Introduction: Translocase of inner mitochondrial membrane 8 homolog B (TIMM8B) is crucial for mitochondrial function, but its role in lung adenocarcinoma (LUAD) remains underexplored. Objective: This study investigates TIMM8B expression patterns, prognostic value, and potential therapeutic implications in LUAD. Methods: The expression and prognostic potential of TIMM8B in LUAD were analyzed using data from The Cancer Genome Atlas (TCGA), Genotype-Tissue Expression, Gene Expression Omnibus, and Gene Expression Profiling Interactive Analysis 2, with survival analysis performed through Kaplan–Meier plotter. The prognostic value was validated using a LUAD tissue microarray and a nomogram. TIMM8B-related differentially expressed genes were identified using TCGA and LinkedOmics, and were functionally annotated using the Gene Ontology and Kyoto Encyclopedia of Genes and Genomes databases. Immunological features were assessed using TCGA data through the XCELL and tumor immune dysfunction and exclusion algorithms. Associations among TIMM8B, m6A modification, ferroptosis-related genes, and tumor genetic mutations were analyzed using TCGA data. Drug response correlations were explored using the Genomics of Drug Sensitivity in Cancer and Comparative Toxicogenomics databases. TIMM8B-depleted LUAD cell lines were analyzed using ribonucleic acid sequencing and subjected to cell cycle analysis. Results: TIMM8B is overexpressed in multiple cancers, including LUAD. High TIMM8B expression correlates with poorer overall survival in LUAD. A nomogram incorporating TIMM8B and pathological tumor-node-metastasis stage showed reliable predictive performance. TIMM8B-related gene analyses suggest roles in cell adhesion, chromosome segregation, and critical cancer pathways. TIMM8B shapes an immunosuppressive tumor microenvironment in LUAD, affecting immune cell infiltration and immunotherapy response. Elevated TIMM8B expression is associated with TP53 mutations and chemotherapy resistance. Knockdown of TIMM8B in H1299 cells downregulates PD-L1, induces G1 phase arrest, and triggers a chemokine (C-C motif) ligand 2-mediated inflammatory response, highlighting roles in cell cycle regulation and inflammatory pathways. Conclusion: These findings underscore TIMM8B’s multifaceted role in cancer progression and its potential as a prognostic marker and therapeutic target in LUAD.

Background TIMM8B is crucial for mitochondrial function, but its role in lung adenocarcinoma (LUAD) remains unexplored. This study investigates TIMM8B expression patterns, prognostic value, and potential therapeutic implications in LUAD. Methods TIMM8B expression in cancers versus normal tissues was analyzed using TCGA, GTEx, and GEO datasets. Prognostic analysis was conducted with TCGA, GEPIA2, Kaplan-Meier plotter, and GEO datasets. Validation was performed using a LUAD Tissue Microarray (TMA). A nomogram for LUAD prognosis was developed and validated. TIMM8B-related DEGs were identified using TCGA and LinkedOmics, followed by GO and KEGG analysis. Immunological features were assessed using XCELL and TIDE with TCGA data, and its predictive value for immunotherapy was evaluated using the Kaplan-Meier plotter. Associations between TIMM8B, m6A, and ferroptosis-related genes were analyzed, and genetic mutation profiles were compared using TCGA data. Drug response correlations were explored using the GDSC and CTD databases. TIMM8B and PDL1 expression in cell lines was examined via Western blot. TIMM8B knockdown in LUAD cell lines was followed by RNA sequencing and bioinformatic analysis of DEGs, as well as cell cycle analysis. Results TIMM8B is overexpressed in multiple cancers, including LUAD. High TIMM8B expression correlates with poorer overall survival (OS) in LUAD. A nomogram incorporating TIMM8B and pTNM stage showed reliable predictive performance. TIMM8B-related gene analyses suggest roles in cell adhesion, chromosome segregation, and critical cancer pathways. TIMM8B shapes an immunosuppressive tumor microenvironment (TME) in LUAD, affecting immune cell infiltration and immunotherapy response. Higher TIMM8B expression is associated with TP53 mutations and chemotherapy resistance. Knockdown of TIMM8B in H1299 cells downregulates PDL1, induces G1 phase arrest, and triggers a CCL2-mediated inflammatory response, highlighting roles in cell cycle regulation and inflammatory pathways. Conclusions These findings underscore TIMM8B's multifaceted role in cancer progression and its potential as a prognostic marker and therapeutic target in LUAD.

