Identification of immune-associated biomarker for predicting lung adenocarcinoma: bioinformatics analysis and experiment verification of PTK6.

BACKGROUND: Abnormal expression of protein tyrosine kinase 6 (PTK6) has been proven to be involved in the development of gynecological tumors. However, its immune-related carcinogenic mechanism in other tumors remains unclear. OBJECTIVE: The aim of this study was to identify PTK6 as a novel prognostic biomarker in pan-cancer, especially in lung adenocarcinoma (LUAD), which is correlated with immune infiltration, and to clarify its clinicopathological and prognostic significance. METHODS: The prognostic value and immune relevance of PTK6 were investigated by using bio-informatics in this study. PTK6 expression was validated in vitro experiments (lung cancer cell lines PC9, NCI-H1975, and HCC827; human normal lung epithelial cells BEAS-2B). Western blot (WB) revealed the PTK6 protein expression in lung cancer cell lines. PTK6 expression was inhibited by Tilfrinib. Colony formation and the Cell Counting Kit-8 (CCK-8) assay were used to detect cell proliferation. The wound healing and trans-well were performed to analyze the cell migration capacity. Then flow cytometry was conducted to evaluate the cell apoptosis. Eventually, the relationship between PTK6 and immune checkpoints was examined. WB was used to estimate the PD-L1 expression at different Tilfrinib doses. RESULTS: PTK6 was an independent predictive factor for LUAD and was substantially expressed in LUAD. Pathological stage was significantly correlated with increased PTK6 expression. In accordance with survival analysis, poor survival rate in LUAD was associated with a high expression level of PTK6. Functional enrichment of the cell cycle and TGF-ß signaling pathway was demonstrated by KEGG and GSEA analysis. Moreover, PTK6 expression considerably associated with immune infiltration in LUAD, as determined by immune analysis. Thus, the result of vitro experiments indicated that cell proliferation and migration were inhibited by the elimination of PTK6. Additionally, PTK6 suppression induced cell apoptosis. Obviously, PD-L1 protein expression level up-regulated while PTK6 was suppressed. CONCLUSION: PTK6 has predictive value for LUAD prognosis, and could up regulated PD-L1.

Corrigendum to "Comprehensive Humoral and Cellular Immune Responses to SARS-CoV-2 Variants in Diverse Chinese Population".

[This corrects the article DOI: 10.34133/2022/9873831.].

Comprehensive Humoral and Cellular Immune Responses to SARS-CoV-2 Variants in Diverse Chinese Population.

The SARS-CoV-2 variants have been emerging and have made great challenges to current vaccine and pandemic control strategies. It is urgent to understand the current immune status of various Chinese populations given that the preexisting immunity has been established by national vaccination or exposure to past variants. Using sera from 85 individuals (including 21 convalescents of natural infection, 15 cases which suffered a breakthrough infection after being fully vaccinated, and 49 healthy vaccinees), we showed significantly enhanced neutralizing activities against SRAS-CoV-2 variants in convalescent sera, especially those who had been fully vaccinated. The neutralizing antibodies against Omicron were detectable in 75% of convalescents and 44.9% of healthy vaccinees (p = 0.006), with a GMT of 289.5, 180.9-463.3, and 42.6, 31.3-59, respectively. However, the neutralizing activities were weaker in young convalescents (aged < 18 y), with a detectable rate of 50% and a GMT of 46.4 against Omicron. We also examined and found no pan-sarbecovirus neutralizing activities in vaccinated SARS-CoV-1 survivors. A booster dose could further increase the breadth and magnitude of neutralization against WT and variants of concern (VOCs) to different degrees. In addition, we showed that COVID-19-inactivated vaccines can elicit Omicron-specific T-cell responses. The positive rates of ELISpot reactions were 26.7% (4/15) and 43.8% (7/16) in the full vaccination group and the booster vaccination group, respectively, although without statistically significant difference. The neutralizing antibody titers declined while T-cell responses remain consistent over 6 months. These findings will inform the optimization of public health vaccination and intervention strategies to protect diverse populations against SARS-CoV-2 variants. Advances. Breakthrough infection significantly boosted neutralizing activities against SARS-CoV-2 variants as compared to booster immunization with inactivated vaccine. Vaccine-induced virus-specific T-cell immunity, on the other hand, may compensate for the shortfall. Furthermore, the public health system should target the most vulnerable group due to a poorer protective serological response in both infected and vaccinated adolescents.

