Lung cancer is a complex disease with its own challenges, and is considered to be one of the most common causes of cancer death worldwide. The coronavirus disease 2019 (COVID-19) pandemic, caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), has exacerbated these challenges. The aim of this review is to explore the impact of the COVID-19 pandemic on the screening, diagnosis and treatment of lung cancer. We hope to provide some experience and help for the whole process management of lung cancer patients.
ObjectiveTo investigate the relationship between DDX46 genes and invasion and migration of esophageal squamous cell carcinoma cells. MethodsHuman esophageal squamous cell carcinoma cells TE-1 were transfected by fluorescent marker shRNA lentivirus (shDDX46 group), and an empty vector was transfected as a control (shCtrl group). The expression rate of green fluorescent protein under the microscope was used to evaluate the cell transfection efficiency. Real-time fluorescence quantitative polymerase chain reaction (RTFQ-PCR) and Western blotting (WB) detected the knockdown efficiency of the target gene at the mRNA and protein expression levels. Wound healing, invasion assay and migration assay detected the changes of invasion and metastasis ability. Classical pathway analysis was used to explore signaling pathway changes and the possible mechanism of DDX46 in the invasion and metastasis was explored by detecting fibronectin expression. ResultsDDX46 gene at mRNA and protein levels was significantly inhibited after lentiviral transfection. Wound healing showed that after 8 h the cell mobility of TE-1 cells decreased significantly (P=0.001). Invasion assay showed that after 24 h the average cell metastasis rate of TE-1 cells was lower in the shDDX46 group than that in the shCtrl group (P<0.001). The cell metastasis rate in the shDDX46 group corresponding to observation points in the transwell assay was lower than that in the shCtrl group (P<0.001) after 24 h culture. The results of the classical pathway analysis showed that the integrin signaling pathway activity was inhibited, further exploration of the mechanism of action found that the expression of fibronectin associated with cell adhesion was decreased. ConclusionDDX46 gene is related to the invasion and migration ability of esophageal squamous cell carcinoma cells. Knockdown of DDX46 genes may reduce cell adhesion by downregulating the integrin pathway signaling.
Objective To systematically evaluate the effect and safety of neoadjuvant PD-1/PD-L1 inhibitors combined with chemotherapy for resectable non-small cell lung cancer (NSCLC). Methods The PubMed, EMbase, The Cochrane Library, CNKI, and Wanfang data were searched by computer to identify relevant studies on anti PD-1 /PD-L1 combined with chemotherapy for resectable NSCLC from inception to March 2023. Two authors independently screened the literature, extracted the data, and evaluated the risk of bias in the included studies. The single-arm study was evaluated for quality using the methodological index for non-randomized studies (MINORS). Meta-analysis was conducted by RevMan 5.4 software. Results Twenty-six studies with 965 patients were included in this meta-analysis. MINORS scores of single-arm studies were ≥12 points. The meta-analysis results showed that the pooled pathologic complete response, major pathologic response, and objective response rates as well as partial response, surgical rate and R0 surgical resection rate of neoadjuvant PD-1/PD-L1 inhibitors combined with chemotherapy were 39% [RD=0.39, 95%CI (0.31, 0.47) ], 59% [RD=0.59, 95%CI (0.53, 0.65) ], 72% [RD=0.72, 95%CI (0.65, 0.80) ], 62% [RD=0.62, 95%CI (0.56, 0.69) ], 86% [RD=0.86, 95%CI (0.81, 0.92) ], and 94% [RD=0.94, 95%CI (0.92, 0.97) ], respectively. In terms of safety, the rate of adverse events (AEs) was 65% [RD=0.65, 95%CI (0.52, 0.78) ], and the rate of grade 3 to 5 AEs was 16% [RD=0.16, 95%CI (0.10, 0.23) ]. Conclusion The combination of neoadjuvant PD-1/PD-L1 inhibitors with chemotherapy has good efficacy and safety in the treatment of patients with resectable NSCLC.
Objective To evaluate the clinical efficacy of fistula repair by stapler technique in patients with cervical tracheoesophageal fistula. Methods Retrospective analysis of 8 patients with cervical tracheoesophageal fistula who accepted operative treatment in the Department of Thoracic Surgery, Lanzhou University Second Hospital from October 2014 to October 2016 was conducted. There were 5 males and 3 females at a mean age of 46.4±13.9 years ranging from 23 to 67 years. The fistula was induced by tracheal intubation in 4 patients, by esophageal foreign bodies in 2, by tracheal stent in 1 and by esophageal diverticulum in 1. The fistula was closed by stapler technique. The surgical effects were evaluated through Karnofsky performance score (KPS), image assessment, patient satisfaction score and assessment of improvement in feeding-induced bucking. Results The operations were performed successfully with time of 117.5±6.6 min and intraoperative blood loss of 60.0±7.0 ml. After the operations, the patients did not suffer incision bleeding and infection, hoarseness, dyspnea, drinking-induced bucking, fistula relapse, tracheoesophageal stenosis or any other complications, and no death occurred during the perioperative period. The chest X-ray test was performed 1 week later showed that the pulmonary infection disappeared, and only 1 patient suffered from esophageal stenosis 1 year later. The postoperative KPS score was 90.0±7.0 points, which significantly improved in contrast to preoperation (P<0.01). Postoperative pulmonary infection area reduced significantly (P<0.05), tracheoesophageal fistula disappeared, postoperative patients satisfaction rate was 90%, and assessment of feeding-induced bucking was excellent. Conclusion Using stapler technique to repair cervical tracheoesophageal fistula is safe, easy and useful, with less operation time and postoperative complications.