Background:Currently, patients with cT1 stage non-small cell lung cancer measuring less than 2 cm are recommended to undergo sublobar resection. However, it should be noted that there is tumor heterogeneity within these lung nodules. Potential visceral pleural invasion (VPI) is regarded as a significant factor that contributes to local recurrence and poorer prognosis after sublobar resection and postoperative upstaging of the T-stage. Currently, there are no effective techniques for preoperative or intraoperative prediction of the status of VPI in lung nodules. The primary objective of this study is to develop a machine learning model for the non-invasive prediction of VPI, thereby providing surgical decision-making support for surgeons during operations. Methods:A total of 983 patients with nodules located within 5 mm distance from the pleura were included. Machine learning models were developed utilizing preprocessed 2D, 2.5D, and 3D computed tomography (CT) imaging data. These models were employed to predict the status of VPI, leveraging radiomics and deep learning techniques. The aforementioned three groups of data were further categorized into region of interest (ROI)-only (exclusively focused on the ROI) and ROI-rect (the minimum bounding rectangle or cuboid of the ROI) groups, based on whether they included images outside the ROI. Receiver operating characteristic (ROC) curves were created for the assessment of predictive accuracy across different models. Employing the Youden's index, patients were categorized into high-risk and low-risk groups based on the model's criteria, which was then followed by an in-depth analysis of overall survival rates among the distinct patient cohorts. Results:This study included a training cohort of 786 patients and a validation cohort of 197 patients. In comparison to radiomic and radiological models, deep learning models, especially the 2D-rect model, demonstrated better predictive performance. Although the 3D-ROI-only model exhibited the highest areas under the curve (AUC) value (0.952), its predictive performance for the status of VPI was found to be inferior according to the decision curve, calibration curve, and survival analysis. Conclusions:The developed deep learning signature offers a robust instrument for the precise prognostication of vascular invasion in stage cT1 lung adenocarcinoma, thereby enhancing stratification for prognostic evaluation. Moreover, the application of this advanced computational model aids in the refinement of therapeutic approach formulation for individuals diagnosed with cT1 lung adenocarcinoma.

Multiple primary lung cancer (MPLC) is an increasingly prevalent subtype of lung cancer. According to recent genomic studies, the different lesions of a single MPLC patient exhibit functional similarities that may reflect evolutionary convergence. We perform whole-exome sequencing for a unique cohort of MPLC patients with multiple samples from each lesion found. Using our own and other relevant public data, evolutionary tree reconstruction reveals that cancer driver gene mutations occurred at the early trunk, indicating evolutionary contingency rather than adaptive convergence. Additionally, tumors from the same MPLC patient are as genetically diverse as those from different patients, while within-tumor genetic heterogeneity is significantly lower. Furthermore, the aberrant molecular functions enriched in mutated genes for a sample show a strong overlap with other samples from the same tumor, but not with samples from other tumors or other patients. Overall, there is no evidence of adaptive convergence during the evolution of MPLC. Most importantly, the similar between-tumor diversity and between-patient diversity suggest that personalized therapies may not adequately account for the genetic diversity among different tumors in an MPLC patient. To fully exploit the strategic value of precision medicine, targeted therapies should be designed and delivered on a per-lesion basis.

To explore the efficiency of ectopic thymectomy by the three surgical approaches of trans-sternum, right unilateral thoracoscopy and thoracoscopic subxiphoid in patients with non-thymomatous myasthenia gravis. 155 consecutive non-thymomatous myasthenia gravis patients who underwent extended thymectomy by 3 approaches including trans-sternum, right unilateral thoracoscopy and thoracoscopic subxiphoid in 1st affiliated hospital of Sun Yat-Sen University from January 2017 to October 2019 were reviewed. Differences of perioperative clinical characteristics in three surgical approaches were analyzed. Time to onset of myasthenia gravis (early or late) (p = 0.018), blood loss (p < 0.001), duration of operation (p = 0.031), duration and volume of thoracic drainage (p = 0.039 and p = 0.026), length of hospitalization (p = 0.039), the efficiency of ectopic thymectomy (p = 0.037), and the detection rate of ectopic thymus in the second quadrant (p = 0.018) were different among the three surgical approaches. In univariate logistic regression analysis, higher efficiency of ectopic thymectomy were associated with transsternal (OR 2.36, 95% CI 1.32–4.22, p = 0.011) and thoracoscopic subxiphoid approaches (OR 2.07, 95% CI 1.12–3.82, p = 0.033). In the multiple logistic regression analysis, the transsternal approach (OR 2.02, 95% CI 1.10–3.71, p = 0.024) was an independent protective factor for the efficiency of ectopic thymectomy. Both the right unilateral thoracoscopic and thoracoscopic subxiphoid approaches have advantages over the transsternal approach in short-term postoperative recovery. Transsternal approach is still the best choice for ectopic thymectomy while thoracoscopic subxiphoid approach show the potential as an alternative way.