HNRNPA2B1 Demonstrates Diagnostic and Prognostic Values Based on Pan-Cancer Analyses.

Some studies have suggested heterogeneous nuclear ribonucleoprotein A2/B1 (HNRNPA2B1) to be a promoter in cancer development. Nonetheless, no detailed pan-cancer investigation has been reported. Thus, this study explored the possible oncogenic role of HNRNPA2B1, such as its expression levels, gene alteration, protein-protein interaction network, immune infiltration, and prognostic value in different cancer types using The Cancer Genome Atlas web platform. Many types of cancer exhibit HNRNPA2B1 overexpression, which is notably associated with poor prognosis. We also found that HNRNPA2B1 with different methylation levels causes a varied prognosis in lung adenocarcinoma (LUAD). It is noteworthy that HNRNPA2B1 levels are connected with cancer-associated fibroblasts in cancers, such as adrenocortical carcinoma, LUAD, and stomach adenocarcinoma. In addition, HNRNPA2B1 participates in the spliceosome- and cell cycle-associated pathways. Finally, HNRNPA2B1 is highly valued in the diagnosis of LUAD, lung squamous cell carcinoma, breast invasive carcinoma, esophageal carcinoma, and liver hepatocellular carcinoma. This systematic study highlighted the role of HNRNPA2B1 in pan-cancer progression.

Long noncoding RNA NR2F1-AS1 stimulates the tumorigenic behavior of non-small cell lung cancer cells by sponging miR-363-3p to increase SOX4.

Long noncoding RNA (lncRNA), specifically the upregulation of lncRNA NR2F1 antisense RNA 1 (NR2F1-AS1), has been involved in the progression of non-small cell lung cancer (NSCLC), but the mechanisms that underlie this remain unclear. In this study, the expression of NR2F1-AS1, miR-363-3p, and SOX4 was assessed in NSCLC cells. A loss-of-function assay was used to measure the tumorigenicity of NSCLC cells. The glycolysis and glutamine metabolism of NSCLC cells was also measured via extracellular acidification rate, consumption of glucose and glutamine, and production of lactate and ATP. The relationships among NR2F1-AS1, miR-363-3p, and SOX4 were detected via dual-luciferase reporter assay. HK-2, GLS1, and SOX4 levels were also analyzed. We found that both NSCLC tissues and cells had higher levels of NR2F1-AS1. Silencing of NR2F1-AS1 inhibited the tumorigenicity of cells in vitro and reduced the glycolysis and glutamine metabolism of NSCLC cells. Regarding its mechanism, NR2F1-AS1 positively regulated the SOX4 level by sponging miR-363-3p. Furthermore, miR-363-3p inhibition or SOX4 overexpression reversed the repressing role of sh-NR2F1-AS1 in the tumorigenicity of NSCLC cells. In summary, NR2F1-AS1 promotes the tumorigenicity of NSCLC cells by regulating miR-363-3p/SOX4.

Circular RNA SOX13 promotes malignant behavior and cisplatin resistance in non-small cell lung cancer through targeting microRNA-3194-3p/microtubule-associated protein RP/EB family member 1.

