The evolutionarily conserved Integrator complex, which is composed of over 10 subunits, orchestrates diverse RNA-processing events such as 3'-end maturation of small nuclear RNAs (snRNAs), transcription termination of RNA Polymerase II, and DNA damage response signaling pathways; however, the functional roles of individual Integrator complex subunits in lung adenocarcinoma (LUAD) remain poorly characterized, and this study aimed to systematically investigate the potential oncogenic functions and prognostic values of these subunits in LUAD. To achieve this goal, the expression profiles of Integrator complex subunits were profiled using transcriptomic data from the The Cancer Genome Atlas (TCGA) database, survival analyses (including Kaplan-Meier and Cox regression models) were performed to evaluate the correlations between subunit expression levels and patient survival outcomes (overall survival (OS) and disease-free survival (DFS)), co-expression network analysis was conducted to annotate the potential biological functions of key subunits, and functional validation was performed using CCK-8 assays and flow cytometry to assess the impact of INTS7 depletion on cell proliferation and cycle progression in LUAD cell lines. The findings of this study showed that Integrator complex subunits were significantly overexpressed in LUAD tissues compared to normal lung parenchyma; among these subunits, INTS7 expression was most strongly associated with shortened OS and DFS, indicating its pivotal role in LUAD pathogenesis, while bioinformatics analyses revealed that INTS7 is involved in regulating critical biological processes including cell cycle progression, transcriptional regulation, and RNA metabolism, and loss-of-function experiments demonstrated that genetic silencing of INTS7 significantly inhibited cell proliferation and induced cell cycle arrest in LUAD cells. Ultimately, this study provides the first evidence that INTS7, a core component of the Integrator complex, serves as a functional and prognostic regulator in LUAD, highlighting its potential as a therapeutic target for this malignancy.
OBJECTIVE:This study aimed to identify biomarkers of esophageal cancer and elucidate their mechanisms of action in esophageal cancer. METHODS:Differential protein expression between esophageal tumor tissue and adjacent normal tissue was analyzed using proteomics in a mouse model of esophageal cancer. Differential proteins were identified through bioinformatics analysis. The mechanisms of action of differential proteins in esophageal cancer were validated using techniques such as western blotting and immunohistochemistry. RESULTS:Proteomic analysis revealed that IL-38 exhibited the greatest differential expression. Molecular biology techniques including western blotting and immunohistochemistry demonstrated that IL-38 modulates Regulatory T cell (Treg)/ T helper 17 cell (Th17) balance through the Sirtuin 1 (SIRT1)/ hypoxia-inducible factor 1-alpha (HIF-1α) signaling pathway in esophageal cancer. CONCLUSION:IL-38 is a novel biomarker for esophageal cancer and regulates Treg/Th17 balance through the Sirt1/HIF-1α signaling pathway, providing new insights for the treatment of esophageal cancer.
BackgroundLung adenocarcinoma (LUAD) has a complex tumor heterogeneity. Our research attempts to clearness LUAD subtypes and build a reliable prognostic signature according to the activity changes of the hallmark and immunologic gene sets.MethodsAccording to The Cancer Genome Atlas (TCGA) - LUAD dataset, changes in marker and immune gene activity were analyzed, followed by identification of prognosis-related differential gene sets (DGSs) and their related LUAD subtypes. Survival analysis, correlation with clinical characteristics, and immune microenvironment assessment for subtypes were performed. Moreover, the differentially expressed genes (DEGs) between different subtypes were identified, followed by the construction of a prognostic risk score (RS) model and nomogram model. The tumor mutation burden (TMB) and tumor immune dysfunction and exclusion (TIDE) of different risk groups were compared.ResultsTwo LUAD subtypes were determined according to the activity changes of the hallmark and immunologic gene sets. Cluster 2 had worse prognosis, more advanced tumor and clinical stages than cluster 1. Moreover, a prognostic RS signature was established using two LUAD subtype-related DEGs, which could stratify patients at different risk levels. Nomogram model incorporated RS and clinical stage exerted good prognostic performance in LUAD patients. A shorter survival time and higher TMB were observed in the high-risk patients.ConclusionsOur findings revealed that our constructed prognostic signature could exactly predict the survival status of LUAD cases, which was helpful in predicting the prognosis and guiding personalized therapeutic strategies for LUAD.
