seventy-three patients with a diagnosis of NSCLC at our hospital were recruited. They were divided into the TP53 mutation status (minor) (TP53 MU) and TP53 wild-type (major) (TP53 WT) groups according to their clinical characteristics after their mutation data and clinical information were collected. Serum markers were compared between groups using Mann-Whitney U test. Other clinical factors were compared between groups using χ2 test and Fisher exact test. The log-rank test was used to compare survival curves. Results: Of the 73 patients with NSCLC, 37 (50.68%) were found to carry TP53 mutation. TP53 MU and TP53 WT groups (n = 36) showed a significant difference in the number of smokers, incidence of squamous cell carcinoma, EGFR mutation, and number of advanced patients (P < .05), while gender, age, lymph node metastasis, and KRAS mutation did not differ significantly between the 2 groups. The survival curves in the TP53/KRAS and the TP53/EGFR co-mutation groups suggest that patients with NSCLC may have a shorter progression-free survival (PFS) if they carry one of the 2 types of co-mutation. Conclusions: TP53 gene mutations are more common in patients with NSCLC and squamous cell carcinoma. New predictive markers for NSCLC prognosis may be TP53/KRAS and TP53/EGFR co-mutations.

miR-452-5p suppressed the metastasis of Non-small cell lung cancer through regulating Moesin.

Background: Non-small cell lung cancer (NSCLC) is a common malignant tumor, and it is characterized by high mortality. MicroRNA-452-5p (miR-452-5p) and Moesin (MSN) have been proved to be related with regulation of tumors. If miR-452-5p could regulate NSCLC through targeting MSN remain unclear. Methods: TargetScan data and GEPIA databases were used to predict binding site and analyze gene expression, respectively. EdU staining, wound healing, and Transwell assays were performed to measure cell proliferation, migration, and invasion, respectively. Results: The binding site between miR-452-5p and MSN was predicted and validated. Overexpression of miR-452-5p cell lines were constructed, and miR-452-5p mimics markedly inhibited the migration, invasion, and proliferation ability of both H322 and A549 cells, but these effects of miR-452-5p were reversed by pcDNA-MSN. pcDNA-MSN significantly reversed the influence of miR-452-5p mimics on the EMT related proteins expression in H322 and A549 cell lines by decreasing E-cadherin and increasing N-cadherin. Significant higher expression of MSN in lung adenocarcinoma and lung squamous cell carcinoma was observed through GEPIA and TCGA data base analysis. Higher expression of MSN is positively correlated with advanced lung cancer and suggests poor prognosis. Conclusions: We demonstrated that miR-452-5p modulated the cell proliferation, migration, invasion, and EMT process of H322 and A549 cell lines through targeting MSN. This research might provide a novel prevention and treatment target for NSCLC.

USP2 Inhibits Lung Cancer Pathogenesis by Reducing ARID2 Protein Degradation via Ubiquitination.

Background: Ubiquitination is an important regulator in physiological and pathological conditions. Ubiquitin-specific protease 2 (USP2), as a member of the USP family, exhibits oncogenic effects in multiple malignancies. However, the exact role of USP2 has not been well clarified in lung cancer pathogenesis and progression. Therefore, we aimed to further investigate the regulatory roles of USP2 in lung cancer in this study. Methods: Firstly, immunoprecipitation-Mass Spectrometry (IP-MS), Co-immunoprecipitation (Co-IP), combined with immunofluorescent colocalization method, was conducted for USP2 protein interaction analysis in lung cancer cell lines. qRT-PCR, Western blot, and immunohistochemistry assays explored the USP2 expression pattern and USP2/ARID2- (AT-rich interactive domain 2-) specific shRNAs and overexpression vectors. Co-IP assays were designed to validate USP2-ARID2 protein interaction. Further functional studies including CHX chase assay, transwell assay, and wound healing assay were subsequently applied to evaluate the impact of USP2 modulation on lung cancer cells. Results: USP2 suppression was characteristic in lung cancer cell line models and lung cancer samples. USP2 and ARID2 demonstrated protein-protein interaction and overlapping localization in cancer cell models. Functional experiments suggested USP2 inhibited lung cancer cell invasion and migration by reducing ARID2 protein degradation. Subsequent ubiquitination assays indicated ARID2 protein degradation via the ubiquitination was significantly reduced by USP2 interaction. Conclusions: Our study provided novel insight that USP2 might suppress lung cancer by reducing ARID2 protein degradation via ubiquitination.