Circular RNA (circRNA) presents an essential regulatory role in affecting the occurrence and acquired resistance in non-small cell lung cancer (NSCLC), but how circSOX13 impacts NSCLC is unclear. In this work it was found that compared with adjacent normal tissues, circSOX13 and the microtubule-associated protein RP/EB family member 1 (MAPRE1) were signally up-regulated in NSCLC while miR-3194-3p was signally lowered. Pulmonary function tests (PETs) revealed that knocking down circSOX13 or overexpressing miR-3194-3p inhibited NSCLC proliferation, invasion and migration but promoted its apoptosis. The promoting effect of overexpressing circSOX13 on NSCLC was reversed via knocking down MAPRE1. Additionally, knocking down circSOX13 reduced cisplatin resistance in NSCLC. Furthermore, circSOX13 mediated MAPRE1 expression via competitively binding miR-3194-3p to exert its tumorigenic impact. To conclude, this work clarified the carcinogenic impact of circSOX13-miR-3194-3p-MAPRE1 axis on NSCLC and DDP resistance. CircSOX13 can be a potential diagnostic marker and therapeutic target for NSCLC, thus providing a new insight for clinically reversing its acquired resistance.

The RNA N6 -methyladenosine modulator HNRNPA2B1 is involved in the development of non-small cell lung cancer.

The key N6  methyladenosine (m6 A) RNA methylation regulator is associated with multiple tumour progression. However, the m6 A-associated regulators that influence non-small cell lung cancer (NSCLC) development have not been fully clarified. The m6 A regulator expression pattern of NSCLC patients from The Cancer Genome Atlas (TCGA) dataset was identified. Aberrations of m6A modulators are related to NSCLC development via cBioPortal database. Furthermore, we found that IGF2BP2, IGF2BP3, HNRNPA2B1, and FTO are significantly correlated with advanced stage disease or clinical outcomes in NSCLC by UALCAN and Kaplan-Meier plot. Bioinformatics analysis showed that m6 A modulators (IGF2BP2, IGF2BP3, HNRNPA2B1, and FTO) are associated with immunomodulator and immune infiltration expression in NSCLC via the Tumor Immune Estimation Resource (TIMER) database. The co-expression between these m6A-associated modulators was analysed by protein-protein interaction networks. Finally, we found that HNRNPA2B1 promotes NSCLC development in vitro by regulating cell proliferation and metastasis functions via Cell Counting Kit 8 (CCK8) and transwell assay. Our study showed that HNRNPA2B1 is a promising target and biomarker for cancer therapy in NSCLC.

Salvianolic acid A blocks vasculogenic mimicry formation in human non-small cell lung cancer via PI3K/Akt/mTOR signalling.

Vasculogenic mimicry (VM) is associated with aggressive cancer cells. Salvianolic acid A (Sal-A), an antioxidant and anti-inflammatory agent, has bioactive properties from Salvia miltiorrhiza Bunge. Current investigation aspired to explore the activity of Sal-A in the VM formation of non-small cell lung cancer (NSCLC) and the mechanism underling this function. The CCK8, the scratch and boyden chemotaxis assay were presented to describe NSCLC cells viability, migration and invasion capabilities, respectively. The protein expression was verified by western blotting. In this report, Sal-A caused a reduction in viability, metastasis and capillaries structure formation of NSCLC cells. Additionally, Sal-A markedly prevented the key VM related proteins, containing EphA2, VE-cadherin and MMP2. Besides, Sal-A significantly diminished p-PI3K, p-Akt and p-mTOR level in NSCLC cells. More importantly, SC79 pretreatment reversed Sal-A inhibits NSCLC cells viability, metastasis and VM formation. These data exhibit that Sal-A could block VM network formation in NSCLC cells through modulating the PI3K/Akt/mTOR signalling pathway.

LncRNA MIR210HG Facilitates Non-Small Cell Lung Cancer Progression Through Directly Regulation of miR-874/STAT3 Axis.