Lung adenocarcinoma (LUAD) is a study that examines the prognostic value of lactate metabolism genes in tumor cells, which are associated with clinical prognosis. We analyzed the expression and clinical data for LUAD from The Cancer Genome Atlas database, using the GSE68465 dataset from the Gene Expression Omnibus and the MSigDB database. LASSO Cox regression and stepwise Cox regression were used to identify the optimal lactate metabolism gene signature. Differences in immune infiltration, tumor mutation burden (TMB), and response to immune checkpoint blockade (ICB) therapy were evaluated between groups. LASSO and Cox regression analyses showed an eight-lactate metabolism gene signature for model construction in both TCGA cohort and GSE68465 data, with higher survival outcomes in high-risk groups. The lactate metabolism risk score had an independent prognostic value (hazard ratio: 2.279 [1.652-3.146], P < .001). Immune cell infiltration differed between the risk groups, such as CD8+ T cells, macrophages, dendritic cells, mast cells, and neutrophils. The high-risk group had higher tumor purity, lower immune and stromal scores, and higher TMB. High-risk samples had high tumor immune dysfunction and exclusion (TIDE) scores and low cytolytic activity (CYT) scores, indicating a poor response to ICB therapy. Similarly, most immune checkpoint molecules, immune inhibitors/stimulators, and major histocompatibility complex (MHC) molecules were highly expressed in the high-risk group. The 8-lactate metabolism gene-based prognostic model predicts patient survival, immune infiltration, and ICB response in patients with LUAD, driving the development of therapeutic strategies to target lactate metabolism.
Mitochondrial DNA is implicated in hypertrophic cardiomyopathy (HCM) development. We aimed to identify valuable mtDNAs that contribute to the development of HCM. Differentially expressed mitochondrial DNAs (DEMGs) between HCM and controls were screened. GO and KEGG functional enrichment analyses were performed, and the optimum genes were explored using the LASSO regression mode and SVM-RFE model. A diagnostic scoring model was constructed and verified using ROC curves. Mitochondria-based subtypes were identified. Immune performance among the subtypes including immune cells, immune checkpoint genes, and HLA family genes was analyzed. Finally, an mRNA-transcription factor (TF)-miRNA network was constructed using Cytoscape software. Twelve DEMGs in HCM were selected. Among them, 6 DEMGs, including PDK4, MGST1, TOMM40, LYPLAL1, GATM, and CPT1B were demonstrated as DEMGs at the point of intersection of Lasso regression and SVM-RFE. The ROC of the model for the training and validation datasets was 0.999 and 0.958, respectively. Two clusters were divided, and 4 immune cell types were significantly different between the 2 clusters, including resting mast cells, macrophages M2, and plasma cells. Nine upregulated KEGG pathways were enriched in cluster 1 vs. cluster 2 including O-glycan biosynthesis, the ErbB signaling pathway, and the GnRH signaling pathway. Meanwhile, 49 down-regulated pathways were enriched such as the toll-like signaling pathway and natural killer cell-mediated cytotoxicity pathway. The 6 gene-based mRNA-TF-miRNA networks included other 133 TFs and 18 miRNAs. Six DEMGs in HCM, including PDK4, MGST1, TOMM40, LYPLAL1, GATM, and CPT1B, can be indicative of HCM prognosis or disease progression.
Objective: Abnormal DNA methylation can regulate carcinogenesis in lung adenocarcinoma (LUAD), while transcription factors (TFs) mediate methylation in a site-specific manner to affect downstream transcriptional regulation and tumor progression. Therefore, this study aimed to explore the TF-methylation-gene regulatory relationships that influence LUAD prognosis. Methods: Differential analyses of methylation sites and genes were generated by integrating transcriptome and methylome profiles from public databases. Through target gene identification, motif enrichment in the promoter region, and TF prediction, TF-methylation and methylation-gene relation pairs were obtained. Then, the prognostic TF-methylation-gene network was constructed using univariate Cox regression analysis. Prognostic models were constructed based on the key regulatory axes. Finally, Kaplan-Meier curves were created to evaluate the model efficacy and the relationship between candidate genes and prognosis. Results: A total of 1878 differential expressed genes and 1233 differential methylation sites were screened between LUAD and normal samples. Then 10 TFs were predicted to bind 144 enriched motifs. After integrating TF-methylation and methylation-gene relations, a prognostic TF-methylation-gene network containing 4 TFs, 111 methylation sites, and 177 genes was constructed. In this network, ERG-cg27071152-MTURN and FOXM1-cg19212949-PTPR regulatory axes were selected to construct the prognostic models, which showed robust abilities in predicting 1-, 3-, and 5-year survival probabilities. Finally, ERG and MTURN were downregulated in LUAD samples, whereas FOXM1 and PTPR were upregulated. Their expression levels were related to LUAD prognosis. Conclusion: ERG-cg27071152-MTURN and FOXM1-cg19212949-PTPR regulatory axes were proposed as potential biomarkers for predicting the prognosis of LUAD.