Pembrolizumab combined with paclitaxel and platinum as induction therapy for locally advanced esophageal squamous cell carcinoma: a retrospective, single-center, three-arm study.

Background: Pembrolizumab has been shown to have a powerful benefit for locally advanced or metastatic esophageal cancer. The aim of present study was to evaluate the efficacy and safety of pembrolizumab combined with neoadjuvant chemotherapy for locally advanced and potentially resectable esophageal squamous cell carcinoma (ESCC). Methods: Patients diagnosed with clinical stage III-IV ESCC and have a chance of resectability at Fujian Provincial Hospital were included into this study. Patients received pembrolizumab in combination with paclitaxel and nedaplatin as induction therapy once every 3 weeks in the first stage. After 4 cycles of pembrolizumab therapy, the patients then chose to undergo radical surgery (group A), radical radiotherapy (group B), or neither (group C). In the third stage, maintenance treatment with pembrolizumab was administered to all patients. Results: A total of 39 patients (33 male and 6 female) with a median age of 64 years were included. After immune response evaluation in the first stage, 34 (87.2%) patients achieved immune partial response (iPR), and 5 (12.8%) patients achieved immune stable disease (iSD). The objective response rate (ORR) was 87.2% (34/39), and the disease control rate (DCR) was 100%. In the second stage, 22 patients received radical surgery, all of whom achieved R0 resection. The major pathological response (MPR) rate was 68.2% (15/22), and the pathological complete response (pCR) rate was 45.5% (10/22). Of the patients, 9 chose radiotherapy as the radical therapeutic method and 8 chose not to undergo any radical therapy. The median period of pembrolizumab therapy was 8 cycles (4-22 cycles). The median follow-up time was 14 months (3-34 months). The median overall survival and progression-free survival (PFS) times were not reached. The incidence of severe adverse events (AEs) (grade ≥3) was 15.4% (6/39). Conclusions: Pembrolizumab combined with paclitaxel and platinum for locally advanced and potentially resectable ESCC has a high ORR, high surgical conversion, MPR, pCR, and R0 resection rates, and tolerable AEs. Also, pembrolizumab could provide good benefits in sequential treatment with radical radiotherapy or maintenance therapy.

CircMMD_007 promotes oncogenic effects in the progression of lung adenocarcinoma through microRNA-197-3p/protein tyrosine phosphatase non-receptor type 9 axis.

Circular RNAs play important roles in cancer biology. In this research, we explored the underlying function and mechanism of cirMMD_007 in lung adenocarcinoma (LC). Clinical lung adenocarcinoma samples were obtained from surgery. Bioinformatic databases were used to predict miRNAs that can potentially target circRNAs and miRNA target genes. hsa_circMMD_007, miR-197-3p, and PTPN9 mRNA expressions were investigated by qRT-PCR. Protein expressions were examined using Western blot. The proliferation abilities were assessed by Cell Counting Kit-8 assays. Wound healing cell migration assay was applied to evaluate cell migration ability. Luciferase reporter assay and rescue experiments were then performed to elucidate the underlying mechanism. We found that the expression of circMMD_007 was abnormally increased in LC. The expression of circMMD_007 was higher in advanced stages. Knockout of circMMD_007 hindered the tumorigenesis of LC in vivo and in vitro. circMMD_007 could negatively regulate the expression of miR-197-3p. PTPN9 behaved to be a molecular target of miR-197-3p. In summary, this research demonstrated that circular RNA circMMD_007 could promote the oncogenic effects in the progression of LC through miR-197-3p/PTPN9 axis.

TRIM55 suppresses malignant biological behavior of lung adenocarcinoma cells by increasing protein degradation of Snail1.