BACKGROUND: Long noncoding RNAs are involved in the progression of multiple cancers. However, the expression and mechanism of microRNA (miR)210HG in non-small cell lung cancer (NSCLC) remain unclear. METHODS: The levels of miR210HG and miR-874 were measured by quantitative real-time polymerase chain reaction in NSCLC tissue samples and cells. Non-small cell lung cancer cell proliferation, migration, and invasion were measured by Cell Counting Kit-8 and transwell assays. Luciferase analysis confirmed the interaction between miR210HG and miR-874. RESULTS: Here, our data showed that miR210HG was overexpressed in NSCLC tissue samples and cells. In vitro functional assays showed that silencing miR210HG blocked NSCLC cell proliferation, migration, and invasion while promoting NSCLC cell radiosensitivity and chemoresistance. Mechanistically, miR-874 was directly regulated by miR210HG. Furthermore, miR-874 expression was reduced in NSCLC tissues and cells. The miR-874 mimic could mitigate the promoting effect of miR210HG on NSCLC cell progression. The data also showed that miR210HG promoted NSCLC cell progression through miR-181a expression by targeting STAT3. CONCLUSIONS: Our observations suggest that miR210HG is associated with NSCLC cell progression by regulating the miR-874/STAT3 axis.

Long noncoding RNA Linc01296 promotes hepatocellular carcinoma development through regulation of the miR-26a/PTEN axis.

Long noncoding RNA 01296 (Lnc01296) is dysregulated in malignant tumors. However, the detailed effect of Linc01296 on hepatocellular carcinoma (HCC) remains largely unknown. In this study, we identified the biological role of Linc01296 in HCC. The levels of Linc01296 in HCC tissues and a panel of cell lines were assessed by quantitative real-time polymerase chain reaction (qRT-PCR). The effects of Linc01296 on HCC progression were explored using a Cell Counting Kit-8 (CCK-8), flow cytometry, migration and Transwell invasion assays. The interactions among Linc01296, miR-26a and PTEN were determined using luciferase, RNA immunoprecipitation (RIP) and Western blot assays. Tumor xenograft models were utilized to confirm the in vivo functional roles of Linc01296 in HCC development. Linc01296 expression was increased in both HCC tissue samples and cell lines. Knockdown of Linc01296 suppressed HCC cell processes, such as proliferation, migration and invasion, and enhanced apoptosis in vitro; these effects were reversed by a miR-26a mimic or PTEN overexpression. Furthermore, knockdown of Linc01296 suppressed HCC growth in vivo. These findings indicated that Linc01296 is involved in HCC progression via regulating miR-26a/PTEN.

Long noncoding RNA LINC-PINT inhibits non-small cell lung cancer progression through sponging miR-218-5p/PDCD4.

Long noncoding RNA, long intergenic non-protein-coding RNA p53-induced transcript (LINC-PINT) was showed to be involved in cancer development. However, the biological effect of LINC-PINT on non-small cell lung cancer (NSCLC) remains unknown. Here, we aimed to investigate the role and underlying mechanism of LINC-PINT in NSCLC. Quantitative real-time polymerase chain reaction (qRT-PCR) was used to measure the level of LINC-PINT in NSCLC tissues and cell lines. Cell counting kit-8 (CCK-8), flow cytometry, migration and transwell invasion assays were used to investigate cell proliferation, cell cycle, cell migration and invasion, respectively. The targets of LINC-PINT were verified by both luciferase reporter assay and RNA immunoprecipitation assay. Tumour xenografts were used to reveal the effect of LINC-PINT on tumourigenesis in vivo. We observed that LINC-PINT expression increased in both NSCLC tissues and cell lines. Function assays exhibited that LINC-PINT reduced NSCLC cell proliferation, cell cycle, cell migration and invasion in vitro. We also indicated that LINC-PINT mediated inhibitory effect on cell proliferation, cell cycle, cell migration and invasion by miR-208a-3p/programmed cell death 4 (PDCD4) in NSCLC cells. These findings indicated that LINC-PINT functions as a tumour-suppressor that exerts important regulatory roles in NSCLC progression by sponging miR-208a-3p/PDCD4.

HDAC1 knockdown inhibits invasion and induces apoptosis in non-small cell lung cancer cells.