Objective:To compare effect of internal fixation of ribs assisted by complete thoracoscopy and thoracotomy for flail chest.Methods:A retrospective cohort study was used to analyze the clinical data of 86 patients with flail chest treated at No.2 Hospital of Nanping City and 900th Hospital of Joint Logistics Support Force between January 2019 and December 2020, including 58 males and 28 females; aged 25-69 years [(42.9±9.5)years]. A total of 45 patients underwent internal fixation of ribs assisted by complete thoracoscopy (thoracoscopy group), and 41 patients by thoracotomy (thoracotomy group). The operation time, number of fixed ribs, intraoperative blood loss, ventilation time, postoperative length of hospital stay, hemodynamic indicators [partial pressure of oxygen (PaO 2), partial pressure of carbon dioxide (PaCO 2), oxygenation index (PaO 2/FiO 2)] before surgery and at 1 day after surgery, respiratory function [forced vital capacity (FVC), forced expiratory volume in one second (FEV1), maximal voluntary ventilation (MVV)] at 1, 3, 6 and 12 months after surgery and postoperative complications were compared between the two groups. Results:All patients were followed up for 12-18 months [(14.1±1.9)months]. Thoracoscopy group showed prolonged operation time [(139.5±36.4)minutes vs. (114.8±32.5)minutes], reduced intraoperative blood loss [(124.6±42.4)ml vs. (198.6±62.6)ml] as well as shortened ventilation time [(4.0±1.1)days vs. (6.7±1.6)days] and postoperative length of hospital stay [(14.9±2.4)days vs. (17.9±3.7)days] when compared with thoracotomy group (all P<0.01). There was no statistical significance in the number of fixed ribs between the two groups ( P>0.05). There were no statistical differences in PaO 2, PaCO 2 or PaO 2/FiO 2 between the two groups before surgery (all P>0.05). At day 1 after surgery, the PaO 2 and PaO 2/FiO 2 in thoracoscopy group were (86.2±5.4)mmHg and 321.4±36.1, higher than (80.1±6.2)mmHg and 286.0±29.3 in thoracotomy group (all P<0.01); the PaCO 2 was (37.4±2.4)mmHg in thoracoscopy group, lower than (40.0±3.1)mmHg in thoracotomy group ( P<0.01). At 1 month, 3 months, 6 months and 12 months after surgery, the FVC was (75.5±10.9)%, (84.5±10.5)%, (93.1±12.8)% and (102.6±17.5)% in thoracoscopy group, higher than (69.2±9.9)%, (78.3±8.9)%, (86.2±10.4)% and (92.4±14.8)% in thoracotomy group; the FEV1 was (76.9±9.3)%, (88.4±12.9)%, (92.4±13.9)% and (98.5±10.6)% in thoracoscopy group, higher than (72.9±8.5)%, (82.8±11.4)%, (86.4±12.7)% and (93.5±11.9)% in thoracotomy group; the MVV was (78.3±13.4)L/min, (87.5±13.5)L/min, (94.6±14.7)L/min and (100.1±11.9)L/min in thoracoscopy group, higher than (72.5±11.6)L/min, (80.5±12.7)L/min, (86.5±13.5)L/min and (92.8±10.3)L/min in thoracotomy group (all P<0.05). There were no thoracic deformities in the two groups after surgery. There was no statistical significance in incision infection rate between the two groups ( P>0.05). The incidence rate of pulmonary infection, atelectasis and pleural effusion was 11.1% (5/45), 6.7% (3/45) and 11.1% (5/45) in thoracoscopy group, lower than 29.3% (12/41), 24.4% (10/41) and 31.7% (13/41) in thoracotomy group (all P<0.05). Conclusion:Although internal fixation of ribs with complete thoracoscopy has longer surgical time than thoracotomy in the treatment of flail chest, it can decrease intraoperative blood loss, ventilation time and length of hospital stay and is more conducive to improving the respiratory function and reducing complication rate.