Up until now, cancer refractoriness and distal organ metastatic disease remain as major obstacles for oncologists to achieve satisfactory therapeutic effects for lung adenocarcinoma patients. Previous studies indicated that TRIM55, which participates in the natural development of muscle and cardiovascular system, plays a protective role in hepatocellular carcinoma (HCC) pathogenesis. Therefore, in this study, we aimed to unveil the detailed molecular mechanism of TRIM55 and identify the potential target for lung adenocarcinoma patients. Surgical samples and lung cancer cell lines were collected to detect the TRIM55 expression for patients with or without lymph node/distal organ metastasis. Cellular functional assays including transwell assay, wound healing assay, cellular survivability assay, etc. as well as ubiquitination assay were performed to evaluate the impact of TRIM55/Snail1 regulatory network via the UPP pathway on lung cancer tumor cell migration and chemo-resistance. Lung cancer tissues and tumor cell lines exhibited significantly lower levels of TRIM55 expression. Functional study further indicated that TRIM55 inhibited chemo-resistance, migration, and cancer stem-cell like phenotype of tumor cells. Further detailed molecular experiments indicated that TRIM55 promoted degradation of Snail1 via the UPP pathway, which played an interesting role in the regulation of cancer cell malignancy. This study provided novel theory that TRIM55 acted as a potential tumor suppressor by inhibition of tumor cell malignancy through enhancement of Snail1 degradation via the UPP pathway. Our research will inspire further exploration on TRIM55 to promote therapeutic effects for lung adenocarcinoma patients.

Prognostic relevance of rib invasion and modification of T description for resected NSCLC patients: A propensity score matching analysis of the SEER database.

Introduction: The impact of rib invasion on the non-small cell lung cancer (NSCLC) T classifications remains unclear. Our study aims to verify the impact of rib invasion on survival in patients with NSCLC through multicenter data from the Surveillance, Epidemiology, and End Results (SEER) database, and proposed a more appropriate pT for the forthcoming 9th tumor-node-metastasis (TNM) classifications. Method: The SEER database was used to collect T2b-4N0-2M0 NSCLC cases from the period of 2010-2015 according to the 7th TNM classification system. Subsequently, the T classification was restaged according to the 8th TNM classification system based on the following codes: tumor size and tumor extension. Cases with T1-2 disease and incomplete clinicopathological information were excluded. Finally, 6479 T3 and T4 NSCLC patients were included in the present study and divided into a rib invasion group (n = 131), other pT3 group (n = 3835), and pT4 group (n = 2513). Propensity-score matching (PSM) balanced the known confounders of the prognosis, resulting in two sets (rib invasion group vs. other pT3 and pT4 group). Overall survival (OS) and cancer-specific survival (CSS) were investigated using Kaplan-Meier survival curves, and predictive factors of OS and CSS were assessed by Cox regression. Result: Survival outcomes of the rib invasion group were worse than the other pT3 group (OS: 40.5% vs. 46.5%, p = 0.035; CSS: 49.2% vs. 55.5%, p = 0.047), but comparable to the pT4 group (OS: 40.5% vs. 39.9%, p = 0.876; CSS: 49.2% vs. 46.3%, p = 0.659). Similar results were obtained after PSM. Multivariate analyses for all patients revealed that age at diagnosis, gender, N stage, T stage, surgical modalities, and adjuvant therapy had a predictive value for the prognosis. Conclusion: The rib invasion group had a worse prognosis than the other pT3 groups, but was similar to the pT4 group. Our recommendation is to change the classification of rib invasion to pT4 disease and further validate this in the forthcoming 9th TNM classification.

Metastatic sites as predictors in advanced NSCLC treated with PD-1 inhibitors: a systematic review and meta-analysis.