Non-small cell lung cancer (NSCLC) is a common malignant tumor. Although the abnormal expression and potential clinical prognostic value of histone deacetylase 1 (HDAC1) were recently discovered in many kinds of cancer, the roles and molecular mechanisms of HDAC1 in NSCLC is still limited. The CCK-8 assay is used to evaluate the viability of NSCLC cells. Downregulation of HDAC1 by shRNA. The TUNEL assay was used to evaluate the role of HDAC1 in NSCLC apoptosis. To evaluate the role of HDAC1 in NSCLC cells migration, the Boyden chamber transwell assay and wound healing assay were used. To evaluate the cells invasion, the matrigel precoated Transwell assay was used. Enzyme-linked immunosorbent assays (ELISAs) were used to detect the level of vascular endothelial growth factor (VEGF) and IL-8 in NSCLC. To investigate the role of HDAC1 in angiogenesis, the tube formation assay was investigated. In this study, we showed that HDAC1 expression was elevated in NSCLC lines compared to that in normal liver cells LO2. Furthermore, downregulation of HDAC1 inhibited cell proliferation, prevented cell migration, decreased cell invasion, reduced tumor angiogenesis and induced cell apoptosis. In summary, HDAC1 may be regarded as a potential indicator for NSCLC patient treatment.

Neural Stem Cell Transplantation Is Associated with Inhibition of Apoptosis, Bcl-xL Upregulation, and Recovery of Neurological Function in a Rat Model of Traumatic Brain Injury.

Traumatic brain injury (TBI) is a common disease that usually causes severe neurological damage, and current treatment is far from satisfactory. The neuroprotective effects of neural stem cell (NSC) transplantation in the injured nervous system have largely been known, but the underlying mechanisms remain unclear, and their limited sources impede their clinical application. Here, we established a rat model of TBI by dropping a weight onto the cortical motor area of the brain and explored the effect of engrafted NSCs (passage 3, derived from the hippocampus of embryonic 12- to 14-d green fluorescent protein transgenic mice) on TBI rats. Moreover, RT-PCR and Western blotting were employed to investigate the possible mechanism associated with NSC grafts. We found rats with TBI exhibited a severe motor and equilibrium dysfunction, while NSC transplantation could partly improve the motor function and significantly reduce cell apoptosis and increase B-cell lymphoma-extra large (Bcl-xL) expression at 7 d postoperation. However, other genes including Bax, B-cell lymphoma 2, Fas ligand, and caspase3 did not exhibit significant differences in expression. Moreover, to test whether Bcl-xL could be used as a therapeutic target, herpes simplex virus (HSV) 1 carrying Bcl-xL recombinant was constructed and injected into the pericontusional cortices. Bcl-xL overexpression not only resulted in a significant improvement in neurological function but also inhibits cell apoptosis, as compared with the TBI rats, and exhibits the same effects as the administration of NSC. The present study therefore indicated that NSC transplantation could promote the recovery of TBI rats in a manner similar to that of Bcl-xL overexpression. Therefore, Bcl-xL overexpression, to some extent, could be considered as a useful strategy to replace NSC grafting in the treatment of TBI in future clinical practices.

Dividing inferior pulmonary ligament may change the bronchial angle.

BACKGROUND: Whether dissecting the inferior pulmonary ligaments (IPLs) during superior video-assisted thoracoscopic (VATS) lobectomy for early stage lung cancer remains controversial. This study aimed to evaluate the influence of dissecting the IPLs during VATS superior lobectomy on bronchial distortion and recovery of pulmonary function. MATERIALS AND METHODS: This was a retrospective study of 72 patients with non-small cell lung cancer who underwent VATS superior lobectomy from March 2012-August 2013 at the First People's Hospital of Yunnan Province. Patients were grouped according to IPLs preservation (group P) or dissection (group D). The preoperative and postoperative pulmonary function and the postoperative complications were analyzed. The changes in bronchi angles and pulmonary capacity were measured using computed tomography. RESULTS: There were no significant differences in the complication rate and volume of chest drainage between the two groups. The changes in bronchus angle in group P were significantly smaller than those in group D after left lung operation (P = 0.046 at 3 mo; P = 0.038 at 6 mo); in the right lung, the changes were not significant between the two groups (P = 0.057 at 3 mo; P = 0.541 at 6 mo). The forced expiratory volume of 2% and forced expiratory volume in 1 s (FEV1%) were significantly better in group P than those in group D at 3 and 6 mo (P < 0.05). The pulmonary capacity in group P was significantly larger than that in group D at 6 mo (P = 0.002). CONCLUSIONS: Preservation of IPLs during VATS lobectomy might have an impact on the bronchus angle, lung function, and lung volume.