e21079 Background: Although the administration of immune checkpoint inhibitors (ICIs) and antiangiogenic agents in advanced non–small-cell lung cancer (NSCLC) has been well established, evidence supporting the combination of immune checkpoint inhibitors plus antiangiogenic drugs in previous treatment patients with advanced NSCLC is insufficient. We aimed to investigate the efficacy and safety of nivolumab combined with recombinant human endostatin (rh-Endostatin) as second-line or later treatment for advanced NSCLC. Methods: In this prospective and multicentre phase 2 trial we enrolled patients with advanced NSCLC who had not responded to standardized first-line treatment regimen from two cancer centres in China. Eligible patients were those aged 18-75 years without ICIs in first-line treatment who received nivolumab (3mg/kg, intravenous drip, day 1) every 2 weeks and rh-Endostatin (30 mg, 24-hour continous intravenous infusion，day 1–7) every 4 weeks till disease progression or discontinuation. The primary end points were objective response rate and safety. This study is registered with Chinese Clinical Trial Registry, number ChiCTR1900023664. Results: A total of 35 patients (median age, 60 years; range, 37-72 years) received nivolumab and rh-Endostatin. Median previous treated line of eligible patients was 2 lines (range, 1-7 lines). Patients received a median of 2 cycles of therapy (range, 1-14 cycles). Eleven of 33 evaluable patients achieved confirmed partial response with an objective response rate of 33.3% (11/33, 95% confidence interval [CI]: 17.2% – 49.4%) and disease control rate of 60.6% (20/33,95%CI:43.9%–77.3%). Median follow-up was 8.2 months (range: 0.9 –17.1). Median progression-free survival was 7.1 months (95% CI: 1.2m–13.0m), median overall survival was not reached and the 6-month overall survival rate was 54.5% (95% CI:37.6%–71.4%). The predominant grade 1-2 adverse events were thyroiditis, arrhythmia, hypertension. The grade 3 treatment-related adverse events were pneumonitis (3/35, 8.6%), hypertension (1/35, 2.9%) and atrial fibrillation (1/35, 2.9%), respectively. No grade 4 or 5 treatment-related adverse events were observed. Conclusions: To the best of our knowledge, this is the first prospective study that assessed nivolumab combined with rh-Endostatin as second-line or later treatment in pretreated patients with advanced NSCLC. In view of its encouraging efficacy and safety profile, nivolumab plus rh-Endostatin represents a promising treatment regimen in this patient population. Clinical trial information: ChiCTR1900023664.

Esophageal cancer (EC) is a highly malignant gastrointestinal tumor, and esophageal squamous cell carcinoma (ESCC) is one of the most common histological types of EC. MicroRNAs (miRNAs) are small noncoding RNAs closely related to tumorigenesis and tumor progression. In addition, Nestin is an intermediate filament protein (class VI) and contributes to the progression of numerous tumors. However, the correlation between miRNAs and Nestin in ESCC remains unclear. This study aimed to investigate the relationship between miR-204-5p and Nestin in ESCC. First, Nestin-related miRNAs in ESCC were explored using RNA sequencing. In ESCC tissues and cell lines, the expression of miR-204-5p was decreased detected by quantitative real-time polymerase chain reaction (qPCR), whereas Nestin protein level was upregulated identified by Western blotting (WB). Besides, Nestin was the direct target of miR-204-5p in ESCC determined via the luciferase reported assay. Moreover, miR-204-5p regulated Nestin to inhibit ESCC cell proliferation detected by the colony formation assay and promote ESCC cell apoptosis identified using the flow cytometry and TUNEL assay. Furthermore, miR-204-5p suppressed tumorigenesis in vivo evaluated by the murine xenograft tumor model. In conclusion, these results indicated that miR-204-5p inhibited cell proliferation and induced cell apoptosis in ESCC through targeting Nestin, which might provide novel therapeutic targets for ESCC therapy.