BACKGROUND: Programmed cell death protein 1 (PD-1) inhibitors are the first-line treatment for advanced non-small-cell lung cancer (NSCLC) patients. However, their efficacy in metastatic NSCLC patients remains controversial. AIM OF THE STUDY: The aim of our study was to evaluate the prognosis of advanced metastatic NSCLC patients treated with PD-1 inhibitors, and discuss the predictive effect of metastatic site on the long-term outcome. METHODS: The Embase, Ovid Medline, Cochrane Central Register of Controlled Trials, and PubMed databases were systematically screened up to February 10, 2020. Twenty-five eligible studies, involving 8,067 patients that assessed the impact of metastatic sites on survival outcome were incorporated in our study. Overall survival (OS) and progression-free survival (PFS) were described as hazard ratio (HR) with 95% confidence interval (CI). RESULTS: Among the advanced NSCLC patients, the median proportion of brain, liver, bone, and adrenal gland metastases were 21%, 17%, 35%, and 21%, respectively. Patients with metastases to the brain, liver, and bone had worse OS compared to patients without these metastases when treated with PD-1 inhibitors. Similarly, patients with metastasis to the brain and liver were more likely to progress when treated with PD-1 inhibitors. Besides, patients with multiple metastatic sites had worse PFS compared to patients with one metastatic site, while no significant difference was found in terms of OS. CONCLUSIONS: Based on the findings of our systematic review and meta-analysis, metastatic sites were independent predictors of the survival outcome for advanced NSCLC patients treated with PD-1 inhibitors.

LncRNA GAS5 inhibits Invasion and Migration of Lung Cancer through influencing EMT process.

Background: Lung cancer is a malignant tumor in mammary gland epithelium with high morbidity and mortality among women worldwide. Long noncoding RNA GAS5 (GAS5) has been proved to be closely related with tumor progression. However, the influence of GAS5 on lung cancer and the specific mechanism remain unclear. Methods: Cell invasion, cell migration, cell apoptosis and cell cycle were investigated after transfection with pcDNA-GAS5 and sh-GAS5. Sizes of tumors were measured by establishing transplanted tumor model in vivo. E-cadherin and N-cadherin expressions were investigated. Results: Cell invasion and migration were inhibited markedly in GAS5 overexpressed cell line. Cell cycle results indicated that the percentage of S-phase cells was increased, and G2-phase was reduced in the GAS5 overexpression cell line. Tumor size was suppressed obviously after GAS5 overexpression treatment. GAS5 markedly inhibited the expression of E-cadherin and induced the expression of N-cadherin. GAS5 overexpression significantly inhibited lung cancer cell proliferation by increasing the E-cadherin and decreasing N-cadherin. Conclusions: These findings provide novel evidence that GAS5 can be viewed as an anti-lung cancer agent through affecting EMT pathway.

Two cases of non-small cell lung cancer patients with somatic or germline EGFR R776H mutation.

The development of epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors (TKIs) has revolutionized the treatment for non-small cell lung cancer (NSCLC). Comprehensive genomic profiling for NSCLC enables clinicians to identify more uncommon genetic alterations in EGFR. It remains unclear whether patients with certain rare EGFR mutations can benefit from EGFR inhibitors. On the other hand, emerging evidence has also showed the involvement of inherited factors in lung cancer development. However, only few germline EGFR mutations have been reported, and their association with NSCLC familial risk remains ambiguous. Here, we report two cases of NSCLCs with uncommon EGFR mutation R776H. One patient carrying somatic EGFR R776H and L861Q was treated with afatinib and achieved a durable response. The other patient harbored a germline EGFR R776H and her son inherited the same germline R776H mutation whose CT examination showed multiple ground-glass nodules in both lungs requiring further follow-up and diagnosis. Our study demonstrated the responsiveness of compound R776H-L861Q mutations to afatinib. We also revealed the transmission of EGFR R776H and suggested it may confer the high susceptibility to lung cancer.

Evaluation of pembrolizumab for the treatment of advanced non-small cell lung cancer: a retrospective, single-centre, single-arm study.