Change of CMTM7 expression, a potential tumor suppressor, is associated with poor clinical outcome in human non-small cell lung cancer.

BACKGROUND: CKLF-like MARVEL transmembrane domain-containing 7 (CMTM7) located at 3p22.3, is a frequent deletion site and a tumor suppressor gene (TSG) locus in many cancer, which suggests CMTM7 may be a potential TSG. The aim of this study was to investigate the correlations of CMTM7 expression and survival rate in patients with non-smallcell lung cancer (NSCLC). METHODS: Surgical specimens of 180 cases with pathologically confirmed NSCLC were grouped into 18 tissue microarray slides. CMTM7 expression in these specimens were detected by immunohistochemistry staining and representative cases were confirmed by Western blotting. Univariate and multivariate analyses were performed to identify the association of CMTM7 expression with pathological features and survival of patients with NSCLC. RESULTS: A total of 78.9% of the 180 patients had variations of CMTM7 protein expression, either up-regulated or down-regulated. Univariate analysis showed that the patients' survival rate after surgery was highly correlated with CMTM7 expression (P = 0.0091). In addition, prognostic factors were examined by multivariate Cox regression analysis, and results suggested that CMTM7 expression was a unique prognostic factor in NSCLC survival. CONCLUSIONS: The CMTM7 expression may be related to survival of patients with NSCLC and a unique prognostic factor. CMTM7 may play an important role in NSCLC development.

Influence on the behavior of lung cancer H1299 cells by silencing SLC35F2 expression.

BACKGROUND: To investigate the effects of RNA interference-mediated downregulation of Human Solute Carrier Family 35 member F2 (SLC35F2) expression on the biological behavior of lung cancer H1299 cells. METHODS: The lentiviral vector of small interfering RNA targeting SLC35F2 was introduced into H1299 cells by liposome-mediated transfection. Expression of the SLC35F2 protein was measured by western blot. The proliferation of H1299 cells was determined by Cell Counting Kit-8 assay. The migration of H1299 cells was measured by Transwell migration assay. Cell cycle analysis used fluorescence-activated cell sorting. RESULTS: SLC35F2 expression was markedly downregulated in H1299 cell clone (transfected with the lentiviral vector harboring small interfering RNA targeting SLC35F2). Proliferation decreased significantly compared with that of non-transfected H1299 cells. Transwell migration assay showed that fewer cells moved through the artificial basement membrane compared with untransfected H1299 cells (38.3 ± 5.7 vs. 113.5 ± 8.5, P < 0.05). The cell cycle of H1299 cells was changed, the percentage of H1299 cells in S and G2/M phases being significantly decreased compared with untransfected H1299 cells (S phase: 15.3% ± 3.0% vs. 27.0% ± 5.4%, P > 0.05; G2/M phase; 3.0% ± 1.1% vs. 10.5% ± 1.7%, P < 0.05), whereas the percentage of H1299 cells in G0/G1 phase increased markedly (81.7% ± 4.0% vs. 62.5% ± 1.9%, P < 0.05). CONCLUSION: RNA interference-mediated downregulation of SLC35F2 expression by lentiviral vector can attenuate the proliferation, migration and invasion of H1299 cells.

Completely video-assisted thoracoscopic lobectomy versus open lobectomy for non-small cell lung cancer greater than 5 cm: a retrospective study.

