Risk factors for esophageal anastomotic stricture after esophagectomy: a meta-analysis.

BACKGROUND: The aim of this study was to assess the risk factors for anastomotic stricture in esophageal cancer patients undergoing esophagectomy. Esophageal anastomotic stricture is the most common long-term complication for esophagectomy. The risk factors for esophageal anastomotic stricture still remain controversial. METHODS: MEDLINE, Cochrane Library, and EMBASE were searched to identify observational studies reporting the risk factors for esophageal anastomotic stricture after esophagectomy. A meta-analysis was conducted to investigate the impact of various risk factors on esophageal anastomotic stricture. The GRADE [Grading of Recommendations Assessment, Development and Evaluation] approach was used for quality assessment of evidence on outcome levels. RESULTS: This review included 14 studies evaluating 5987 patients.The meta-analysis found that anastomotic leakage (odds ratio [OR]: 2.75; 95% confidence interval[CI]:2.16-3.49), cardiovascular disease [OR:1.62; 95% CI: 1.22-2.16],diabete [OR: 1.62; 95% CI: 1.20-2.19] may be risk factors for esophageal anastomotic stricture.There were no association between neoadjuvant therapy [OR: 0.78; 95% CI:0.62-0.97], wide gastric conduit [OR:0.98; 95% CI: 0.37-2.56],mechanical anastomosis [OR: 0.84; 95% CI:0.47-1.48],colonic interposition[OR:0.20; 95% CI: 0.12-0.35],and transhiatal approach[OR:1.16; 95% CI:0.81-1.64],with the risk of esophageal anastomotic stricture. CONCLUSIONS: This meta-analysis provides some evidence that anastomotic leakage,cardiovascular disease and diabete may be associated with higher rates of esophageal anastomotic stricture.Knowledge about those risk factors may influence treatment and procedure-related decisions,and possibly reduce the anastomotic stricture rate.

Clinical Analysis of 80 Patients of Multiple Primary Lung Cancers Undergoing Simultaneous Video-Assisted Thoracoscopic Surgery.

Objective: To explore the diagnosis, treatment and prognosis of multiple primary lung cancers (MPLCs) through summarizing and analyzing the clinical data of 80 patients with MPLCs. Methods: The clinical and pathological data of 80 patients who were diagnosed with MPLCs according to the Martini-Melamed criteria and who underwent simultaneous video-assisted thoracoscopic surgery in our hospital from January 2017 to June 2018 were retrospectively analyzed. The Kaplan-Meier method was used for survival analysis. Log-rank test was used for univariate analysis and Cox proportional hazards regression model for multivariate analysis to evaluate the independent risk factors affecting the prognosis of MPLCs. Results: Among the 80 patients, there were 22 cases with MPLCs and 58 cases with double primary lung cancers. The surgical approach was mainly pulmonary lobectomy and pulmonary segmental or wedge resection (41.25%, 33/80), and lesions occurred predominantly in the upper lobe of the right lung (39.8%, 82/206). The pathology of lung cancers was mainly adenocarcinoma (89.8%, 185/206), with invasive adenocarcinoma as a dominant pathological type (68.6%, 127/185), in which acinar subtype was found to be predominant (79.5%, 101/127). The proportion of MPLCs with the same histopathological type (96.3%, 77/80) was higher than that with different histopathological types (3.7%, 3/80). Postoperative pathological staging showed stage I in most patients (86.25%, 69/80). Univariate analysis revealed that the maximum tumor diameter, highest pathological stage and lymph node metastasis were correlated with disease-free survival (P < .05). The overall median survival time of patients was 50 months. Cox multivariate regression analysis indicated that lymph node metastasis was an independent risk factor affecting the prognosis of MPLC patients (P < .05). Conclusion: MPLCs occur principally in the upper lobe of the right lung and pulmonary adenocarcinoma is the most dominant pathological type, with acinar type as the predominant pathological subtype. Lymph node metastasis is an independent risk factor affecting the prognosis of MPLC patients. A favorable prognosis can be achieved through early diagnosis and active surgical treatment for individuals who are highly suspected of MPLCs indicated by imaging examination.