BACKGROUND: Immune checkpoint inhibitors (ICIs) provided a paradigm shift for advanced non-small cell lung cancer (NSCLC) treatment and improved the clinical prognosis of such patients. Pembrolizumab is a humanized anti-programmed death cell protein 1 (PD-1) monoclonal antibody, approved for the treatment of patients with advanced or metastatic NSCLC. This article investigated and reported on the efficacy and safety of pembrolizumab in the treatment of advanced NSCLC in our center since 2019. METHODS: Patients with clinical stage III-IV NSCLC treated with pembrolizumab for ≥4 cycles were enrolled as participants in this study. Pembrolizumab was administered intravenously at a dose of 2 mg/kg every 3 weeks. A cycle was defined as 3 weeks of treatment. We assessed the efficacy and safety of pembrolizumab through the collection of researcher-assessed tumor response, survival, and safety data. RESULTS: A total of 24 patients were included in this study. The median follow-up time was 9 months (3-20 months) and the median period of pembrolizumab therapy was 7 cycles (4-21 cycles). The objective response rate (ORR) was 45.8% and disease control rate (DCR) was 70.8%. The median overall survival (OS) and progression-free survival (PFS) times were not reached. A total of 2 programmed death-ligand 1 (PD-L1)-negative participants were treated with pembrolizumab combined with chemotherapy and there was no significant progression during the follow-up period. During the follow-up period, 8 patients underwent surgery. The major pathological response (MPR) was 75% and pathological complete response (pCR) was 50%. A case that was preoperatively diagnosed with clinical stage IV achieved pCR after 6 cycles of pembrolizumab combined with chemotherapy. The incidence of adverse effects (AEs) was 83.3%, and 16.7% of these were serious AEs (grade ≥3), which was similar to the incidence reported in previous studies. CONCLUSIONS: This real-world data supports the use of pembrolizumab for advanced NSCLC, including those cases that are PD-L1 negative. More importantly, pembrolizumab immunotherapy can also provide the potential of local treatment for patients with advanced NSCLC, which has wide application prospects in the field of surgery.

Photodynamic Therapy in Combination with Sorafenib for Enhanced Immunotherapy of Lung Cancer.

The emerging of cancer immunotherapy is a great progress in cancer therapy. However, accumulating evidences have shown that tumor microenvironment (TME) exerted strong inhibition effects on cancer immunotherapy. In order to solve this issue, a cell membrane vehicle (CMV) was developed and employed to encapsulate both chlorins e6 (Ce6) and sorafenib (Sfn). The obtained drug delivery system (DDS, CMV/C-S was expected to enhance the immune response in cancer therapy by remodeling the TME. The results showed that CMV/C-S was highly stable under physiological environment with responsive drug release upon laser irradiations and high tumor targetability, which all contributed to promising anticancer performance in vitro / in vivo. Especially, the photodynamic nature of Ce6 could exert significant immunogenic cell death (ICD) to trigger immune response. At the same time, with the TME regulation effects of Sfn, the outcome of cancer immunotherapy was significantly enhanced as compare to mono-therapies. The study offers a novel approach for effective cancer immunotherapy.

[Distribution and Pollution Assessment of Nutrients and Heavy Metals in Surface Sediments from Shibalianwei Wetland in Hefei, Anhui Province, China].

Shibalianwei is a large constructed wetland formed at the estuary of the Nanfei River adjoining Lake Chaohu. To investigate the distribution and pollution characteristics of nutrients and heavy metals in surface sediments of Shibalianwei Wetland, sediment samples were collected from 72 sites in July 2018. The source of the pollution was analyzed. Our results showed that the average contents of total nitrogen (TN), total phosphorus (TP), and organic matter (OM) in surface sediments of Shibalianwei were 2108.87 mg·kg-1, 1448.82 mg·kg-1, and 86.2 g·kg-1, respectively; in the external water system of the wetland, they were 2305.81 mg·kg-1, 1268.46 mg·kg-1, and 59.9 g·kg-1, respectively. The average contents of heavy metals of Mn, Cr, Cu, Pb, Cd, As, and Hg in Shibalianwei were 462.58, 42.12, 21.69, 18.05, 0.63, 5.67, and 0.059 mg·kg-1, respectively; in the external water bodies, they were 381.61, 36.85, 24.74, 30.70, 2.49, 6.47, and 0.035 mg·kg-1, respectively. In the assessments of nutrient pollution of internal water bodies of Shibalianwei, TN was at mild to moderate pollution levels, TP was at a heavy pollution level, and the comprehensive pollution index (FF) indicated that nutrients in Shibalianwei were at moderate to heavy pollution levels. The assessment results of the organic pollution index (OI) were consistent with the FF. The potential ecological risk assessments of heavy metals showed that both Cd and Hg reached certain ecological risks, which were indicated by RI and Eri. For external water bodies, the nutrient levels were also high and heavy metal pollution was relatively serious, indicating high ecological risks.