目的 探讨食管癌根治术患者癌组织中血红素加氧酶-1(HO-1)、血管内皮细胞生长因子受体-3(VEGFR-3)表达与其远期预后的关系.方法 取76例食管癌患者术后的癌组织及距瘤体5cm以上的正常组织,比较不同组织、食管癌不同病理特征患者HO-1、VEGFR-3表达情况,分析患者预后的影响因素.结果 食管癌组织HO-1、VEGFR-3阳性表达率高于正常组织(P<0.05).食管癌组织HO-1阳性表达率比较Ⅰ~Ⅱ期
Backgrounds: Esophageal carcinoma (EC), a type of malignant tumor originating from the esophageal mucosa, is frequently encountered in clinical practice. Fatty acids contribute to the polarization of tumor-associated macrophage to the immunosup-pressive M2 phenotype. Fatty acid metabolism is an essential factor in tumor development and progression.Methods: EC expression and clinical data were downloaded from the Cancer Genome Atlas database and GSE53625 dataset. Fatty acid metabolism gene sets were downloaded from the Msigdb database. Differentially expressed fatty acid-related genes (DFAGs) in tumor and normal samples were screened using a t-test, and their prognostic value was investigated. Optimal prog-nostic DFAGs were identified to establish the fatty-acid-risk score (FARS) model. A nomogram was then established based on the independent prognostic factors. Associations between the FARS and clinical features, immune infiltration, tumor mutation burden (TMB), drug sensitivity, and tumor immune dysfunction and exclusion (TIDE) were analyzed using the prophetic pack-age.Results: Six prognostic DFAGs were identified from 161 DFAGs and 13 prognostic genes. Three genes, PDHA1, PTGES3, and CPT2, were identified as optimal prognostic DFAGs to establish the FARS model. Patients with high FARS tended to present shorter survival times in the Cancer Genome Atlas (TCGA) database and GSE53625 cohorts. The tumor stage and FARS were identified as independent prognostic factors for establishing the nomogram. The nomogram showed high conformance with actual survival in predicting 1-, 3-, and 5-year survival rates. High-FARS groups had a high abundance of infiltrating M2 macrophages and higher TMB. Patients with high TMB tended to have low survival. High FARS also correlated with higher sensitivity to cisplatin, gemcitabine, and paclitaxel and a high TIDE score, indicating a poor response to immune checkpoint blockade (ICB) therapy.Conclusions: Predicting model including DHA1, PTGES3 and CPT2 was established. These genes could predict overall EC survival, chemosensitivity, and immunotherapy response and were correlated with aggressive clinicopathologic features.
目的 探讨低分子肝素对食管癌术后患者深静脉血栓形成的预防效果.方法 收集2017年1月至2020年6月在中国人民解放军联勤保障部队第九〇〇医院接受食管癌手术治疗的168例患者临床资料,并根据术后抗凝药物使用情况将其分为对照组(n=76,术后采取常规抗凝干预)和观察组(n=92,术后采取常规抗凝干预+低分子肝素).比较两组患者治疗前后的凝血功能指标[血小板计数(PLT)、凝血酶原时间(PT)、活化部分凝血活酶时间(APTT)、纤维蛋白原(Fib)、D-二聚体(D-D)]、血液流变学指标(全血高切黏度、全血中切黏度、全血低切黏度)、术后胸腔积液引流量、术后并发症发生情况.结果 治疗后,观察组患者的PLT少于对照组患者,Fib、D-D水平均低于对照组患者,PT、APTT均长于对照组患者,差异有统计学意义(P<0.05).治疗后,观察组患者的全血高切黏度、全血中切黏度、全血低切黏度均低于对照组患者,差异均有统计学意义(P<0.05).术后,两组患者的胸腔积液引流量比较,差异无统计学意义(P>0.05).术后,两组患者的血栓性并发症发生率比较,差异有统计学意义(P=0.020).两组患者切口感染的发生率比较,差异无统计学意义(P>0.05).结论 对食管癌术后患者适当给予低分子肝素进行抗凝治疗,可以在短期内有效改善凝血功能指标及血液流变学指标,降低术后血栓性并发症的发生风险,用药安全性较高.