Lung Cancer Stage Prediction Using Multi-Omics Data.

Lung cancer is one of the leading causes of cancer death. Patients with early-stage lung cancer can be treated by surgery, while patients in the middle and late stages need chemotherapy or radiotherapy. Therefore, accurate staging of lung cancer is crucial for doctors to formulate accurate treatment plans for patients. In this paper, the random forest algorithm is used as the lung cancer stage prediction model, and the accuracy of lung cancer stage prediction is discussed in the microbiome, transcriptome, microbe, and transcriptome fusion groups, and the accuracy of the model is measured by indicators such as ACC, recall, and precision. The results showed that the prediction accuracy of microbial combinatorial transcriptome fusion analysis was the highest, reaching 0.809. The study reveals the role of multimodal data and fusion algorithm in accurately diagnosing lung cancer stage, which could aid doctors in clinics.

Dexmedetomidine disrupts esophagus cancer tumorigenesis by modulating circ_0003340/miR-198/HMGA2 axis.

More and more studies have focused on the regulatory role of circular RNAs (circRNAs) in various cancers. However, it is not clear how dexmedetomidine (DEX) affects esophagus cancer progression by affecting the expression of circRNAs. This study aimed to investigate the role of DEX in esophagus cancer and its underlying mechanism. Cell Counting Kit-8 assay and 5-ethynyl-2'-deoxyuridine assays were conducted to evaluate cell proliferation. Flow cytometry analysis and transwell assay were performed for cell apoptosis and invasion. The protein levels of cleaved caspase-3, matrix metallopeptidase 9, and high mobility group AT-hook 2 (HMGA2) were assessed by western blot assay. The expression levels of circ_0003340 and microRNA-198 (miR-198) were determined by quantitative real-time PCR. Dual-luciferase reporter assay was performed to verify the interaction between miR-198 and circ_0003340 or HMGA2. Murine xenograft model was established to investigate the role of circ_0003340 and DEX in vivo. DEX exerted antitumor effects in esophagus cancer cells. DEX hindered proliferation and invasion while inducing apoptosis of esophagus cancer cells, which was abolished by circ_0003340 elevation, HMGA2 overexpression, or miR-198 silencing. miR-198 directly interacted with circ_0003340 and HMGA2 in esophagus cancer cells. Moreover, knockdown of circ_0003340 could improve the anticancer role of DEX in vivo. DEX constrained cell carcinogenesis by regulating circ_0003340/miR-198/HMGA2 axis in esophagus cancer, providing an effective clinical implication for preventing the development of the esophagus cancer by the DEX.

Initial experience of video-assisted thoracic surgery lobectomy after neoadjuvant chemotherapy plus toripalimab in a patient with locally advanced non-small cell lung cancer: a case report.

BACKGROUND: Immune checkpoint inhibitors were used for patients with advanced non-small cell lung cancer (NSCLC) more and more frequently and the effects were thrilling. Toripalimab as a new immune checkpoint inhibitor has been shown to be effective in patients with advanced NSCLC. However, data regarding the safety and feasibility of surgical resection after treatment with toripalimab for NSCLC remain scarce. Here, we present a case with locally advanced NSCLC that received video-assisted thoracic surgery (VATS) lobectomy after treatment with toripalimab in combination with chemotherapy. CASE PRESENTATION: A 62-year-old male patient with a history of coronary artery stenting operation for two times was found a 3.4 × 3.2 cm cavity mass in the upper lobe of the left lung and enlarged left hilar and mediastinal lymph nodes. Pathological results identified squamous cell carcinoma. The patient was diagnosed with a locally advanced NSCLC and received VATS left upper lobectomy and lymph node dissection after neoadjuvant chemotherapy plus toripalimab for 3 cycles. The postoperative pathological results showed complete tumor remission. Short-term follow-up results were excellent, and long-term results remain to be revealed. CONCLUSIONS: Our preliminary results showed that the use of neoadjuvant toripalimab and chemotherapy for the locally advanced NSCLC before surgical resection is safe and feasible.

