With the continuous advancements in immunotherapy and targeted therapy, the treatment management and surgical resection assessment of locally advanced lung cancer have undergone significant changes. In October 2024, the Society of Thoracic Surgeons (STS) released the "STS expert consensus on the multidisciplinary management and resectability of locally advanced non-small cell lung cancer", which provides the latest insights on the evaluation of resectability and multidisciplinary management of locally advanced lung cancer, neoadjuvant (including perioperative) therapy, and adjuvant therapy. This article aims to interpret this consensus, with the goal of introducing the latest perspectives of the STS consensus to thoracic surgeons and providing a reference for the rational implementation of surgical resection, multidisciplinary management, and standardized comprehensive treatment models for non-small cell lung cancer in China.

OBJECTIVES: To investigate the mechanism through which salidroside inhibits proliferation of gastric cancer (GC) cells focusing on glucose metabolic reprogramming pathways. METHODS: High-throughput sequencing combined with bioinformatics analysis was employed to identify the potential targets of salidroside in human GC MGC-803 cells. Liposome-mediated transfection experiments were carried out to validate the functional and mechanistic roles of these targets. CCK-8 and colony formation assays were used to assess the effects of salidroside on GC cell viability and clonogenic ability. qRT-PCR, Western blotting, and biochemical assay kits were used to analyze the regulatory effects of salidroside on the miR-1343-3p-OGDHL/PDHB enzyme complex-pyruvate metabolic pathway in GC cells. RESULTS: Bioinformatics analysis suggested that the tumor-suppressive factor miR-1343-3p negatively regulated the key glycolytic enzyme gene oxoglutarate dehydrogenase-like (OGDHL) in GC cells, and OGDHL and pyruvate dehydrogenase E1 subunit beta (PDHB) were both significantly upregulated in GC tissues, which was close by correlated with reduced survival rates of GC patients. In MGC-803 cells, salidroside treatment significantly enhanced the expression level of miR-1343-3p and downregulated OGDHL expression, resulting in disruption of the stability of PDHB, reduced pyruvate oxidative decarboxylation, and consequently decreased production of acetyl-CoA and ATP. CONCLUSIONS Salidroside inhibits GC cell proliferation possibly by regulating the miR-1343-3p-OGDHL/PDHB enzyme complex-pyruvate metabolic pathway, which provides new insights into its anti-tumor mechanisms and suggests new strategies for targeted therapy for GC.
Humans ; Stomach Neoplasms/pathology* ; MicroRNAs/genetics* ; Cell Proliferation/drug effects* ; Glucosides/pharmacology* ; Phenols/pharmacology* ; Cell Line, Tumor ; Glucose/metabolism* ; Pyruvate Dehydrogenase (Lipoamide)/metabolism*

Objective To investigate the molecular mechanism by which salidroside inhibits the proliferation of gastric cancer(GC)cells through upregulation of miR-1343-3p.Methods RNA databases were used to screen for mRNAs associated with tumor proliferation and with miR-1343-3p,and exhibiting significant changes in their expression levels after salidroside treatment of human GC cells.Gene matching and immunoprecipitation of RNA-binding proteins were conducted to analyze the association between miR-1343-3p and SOX18.Immunocytochemistry was performed to determine the localization of SOX18 protein.The effect of salidroside on the proliferation of human GC cells(MGC-803 and AGS)was determined by CCK-8 assay.Human GC cells were divided into a blank control group and low-and high-dose salidroside groups.The expression of miR-1343-3p and SOX18 mRNA was measured by real-time quantitative fluorescence PCR(qPCR).The protein expression of SOX18 was measured by Western blot.GC cells were co-transfected with miR-1343-3p mimic and miR-1343-3p inhibitor,respectively,via LipofectamineTM 2000 liposomes.The expression of miR-1343-3p and SOX18 mRNA was measured by qPCR,and the protein expression of SOX18 was measured by Western blot.Results Through bioinformatic analysis,SOX18 was identified as a downstream target of miR-1343-3p.Gene alignment confirmed the presence of specific binding sites between the two genes,and immunoprecipitation of RNA-binding proteins validated the targeting relationship between them(P<0.05).Immunocytochemistry demonstrated the nuclear localization of SOX18 protein.CCK-8 assay findings demonstrated that salidroside significantly inhibited the proliferation of GC cells in a time-and dose-dependent manner.Compared with the blank control group,salidroside-treated GC cells showed decreased expression of both SOX18 mRNA and protein(P<0.05)and an increased miR-1343-3p expression(P<0.05).Compared with the control group,GC cells in the miR-1343-3p mimic group exhibited increased expression of miR-1343-3p and decreased expression of SOX18 mRNA and protein.In contrast,GC cells in the miR-1343-3p inhibitor group showed decreased expression of miR-1343-3p and increased expression of SOX18 mRNA and protein(all P<0.05).Conclusion Salidroside may inhibit the proliferation of GC cells by regulating the miR-1343-3p/SOX18 signaling axis and these regulators may present new potential therapeutic targets or biomarkers for gastric cancer.

With the development of low-dose chest computed tomography(CT)and artificial intelligence,the detection rate of multiple pulmonary nodules has been increased year by year.Surgical resection is the preferred treatment for high-risk pulmonary nodules,but some multiple pulmonary nodules cannot be treated surgically for various reasons,so ablation therapy can be used as an alternative to surgical procedures.This paper aims to make a comprehensive review about the research progress in the treatment of multiple pulmonary nodules,focusing on the percutaneous ablation,transbronchial ablation,ablation combined with surgery,ablation combined with drug therapy,etc.