目的 建立CT辅助下肺内置入金属导丝模拟巴马小型猪肺内异物的模型,探索该模型用于研究CT引导下穿刺注射医用胶精准定位肺内异物后行胸腔镜下肺内异物取出术的可行性及安全性.方法 选取4只巴马小型猪,麻醉后CT引导下在巴马小型猪的右侧肺内置入2 cm金属导丝模拟肺内异物.CT扫描确定异物位置后穿刺注射医用胶精准定位肺内异物,然后行胸腔镜下肺内异物取出术.结果 4只巴马小型猪均成功建立CT辅助定位肺内置入金属导丝模拟肺内异物的模型,操作时间6~9 min,平均(7.50±1.29)min;均CT引导下穿刺注射医用胶,定位操作时间18~25 min,平均(21.25±2.99) min;定位后出现气胸1只(25%),气胸量较小,未行处理,无血胸、肺栓塞等其他并发症.均完成胸腔镜下肺内异物取出术,手术时间46~93 min,平均(66.00±20.12)min;其中术中确定异物位置时间7~11 min,平均(8.75±1.71)min;解剖证实切开离体猪肺后,医用胶胶团位于肺内异物旁,胶团直径大小8~12 mm,平均(9.50±1.91)mm;胶团与肺内异物的距离9~13 mm,平均(11.00±1.83)mm;定位成功率为100%.结论 建立CT辅助定位肺内置入金属导丝模拟巴马小型猪肺内异物的模型,证实了该模型用于研究CT引导下穿刺注射医用胶精准定位异物、实施胸腔镜下肺内异物取出术是安全、可行的,为进一步临床应用奠定了基础.
目的 探讨完全单孔胸腔镜肺叶切除在高龄肺癌患者中的临床应用价值.方法 2018年2月至2019年4月,采用单孔全胸腔镜肺叶切除治疗高龄(73.1±5.9)岁肺癌患者45例,进镜和操作均位于同一个孔,取第5肋间,切口长3~5 cm,术后常规放置2根胸腔闭式引流管.结果 全组无手术死亡,无中转开胸,无严重并发症发生.手术时间(121.5±33.2)min,术中出血量(61.4土12.4)mL.术后胸腔引流(3.6±1.3)d,术后住院时间(6.6±2.3)d.清扫淋巴结(15.4±4.7)枚.结论 单孔全胸腔镜肺癌根治术在高龄患者中应用安全、可靠,值得临床推广应用.
Background: The epidermal growth factor receptor (EGFR) mutation status related to the treatment approach for advanced non-small cell lung cancer (NSCLC) patients. This study aimed to evaluate the diagnostic accuracy of peripheral blood circulating tumor DNA (ctDNA) in EGFR mutated advanced NSCLC patients. Method: The related database was systematically searched with keywords until January 19, 2020. Studies contained the histopathological and cytological advanced NSCLC samples were included, and the diagnostic data were recorded for calculating sensitivity and specificity.I(2)statistics were used for detecting heterogeneity across studies, and the meta-regression was performed to seek the source of heterogeneity. Result: A total of 32 studies with 4527 advanced NSCLC patients were included in our meta-analysis. Among them, 87% of the patients were diagnosed as stage IV. The pooled sensitivity of peripheral blood ctDNA was 0.70 (95% CI: 0.63-0.75,I-2 = 81.76) and the pooled specificity was 0.98 (95% CI: 0.96-0.99,I-2 = 88.33). The meta-regression showed that the prospective study design and the ARMS detection method were the main source of heterogeneity for sensitivity (P < .05), and the publication country (Asia or non-Asia) was the main source of heterogeneity for specificity (P < .01). Conclusion: ctDNA biopsy has high specificity and diagnostic accuracy in detection of EGFR mutation in advanced NSCLC patients. When the ctDNA gene test result is negative, we should fully consider the risk of missed diagnosis, and further tissue biopsy is still needed to undertake.
Non-small cell lung cancer (NSCLC) has been considered to be the most common category of lung cancer, comprising approximately 80% of lung cancers. Long non-coding RNAs (lncRNAs) were diffusely documented to modulate carcinogenesis or progression of tumours. However, the role of DDX11-AS1 was still unclear in NSCLC. Bioinformatics analysis and experimental assays including hematoxylin and eosin (H&E) staining, RT-qPCR, colony formation, CCK-8, flow cytometry, western blot and xenograft assays were applied to investigate the biological role and molecular mechanism of DDX11-AS1 in NSCLC. The level of lncRNA DDX11-AS1 was up-regulated in NSCLC tumour tissues and cells. In function aspect, knockdown of DDX11-AS1 caused an apparent inhibitive effect on cell proliferation in vitro and in vivo. DDX11-AS1 inhibition promoted cell apoptosis in vitro. In mechanism, the protein level of phosphorylated AKT was reduced by DDX11-AS1 inhibition but increased by DDX11-AS1 overexpression. These results indicated that DDX11-AS1 exacerbated NSCLC progression via activating PI3K/AKT signalling pathway. All in all, DDX11-AS1 promotes NSCLC development via regulating PI3K/AKT signalling.