MicroRNA-144-3p suppressed TGF-ß1-induced lung cancer cell invasion and adhesion by regulating the Src-Akt-Erk pathway.

Lung cancer remains a leading cause to cancer-related death worldwide. The anti-cancer ability of microRNA-144-3p has been reported in many cancer types. This study focused on the mechanisms underlying miR-144-3p in inhibiting lung cancer. The expression levels of miR-144-3p and steroid receptor coactivator (Src) in different lung cancer cell lines and those in bronchial epithelial cells (16HBE) were compared. miR-144-3p mimic and siSrc were transfected into A549 cells. Under the conditions of transforming growth factor-ß1 (TGF-ß1). Small interfering transfection or TGF-ß1 treatment, cell invasive and adhesive abilities were analyzed by Transwell and cell adhesion assays. miR-144-3p inhibitor and siSrc were co-transfected into A549 cells and the changes in cell invasion and adhesion were detected. The activation of Src-protein kinase B-extracellular-regulated protein kinases (Src-Akt-Erk) pathway was determined using Western blot. The downregulated miR-144-3p and upregulated Src were generally detected in lung cancer cell lines and were the most significant genes in A549 cells. Both miR-144-3p overexpression and Src inhibition could obviously inhibit the invasion and adhesion abilities of A549 cells in the presence or absence of the effects of TGF-ß1. The inhibition of Src could block the promotive effects of miR-144-3p inhibitor and TGF-ß1 on cell invasion and adhesion. Furthermore, we found that miR-144-3p could negatively regulate the phosphorylation levels of Akt and Erk. Our data indicated the essential role of Src in the mechanisms underlying TGF-ß1-induced cell invasion and adhesion of lung cancer, and that miR-144-3p could effectively suppress TGF-ß1-induced aggressive lung cancer cells by regulating Src expression.

D2 dopamine receptor antagonist raclopride induces non-canonical autophagy in cardiac myocytes.

Cell death by autophagy is an important means of maintaining cellular homeostasis in adult cardiac myocytes. Autophagy was previously shown to exert a cardioprotective effect, suggesting that modulation of autophagy pathways is a potential therapeutic strategy in the treatment of heart disease. Although dopamine is known to induce autophagy in neuroblastoma cells, the underlying mechanism and the types of dopamine receptors involved in this process remain unclear. In this study, we used various dopamine receptor antagonists and agonists to identify the specific dopamine receptor that mediates induction of autophagy. We evaluated autophagy induction by the expression of autophagy markers in neonatal rat ventricular cardiac myocytes. We evaluated intracellular calcium levels using Fluo-3/AM and demonstrated autophagy-induced morphological changes in cardiac myocytes using electron microscopy. We also examined the pathway for dopamine-induced autophagy using RNAi-mediated gene knockdown. Raclopride, the well-documented D2 receptor antagonist, significantly upregulated autophagy in cardiac myocytes via an mTOR-independent pathway. There was no difference in intracellular calcium levels between raclopride-treated cells and untreated cells. siRNA-mediated knockdown of Rab9 resulted in decreased expression of autophagy markers in raclopride-treated cells. Interestingly, siRNA-mediated knockdown of Atg7 resulted in a significant increase in Rab9 levels in raclopride-treated cells, suggesting that blocking the classical autophagy pathway results in activation of an alternative pathway. Our study suggests that (1) the D2 dopamine receptor plays a role in autophagy and (2) raclopride mediated a non-canonical autophagy pathway in cardiac myocytes via Rab9.