ObjectiveTo explore the mechanism of dihydrouridine synthase 4-like (DUS4L) on the development of lung adenocarcinoma (LUAD).MethodsThe RNA-seq expression data of LUAD was downloaded from The Cancer Genome Atlas (TCGA), and the relationship between its clinical pathological characteristics and DUS4L mRNA expression was evaluated. The effect of DUS4L knockdown on the proliferation of A549 cells was detected by EDU proliferation assay. The gene expression profile of lung adenocarcinoma A549 cells in the DUS4L knockdown group (KD group) and control group (NC group) was detected by transcriptome sequencing technique. The differential genes were screened by DESeq2. ClusterProfiler was used to perform GO functional enrichment analysis of differential genes.ResultsThe expression of DUS4L mRNA in LUAD tissues was higher than that in normal tissues, and the up-regulation of DUS4L was related to the clinical pathological characteristics of LUAD patients. EDU proliferation assay suggested that knocking down DUS4L could inhibit the proliferation of A549 cells. A total of 456 differential genes were screened, including 289 up-regulated genes and 167 down-regulated genes [|log2(fold change)|>1 and Padj<0.05]. STC2 and TRIB3 were significantly down-regulated (P<0.05). Differential genes were mainly involved in the production of interleukin-8, angiogenesis, vascular endothelial cell proliferation and other biological pathways.ConclusionDUS4L can widely regulate the gene expression of LUAD cells, which provides a new idea for further studying the function and role of DUS4L in the occurrence and development of LUAD and finding new therapeutic targets for LUAD.
ObjectiveTo explore the effect of DDX46 silencing on growth and apoptosis in esophageal squamous cell carcinoma cell TE-1 by the shRNA. MethodsThe relative expression of DDX46 mRNA in TE-1 cells was detected by real-time quantitative polymerase chain reaction (qRT-PCR) and compared with immortalized human esophageal squamous cell Het-1A. DDX46 shRNA-expressing lentivirus was applied to silence DDX46 (experimental group), and non-silencing control lentivirus was added (control group) with a multiplicity of infection of 5 in TE-1 cells. In both groups, cell growth was monitored using high content screening, cell colony-forming capacity was measured by colony formation assay, cell apoptosis were determined by flow cytometry. Further, the Stress and Apoptosis Signaling Antibody Array Kit was used to detect the changes of signaling molecules in TE-1 cells after DDX46 knockdown. ResultsCompared with the control group, cell counting after DDX46 silencing showed that TE-1 cell growth was significantly inhibited (P<0.001). Colony formation assay showed that cell colony-forming capacity was significantly inhibited (P<0.01). Annexin V-APC flow cytometry showed a significant increase in apoptosis (P<0.001). In PathScan® Antibody Array, the expression levels of Akt (Ser473, phosphorylation) and IκBα (Total, N/A) significantly decreased (P<0.01), and the expression of Caspase-3 (Asp175, cleaved) increased (P<0.05). ConclusionDDX46 is overexpressed in TE-1 cells. Targeted gene silencing of DDX46 inhibits cell growth, and induces cell apoptosis. DDX46 silencing probably by negative regulation of Akt/NF-κB signaling pathway, to play a role in inhibiting TE-1 cells growth and inducing apoptosis.
ObjectiveTo investigate the prognostic survival status and influence factors for surgical treatment of esophageal squamous cell carcinoma (ESCC) in pathological stage T1b (pT1b).MethodsThe patients with ESCC in pT1b undergoing Ivor-Lewis or McKeown esophagectomy in Lanzhou University Second Hospital from 2012 to 2015 were collected, including 78 males (78.3%) and 17 females (21.7%) with an average age of 61.4±7.4 years.ResultsThe most common postoperative complications were pneumonia (15.8%), anastomotic leakage (12.6%) and arrhythmia (8.4%). Ninety-three (97.9%) patients underwent R0 resection, with an average number of lymph node dissections of 14.4±5.6. The rate of lymph node metastasis was 22.1%, and the incidence of lymph vessel invasion was 13.7%. The median follow-up time was 60.4 months, during which 25 patients died and 27 patients relapsed. The overall survival rate at 3 years was 86.3%, and at 5 years was 72.7%. Multivariate Cox regression analysis showed that lymph node metastasis (P=0.012, HR=2.60, 95%CI 1.23-5.50) and lympovascular invasion (P=0.014, HR=2.73, 95%CI 1.22-6.09) were independent risk factors for overall survival of pT1b ESCC.ConclusionEsophagectomy via right chest approach combined with two-fields lymphadenectomy is safe and feasible for patients with pT1b ESCC. The progress of pT1b ESCC with lymph node metastasis or lymphovascular invasion is relatively poor.