Although the National Comprehensive Cancer Network and the Chinese Society of Clinical Oncology guidelines recommend comprehensive genomic profiling of lung adenocarcinoma, it has not been widely applied in Chinese hospitals. This observational study aimed to determine real-world evidence of whether comprehensive genomic profiling can benefit the survival of patients with lung cancer. We investigated the frequency of genomic alterations, treatment strategies, and clinical outcomes in 233 patients with advanced non-small cell lung carcinoma who were routinely screened using a 508-gene panel. The most prevalent drivers were mutations of EGFR (51%), KRAS (9%), PIK3CA (7%), ALK (7%), MET (6%), and BRAF (5%). Mutations in tumor suppressor genes included TP53, KEAP1, RB1, PTEN, and APC. Median overall survival (OS) was significantly shorter among patients harboring KRAS (mutant, n = 17; WT, n = 154) and TP53 (mutant, n = 103; WT n =68) mutations (11.3 vs. 24.0 months; P = 0.16 and 18.7 vs. 28.7 months; P = 0.018, respectively). The OS was longer among patients with tumors harboring EGFR (P = 0.069) and ALK (P = 0.51) mutations. Most patients (65.4%) with the driver gene-positive (EGFR, ALK, and ROS1) tumors were received TKI treatment, whereas those with driver gene wild tumors (53.1%) chose platinum-based therapy. Univariate and multivariate analyses associated a shorter OS among patients with tumors harboring concomitant TP53 and EGFR mutations. These findings provide additional evidence from real-world on the potential importance of targeted therapies as a treatment option in NSCLC patients harboring clinically actionable mutation.

Background Single-port inflatable mediastinoscopy with simultaneous laparoscopic-assisted surgery for radical esophagectomy is a promising surgical method with high technical requirements and needs team cooperation. Therefore, it is necessary to define a learning curve to guide personnel training and improve the safety of these surgical techniques. Method This study prospectively analyzed the data of 79 consecutive patients, who underwent the surgery in the Fifth Affiliated Hospital of Sun Yat-sen University from October 2016 to May 2018. All of these patients were treated by the same surgical team with extensive experience in thoracotomy, laparotomy, thoracoscopic surgery and laparoscopic surgery. The learning curve was analyzed by cumulative summation (CUSUM) analysis, with the assessment of operative time, estimated blood loss, and postoperative complications. Result By analyzing these data, The scatter diagram of every measure showing a declining situation. The learning curve decreased beginning at 25 th operation. All patients were chronologically divided into two groups, the group 1(the first 25 patients) and the group 2 (the last 54 patients). The median estimated blood loss of group 2 was lower than group 1(200 vs 100ml, p <0.05). No other clinic or pathologic characteristics were observed as significantly different. Conclusion For a surgical team with extensive experience in thoracotomy, laparotomy, thoracoscopic surgery and laparoscopic surgery, 25 cases are needed before becoming proficient in this surgery.

Introduction. We conducted a cross-sectional study on children with steroid-resistant nephrotic syndrome (SRNS) in a single center in Southern China. Methods. A total of 166 SRNS cases in the Paediatric Nephrology Center of the First Affiliated Hospital of Sun Yat-Sen University from September 1, 2006, to August 31, 2016 were retrospectively analysed. The inclusion criteria were: 1) age ≤ 14 years, 2) diagnosed with SRNS, and 3) without purpura nephritis, immunoglobulin A nephropathy, lupus nephritis, or another secondary nephritis. Incidences of primary/ late steroid-resistance and curative effects were analysed. Results. The median follow-up time was 4.64 (2.64 to 8.11) years. There were 67 cases of complete remission (CR) (40.36%), 46 cases of partial remission (PR) (27.71%), 31 cases of no remission (NR) (18.67%), 18 cases of end-stage renal disease (ESRD, 10.84%, including 7 cases of kidney transplantation), and 4 cases of death due to hematoma and severe infection after renal biopsy; renal failure after progression to ESRD; sepsis during glucocorticoid (GC) + Cyclosporine A (CsA) treatment; and multiple organ failure at the onset of disease, respectively. For the 8 cases with gene mutation, unnecessary drug treatment should be reduced due to their low responsiveness to immunosuppressive treatment. Female, patients with hematuria, primary steroid-resistance (PSR) type and histopathologic focal segmental glomerulosclerosis (FSGS) were more likely to have higher ESRD rate. Subgroup analysis of ESRD suggested that female patients and patients with PSR type were more likely to develop ESRD. Cox-regression analysis showed that female (HR = 3.04, 95% CI: 1.18 to 7.86; P < .05), without hematuria (HR = 0.36, 95% CI: 0.14 to 0.91; P < .05), and LSR type (HR = 0.17, 95% CI: 0.04 to 0.74; P < .05) were significantly associated with ESRD. Kaplan-Meier survival analysis also showed the same trends. Conclusion. Of the 166 SRNS cases, 68.07% of patients achieved CR or PR, 18.67% of cases had NR, 10.84% of cases developed ESRD, and 2.41% of patients died during follow-up. Female gender, hematuria, and PSR type were positively associated with ESRD.