Colorectal cancer(CRC)is one of the most common malignant tumors worldwide,metastasizing most commonly to the liver and lung.Local treatment of pulmonary oligometastases from CRC has an important position in the therapeutic course of the disease,sometimes local therapy is the key to achieve a disease-free state.Surgery is the preferred treatment for pulmonary oligometastases from CRC,but some patients are unable to undergo surgery due to physical conditions or lesion's anatomical location limitations.Because of its minimally-invasive manipulation,repeatable adoption,maximum preservation of lung parenchyma and lung function,and the potential to cure new or recurrent lung metastases,percutaneous ablation therapy has emerged as an important surgical alternative,and its clinical application has been increasing in recent years.Percutaneous ablation techniques mainly include radiofrequency ablation(RFA),microwave ablation(MWA),and cryoablation(CA).RFA produces thermal effect through high-frequency electrical current,and it is easy to operate and applicable for a wide range of treatments.MW A uses efficient microwave heating technique and its energy distribution is uniform,suitable for larger lesions.Through repeated freeze-thaw cycles CA destroys tumor tissues,which is particularly suitable for the lesions near important structures.Besides,percutaneous ablation combined with surgery,medication,etc.can be used for the treatment of pulmonary oligometastases from CRC,this kind of combination therapy has synergistic effect to enhance the curative efficacy.This paper aims to make a comprehensive review about the importance of treating pulmonary oligometastases from CRC,the efficacy,prognosis,and influencing factors of various percutaneous ablation techniques,and the application progress of ablation combined with other therapies.

Objective:To investigate the impact of diabetes mellitus (DM) and stroke on long-term outcomes in patients with acute coronary syndrome (ACS) undergoing percutaneous coronary intervention (PCI).Methods:Total 411 consecutive ACS patients undergoing PCI at the Ninth People′s Hospital of Zhengzhou between December 2014 and June 2018 were recruited, including 319 males and 92 females with a mean age of (64.7±10.1) years. These patients were divided into 4 groups according to the presence or absence of history of diabetes or stroke: non-DM non-stroke group ( n=192) , DM group ( n=140), stroke group ( n=41), and DM+stroke group ( n=38). The data of baseline demographic characteristics, clinical feature, coronary angiographic findings, and cardiovascular adverse events during long-term follow-up were obtained. Kaplan-Meier curves were used to investigate the long-term clinical outcomes among groups. Results:The mean interval of follow-up was (24.1±13.8) months. Patients with DM+stroke had the highest rates of non-fetal myocardial infarction (χ 2=24.932) , non-fetal stroke (χ 2=9.434) , hospitalization due to heart failure/angina (χ 2=69.290) , revascularization (χ 2=22.918) , cardiovascular death(χ 2=13.473)and all-cause death(χ 2=17.724)as well as hard endpoint events (the sum of non-fetal myocardial infarction, non-fetal stroke, and all-cause death) (χ 2=30.268)and combined major adverse cardiovascular events (MACE) (the sum of hard endpoint events, hospitalization due to heart failure/angina, and revascularization) (χ 2=119.556)among 4 groups(all P<0.01). In Kaplan-Meier survival analysis, the cumulative ratio of freedom from all-cause death decreased significantly in DM+stroke group compared with no DM no stroke group ( HR=17.121, 95 %CI: 2.527-115.934, P<0.01), but no statistical difference was observed in the cumulative ratio of freedom from all-cause death between DM+stroke group and DM group or stroke group respectively ( HR=3.178, 95 %CI: 0.744-13.582; HR=1.383, 95 %CI: 0.374-5.118; all P>0.05) . Meanwhile, patients with DM+stroke presented significantly lower cumulated ratio free from combined MACE than patients with non-DM non-stroke ( HR=5.423, 95 %CI:2.941-10.036, P<0.01), and the cumulated ratio free from combined MACE also decreased significantly in DM+stroke group as compared to DM group or stroke group respectively ( HR=1.859,95 %CI: 1.167-2.962; HR=1.991,95 %CI: 1.178-3.364; all P<0.01) . Conclusions:ACS patients with combined history of DM and stroke have a worse long-term outcomes after PCI than those with DM alone or stroke alone or without DM or stroke. DM and stroke seemed to have an additive effect on decrease in the cumulative ratio free from combined MACE in ACS patients following PCI.

Objective To approach the expression and significance of CD30 in Hodgkin lymphoma cells which were transfected with mtr Ⅱ gene. Methods The CD30 expression of Hodgkin lymphoma cells in those transfected with mtr Ⅱ gene was analysed by immunohistochemical technique respectively. Results The CD30 expression rate of Hodgkin lymphoma cells which were transfected with mtr Ⅱ gene was higher than that of Hodgkin lymphoma cells which weren't transfected with mtrⅡ gene (P ＜0.01). Conclusion The mtr Ⅱ gene may be related to the malignant transformation of Hodgkin lymphoma.

Objective To investigate the proliferative activities and significance of Hodgkin's disease cells which were transfected with mtr Ⅱ gene. Methods The ki67 and proliferating cell nuclear antigen (PCNA) expression in Hodgkin's disease cells transfected with mtr Ⅱ gene were determined with immunohistochemistry. Results The ki67 and PCNA expression in cells transfected with mtr Ⅱ gene was more than that of cells without mtrⅡ gene transfected (P<0.05). Conclusion The proliferative activities of Hodgkin's disease cells transfected with mtr Ⅱ gene increased obviously, which may be related to the progress of Hodgkin's disease.

Objective To approach the proliferative activities of Hodgkin's disease cells were transfected with mtrⅡ gene.Methods The ki67 and PCNA expression of Hodgkin's disease cells and those which were transfected with mtrⅡ gene by immunohistochemical technique respectively.Results The expression rate of ki67 and PCNA in Hodgkin's disease cells which were transfected with mtrⅡ gene was higher than that weren't transfected(P