BACKGROUND: Completely video-assisted thoracoscopic lobectomy is a reasonable treatment for early-stage non-small-cell lung cancer (NSCLC). At present, the indication for this procedure is stage Ia and Ib peripheral lung cancer (≤ 5 cm); however, for larger tumors, it remains controversial whether this surgical technique is comparable to open lobectomy. This study aimed to evaluate the safety, completeness, and efficacy of thoracoscopic lobectomy, and to compare this technique with open lobectomy for the treatment of non-small-cell lung cancer when the tumor's diameter was greater than 5 cm. METHODS: From May 2001 to April 2011, 802 patients underwent a lobectomy for treatment of non-small-cell lung cancer at our center. In 133 patients, the tumor was > 5 cm. There were 98 men and 35 women, median age 63 years (range: 29 - 81 years). We divided the patients into two groups, group V (completely video-assisted thoracoscopic surgery), and group T (open lobectomy), and evaluated the two groups for age, gender, tumor size, pathological type, location, duration of surgery, blood loss, lymph node dissection, pathological stage, time of drainage, hospitalization, complications, overall survival and recurrence. RESULTS: There were 46 cases in group V and 87 cases in group T. Age, gender, tumor size, location, pathological type and stage were similar between the two groups. Group V had shorter operative duration ((186.5 ± 62.8) minutes vs. (256.7 ± 67.5) minutes, P < 0.001) and reduced bleeding ((218.5 ± 174.6) ml vs. (556.9 ± 187.2) ml, P < 0.001). There were no significant differences between the two groups in complications, lymph node dissection, time of drainage and hospitalization. The recurrence between the two groups was equivalent (2.4% vs. 3.8%, P = 0.670). The overall survival at 1, 2 and 3 years was 95.1%, 81.6% and 69.6% for group V and 88.3%, 78.8% and 64.0% for group T. Kaplan-Meier survival curves showed that there was no significant differences between the two groups (P = 0.129). CONCLUSIONS: Completely video-assisted thoracoscopic lobectomy was similar to open lobectomy in safety, completeness, and efficacy, but had a shorter operative duration, and reduced bleeding. This is a minimally invasive procedure that is feasible for a subset of non-small-cell lung cancer patients with tumor size > 5 cm.

[Application of endobronchial ultrasound-guided transbronchial needle aspiration in the diagnosis of isolated mediastinal lesions].

OBJECTIVE: To evaluate the role of endobronchial ultrasound-guided transbronchial needle aspiration (EBUS-TBNA) in the diagnosis of isolated mediastinal lesions. METHODS: A retrospective study was conducted of 73 consecutive patients with isolated mediastinal lesions of unknown origin without parenchymal lung abnormalities, who underwent EBUS-TBNA from September 2009 to April 2011. The patients who were nondiagnostic with EBUS-TBNA subsequently underwent surgical biopsies and a minimum of 6 months'clinical and radiologic follow-up. RESULTS: EBUS-TBNA achieved definitive diagnoses in 60 patients of the 73 patients (82.2%, 60/73). Malignancies were diagnosed in 23 patients and benignancies in 37. The sensitivity, specificity, and accuracy of EBUS-TBNA in distinguishing malignant mediastinal lesions were 95.8%(23/24), 100%(49/49) and 98.6%(72/73), respectively. EBUS was well tolerated by all of the patients with no complications. CONCLUSION: EBUS-TBNA of isolated mediastinal lesions is a minimally invasive and safe diagnostic technique with high yield.

[Preliminary comparison research of thoracoscopy and thoracotomy lobectomy for clinical N0 and post-operatively pathological N2 non-small cell lung cancer].