Abstract PurposeThis study aimed to investigate the relationship between miR-204-5p and Nestin in esophageal squamous cell carcinoma (ESCC). MethodsThe expression levels of miR-204-5p and Nestin were tested by quantitative real-time polymerase chain reaction (q-PCR) and Western blotting, respectively. The colony formation assay was used to assess cell proliferation. The flow cytometry and TUNEL assay were used to examine cell apoptosis. Tumorigenesis was evaluated using a murine xenograft tumor model. ResultsESCC tissues and cell lines exhibited decreased miR-204-5p expression and increased Nestin expression, while the opposite results were found in paired para-carcinoma tissues and esophageal epithelial cell lines. The Luciferase reported assay confirmed that Nestin was the direct target of miR-204-5p. In vitro , miR-204-5p inhibited cell proliferation and induced apoptosis through regulating Nestin expression. In vivo , miR-204-5p inhibited xenograft tumor formation. ConclusionIn conclusion, these results indicate that miR-204-5p inhibits cell proliferation and induces cell apoptosis in ESCC through regulating Nestin.

Background: Pneumonia is a common disease with high morbidity and even death. In our country, pneumonia is the leading cause of child death. Therefore, research on the pathogenesis of pneumonia can help improve the treatment of pneumonia. Long non-coding RNA (lncRNA) is an important regulator of disease development, and its regulatory mechanism is closely related to cellular processes. However, the function and regulatory network of lncRNA is not fully elucidated in pneumonia. Material/Methods: Quantitative real-time polymerase chain reaction (qRT-PCR) was applied to detect the expression of CRNDE and miR-141 in lipopolysaccharides (LPS)-induced MRC-5 cells and pneumonia tissues. MTT (3-(4,5-dimethylthiazol-2-yl)-2 5-diphenyl-2-tetrazolium) assay was used to assess cell proliferation. Flow cytometry assay was performed to detect cell apoptosis in LPS-induced MRC-5 cells. Enzyme-linked immunosorbent assay and western blot were used to measure the levels of interleukin (IL)-1 beta, IL-6, and tumor necrosis factor (TNF)-alpha, respectively. In addition, luciferase reporter assay and RNA immunoprecipitation (RIP) assay were applied to prove the relationship between CRNDE and miR-141. Results: In this study, we found that CRNDE expression was induced in LPS-induced MRC-5 cells and pneumonia tissues. Moreover, miR-141 expression was low in LPS-induced MRC-5 cells and was verified was a target miRNA of CRNDE by using luciferase reporter assay and RIP assay. The downregulation of CRNDE and upregulation of miR-141 promoted cell viability, inhibited cell apoptosis, as well as decreased the levels of IL-1 beta, IL-6, and TNF-alpha. Moreover, we demonstrated that si-CRNDE transfection increased cell viability and suppressed cell apoptosis and the levels of IL-1b, IL-6, and TNF-a, which were alleviated by anti-miR-141 transfection in LPS-induced MRC-5 cells. Conclusions: In this study, we found that downregulation of CRNDE and upregulation of miR-141 inhibited cell apoptosis and inflammation response and promoted cell viability in LPS-induced MRC-5 cells. Low CRNDE expression increased cell growth and suppressed inflammation response, which was impaired by inhibition of miR-141. These results suggested that a novel therapeutic target was found in pneumonia treatment.

Minimally invasive esophagectomy (MIE) has been developed for decades. However, conventional MIE requires transthoracic surgery, which can increase the risk of many perioperative cardiopulmonary complications. Therefore, mediastinoscopy-assisted transhiatal esophagectomy has been proposed, but the traditional surgical methods have shortcomings, such as unclear vision, especially during the dissection of mediastinal lymph nodes (LNs). A new approach for mediastinal lymphadenectomy under single-port inflatable mediastinoscopy with one left-neck incision is proposed. There are three difficulties in this procedure. (I) LNs along the left recurrent laryngeal nerve (RLN). After establishing pneumomediastinum, esophagectomy is performed over the aortic arch to the level of the lower edge of the left main bronchus, and lymphadenectomy along the left RLN is also accomplished during this process. (II) LNs along the right RLN. At the level of the lower edge of the right subclavian artery (RSA), between the trachea and the esophagus, instruments are used to access the right RLN. Lymphadenectomy of up to 2 cm can be accomplished at the upper edge of the RSA. (III) Subcarinal LNs. Between the trachea and esophagus, the left and right main bronchi are exposed along the trailing edge of the trachea down to the carina, and lymphadenectomy can be performed here. The surgical procedure described here in detail is the first mediastinal lymphadenectomy under mediastinoscopy with one single left-neck incision.