MiR-504 inhibits cell proliferation and invasion by targeting LOXL2 in non small cell lung cancer.

BACKGROUND: MicroRNAs (miRNAs) play crucial roles in tumor initiation and development. The aim of the study was to explore the clinicopathological role and functional effects of miR-504 in non small cell lung cancer (NSCLC). METHODS: Quantitative reverse transcription polymerase chain reaction (QRT-PCR) was applied to detect the expression of miR-504 in 55 cases of NSCLC tissues and matched adjacent normal tissues in NSCLC patients. MTT, colony formation and transwell invasion assays were performed to evaluate the effects of miR-504 on cell proliferation and invasion, respectively. Dual luciferase reporter assay was used to verify that LOXL2 was a direct target of miR-504. QRT-PCR and western blot analysis were performed to analyze mRNA and protein expression. RESULTS: In the study, we demonstrated that miR-504 was notably downregulated in NSCLC tissues compared with adjacent normal tissues. Lower miR-504 expression positively correlated with lymph node metastasis and advanced TNM stage in patients. Furthermore, upregulation of miR-504 significantly inhibited cell proliferation, cell invasion and EMT process of NSCLC. QRT-PCR, western blot and luciferase reporter assays confirmed that miR-504 could bind to LOXL2 3'UTR region and regulate its expression. Moreover, ectopic expression of LOXL2 could rescue the inhibiting effects on cell proliferation and invasion induced by miR-504 in NSCLC cells. CONCLUSIONS: Our results indicated that miR-504 functioned as a tumor suppressor in NSCLC and may serve as a target of NSCLC treatment.

[Application of vascular repair and reconstruction in surgical treatment of superior vena cava syndrome caused by thoracic tumor].

Objective: To summarize the clinical experience of vascular repair and reconstruction for treating superior vena cava syndrome (SVCS) caused by thoracic tumor. Methods: Between October 2008 and June 2016, 26 patients with thoracic tumor and SVCS were admitted. There were 18 males and 8 females, aged from 27 to 70 years (mean, 45.9 years). Tumor was typed as B1-B3 thymoma in 13 cases, thymic carcinoma in 6 cases, large B-cell lymphoma in 3 cases, T lymphocytic lymphoma in 1 case, malignant teratoma in 1 case, right lung squamous cell carcinoma in 1 case, and carcinoid in 1 case. The tumor diameter ranged from 8 to 15 cm with an average of 10 cm. The patients had different degrees of neck, face, and upper extremity edema, jugular vein distention, and chest wall collateral venous filling. The superior vena cava pressure was 2.45-5.39 kPa. After excision of tumor and invading superior vena cava, 7 patients underwent superior vena cava reconstruction and 19 patients underwent artificial vascular replacement. Results: There was no perioperative death, and the symptoms of superior vena cava obstruction were eliminated. Postoperative pulmonary infection, respiratory muscle weakness, and right chylothorax occurred in 4 cases, 1 case, and 1 case respectively. Twenty-four patients were followed up 2-92 months (mean, 37 months), and 2 patients failed to be followed up. At 1, 3, and 5 years, the survival rate was 83.3% (20/24), 41.7% (10/24), and 25% (6/24), respectively. In 6 patients with 5-year survival, there were 1 case of type B1 thymoma, 3 cases of type B3 thymoma, and 2 cases of large B-cell lymphoma. Conclusion: For preoperative evaluation of SVCS caused by resectable thoracic tumors, vascular repair and recons-truction technique can be used to quickly and effectively relieve the clinical symptoms and improve the quality of life.