OBJECTIVE: To evaluate the safty, thoroughness and efficacy of the video-assisted thoracoscopic surgery compared with open thoracotomy, in treatment of patients with the preoperative staging of lymph node negative and postoperative pathological mediastinal lymph node positive (cN0-pN2) locally advanced non-small cell lung cancer(NSCLC). METHODS: We performed a retrospective review of 616 patients who underwent either VATS lobectomy or open thoracotomy from July 2000 to December 2009. Of which 386 patients were diagnosed with preoperative staging of lymph node negative(cN0) non-small cell lung cancer. Of the 386 patients 76 were diagnosed with postoperative pathological mediastinal lymph node positive (pN2). Twenty-nine patients were operated by video-assisted thoracoscopic surgery (VATS group), 47 patients were operated by open thoracotomy(T group).The patients' preoperative and intraoperative conditions, postoperative survival and recurrence, etc. were compared. RESULTS: The two groups were similar in age, gender distribution, pulmonary function, preoperative complications and the preoperative clinical stage. VATS group was slightly lower than T group in operation time, and blood loss. The station number of mediastinal lymph nodes dissection was (3.3±1.1) vs. (3.3±1.3), P=0.959; the number of lymph nodes dissected (12.7±8.9) vs. (10.5±7.2),P=0.260; positive lymph nodes / lymph nodes dissection 28.7% vs. 32.5%, P=0.592; the postoperative proportion of single-station N2 55.2% vs. 66.0%(P=0.189) in VATS group and T group, respectively. One, three-year disease-free survival rates after operation in VATS and T group were 82.6% vs.69.2%(P=0.088) and 49.3% vs. 51.3% respectively(P=0.996); one, three-year overall survival rates were 84.9% vs. 71.2%(P=0.149) and 64.0% vs. 42.7% (P=0.121). Both groups had the similar pattern of recurrence, most of which were distant metastases. CONCLUSION: With respect to the safety,thoroughness and recent effect, VATS is not inferior to open thoracotomy in the treatment of cN0-pN2 non-small cell lung cancer.

[A retrospective comparative study of the safety, completeness and efficacy of video-assisted thoracoscopic lobectomy versus open lobectomy for non-small-cell lung cancer patients whose tumor size was greater than 5 cm].

OBJECTIVE: To discuss the feasibility of the completely video-assisted thoracoscopic lobectomy for non-small-cell lung cancer (NSCLC) patients whose tumor size was greater than 5 cm. METHODS: From May 2001 to May 2010, 564 patients with NSCLC received lobectomy in our center, of whom, 114 had tumors whose diameters were larger than 5 centimeters (79 males and 35 females, their median age was 63.6 years, ranging from 29 to 81 years). We divided all the patients into two groups, group V (video-assisted thoracoscopic surgery) and group T (Thoracotomy). We compared all the factors, such as age, gender, tumor size, pathological type, location, operation time, blood loss, lymph node dissection, pathological stage, time of drainage, hospitalization, complications, overall survival and recurrence between the two groups. RESULTS: There were 72 cases of lobectomy, 18 cases of composite lobectomy and 24 cases of pneumectomy in all the patients. All of the procedures were carried out safely with no serious complications except for two prioperative deaths resulting from respiratory failure (in group T). There were 34 cases in group V and 80 cases in group T. Age, gender, tumor size, tumor location, pathological type and stage were similar between the two groups. The operation time of group V was significantly shorter than that of group T [(208.2±57.0) min vs. (256.4±70.3) min, P=0.001]. The blood loss of group V was much less than that of group T[(269.1±176.2) mL vs. (591.9±169.7) mL, P<0.001].There were no differences between the two groups, such as complications (13.3% vs. 21.3%, P=0.232), lymph node dissection stages (5.0±2.2 vs. 5.1±1.1, P=0.885) and numbers (18.5±9.6 vs. 19.2±9.1, P=0.714), time of drainage[(8.6± 3.9 d) vs. (9.0±5.0) d,P=0.693] and hospitalization (11.7±6.8) d vs. (12.8±7.1) d,P=0.431].The local recurrence between the two groups was equivalent(3.5% vs. 4.2%, P=0.857).The estimated overall survival at the end of 1, 2 and 3 years was 90.0%, 76.9% and 65.9% for group V and 80.3%, 62.9% and 55.3% for group T, respectively. Kaplan-Meier survival curves showed that there was no significant difference between the two groups (P=0.163). CONCLUSION: Completely video-assisted thoracoscopic lobectomy is a safe and feasible procedure for a part of non-small-cell lung cancer patients whose tumor size is greater than 5 cm.