Background Role of biomarkers for promotion of tumor proliferation (BPTPs) and for promotion of apoptosis (BPAs) in thymic malignant tumors is still unclear. The purpose of this study was to evaluate the relationship between BPTPs and/or BPAs and malignancy of thymic malignant tumors. Methods Studies on thymic malignant tumors and biomarkers were searched in PubMed, ISI Web of Knowledge, and Embase databases, and all statistical analyses were conducted using Review Manager. Results Twelve articles related to biomarkers and thymic malignant tumors were selected and analyzed. A relationship between BPAs and Masaoka stage was demonstrated for four markers, namely Bax, p73, Casp-9 and Bcl-2, included 138 stage I/II patients and 74 stage III/IV patients, and BPAs were significantly correlated with high Masaoka staging ( P = 0.03). We further found a relationship between BPAs and degree of malignancy for four markers, namely Bax, p73, Casp-9 and Bcl-2, included 176 thymoma patients and 36 thymic carcinoma patients, and BPAs were significantly correlated with thymic carcinoma ( P = 0.010). In addition, a relationship between BPTP and Masaoka staging was demonstrated for seven markers, namely Podoplanin, Glut-1, Muc-1, Egfr, Igf1r, c-Jun, and n-Ras, included 373 patients with stage I/II and 212 patients with stage III/IV, and BPTPs were significantly correlated with high Masaoka staging ( P < 0.001). We also found a relationship between BPTPs and degree of malignancy for ten markers, namely Mesothelin, c-Kit (CD117), Egfr, Lat-1, Muc-1,Ema, Glut-1, Igf1r, c-Jun, and n-Ras, included 748 thymoma patients and 280 thymic carcinoma patients, and BPTPs were significantly correlated with thymic carcinoma (P < 0.001). Conclusion These findings show that high levels of BPTPs or BPAs are more closely related to thymic carcinoma and Masaoka stage III/IV, suggesting that BPTPs and BPAs may play an important role in the occurrence and development of thymic malignant tumors.

AbstractPurposeTo determine the postoperative effects of radiotherapy (PORT) on the local recurrence‐free survival (LRFS) and overall survival (OS) of stage III‐N2 non‐small‐cell lung cancer (NSCLC).Materials and Methods183 patients with resected stage III‐pN2 NSCLC from Hunan Cancer Hospital between 2013 and 2016 were divided into two groups for postoperative chemotherapy (POCT) (n = 105) or combination chemotherapy and radiotherapy (POCRT) (n = 78). The LRFS and OS were compared and the factors affecting local recurrence were illustrated in these two groups. The sites of failure based on the lobe of the primary tumor in two groups were described.ResultsPORT leads to a strikingly lower risk for local recurrence and brought superior OS benefit. For different pN2 Subclassification, Patients with multiple‐station pN2 ± pN1 disease had the worst LRFS (11 months) and single‐station pN2 + multiple station pN1 disease had a relatively short LRFS (24 months) in group POCT. Short LRFS is correlated with multiple‐station pN2, older age (Y > 55), patients with a high positive LN ratio > 1/3 and a poor tumor histological differentiation degree. In group POCT, the most frequent failure site occurs at the ipsilateral hilum (21.0%), the bronchial stump (20.0%), followed by LNs4R (19.0%), LNs4L (18.1%), LNs7 (15.2%), most of left‐sided tumors more frequently involved the contralateral mediastinum, whereas the ipsilateral recurrences dominated for right‐sided tumors, especially for LNs4R. In group POCRT, the highest failure site was the bronchial stump (11.5%), followed by LNs4L (8.97%), LNs1 (7.69%), the ipsilateral hilum (6.41%) and LNs4R (6.41%).ConclusionPORT remarkably reduced local recurrence and improved OS in stage III‐pN2 NSCLC, especially in the multiple‐station pN2 group.