Objective Preliminary study on the clinical effect of preoperative ultrasound endoscopy combined with stai-ning labeling technique to locate the actual boundary of esophageal and gastric cancer Methods From September 1, 2015 to October 30, 2017, 18 patients with esophageal adenocarcinoma were enrolled in this study. The actual boundaries of esophage-al and gastric-derived adenocarcinoma lesions were localized by endoscopic ultrasonography and staining. There were 10 males and 8 females. After completing the preoperative examination, 1-2 days before operation, endoscopic ultrasonography was used to locate the edge of the lesion. Two point injection of carbon nano suspension was used to mark the location of 1cm at the lon-gest distance from the longitudinal axis of the tumor. According to the length of longitudinal axial staining, the thoracotomy was performed. Intraoperative proximal margin resection was used to send frozen pathology. According to the results of freezing, the operation was decided. After the operation, the specimens from the margin of the tumor were segmented into paraffin section, which was about 0. 5cm in each segment, and the tumor cells were observed under the electron microscope at all levels of the paraffin sections. Results The average time of preoperative endoscopic ultrasonography staining was(10. 16 ± 1. 38) min, and the diameter of nano carbon diffusion was(1.43 ±0.41)cm. All patients in the operation could clearly see the nano carbon staining area under the naked eye. In the field, the average time of locating lesions was(1.27 ±0.53)min. 5 patients under-went thoracoabdominal surgery and 13 underwent abdominal surgery. The average length of the cut margin of the tumor was(4. 74 ±1.12)cm, and the frozen pathology of the incision margin was negative, and no additional operation was performed. The routine pathology confirmed that all the specimens were negative. Conclusion The staining and labeling technique for adeno-carcinoma of the esophagogastric junction under endoscopic ultrasonography can detect the tumor edge and the scope of invasion accurately. It provides guidance and guarantee for the smooth implementation of AEG precision surgery. It is a safe, rapid and effective positioning technique.
Background: Immunoscore, as a prognostic tool defined to quantify in situ immune cell infiltrates, appears to be superior to the TNM staging system. In esophageal squamous cell carcinoma (ESCC), no immunoscore has been established; however, in situ tumor immunology is recognized as highly important. Our study aimed to construct a comprehensive immunoprofile for ESCC. Methods: The infiltration of four immune cell types (CD8+/CD4+/Foxp3+/CD33+ cells), the expression of both inhibitory (PD-1/PD-L1/Tim-3/LAG-3) and stimulatory checkpoints (OX-40/ICOS), and IDO1 were evaluated by IHC staining and multi-color immunofluorescence in two independent cohorts (95 patients in the primary cohort and 55 patients in the validation cohort). The association with patients' overall survival was analyzed by the Kaplan-Meier method and the Cox model. Nomogram-based immunoprofile was established using the independent prognostic variables. To determine its predictive accuracy and discriminatory capacity, the C-index and calibration curve were calculated. Results: Significant correlation of PD-L1 expression in tumor cells with PD-1+ T cell infiltration was found (P=0.035), indicating the activation of the inhibitory PD-1/PD-L1 pathway in ESCC cases. More PD-L1+ICs, Tim-3+ ICs and LAG-3+ ICs were found in the CD8-rich tumor microenvironment, which is in accordance with the feedback nature of immune system. After adjustment by TNM stage, four immune variables including the infiltration of CD8+/Foxp3 +/CD33+ cells and the PD-L1 expression by tumor cells were selected to construct a prognostic nomogram. The calibration curves showed good accuracy of the nomogram for survival prediction. To overcome the complexity of applying a nomogram in a clinical setting, a simple immunoprofile was then established according to the points of each factor from the nomogram. Our immunoprofile model could separate same-stage patients into different risk subgroups, and showed superior accuracy for survival prediction than the TNM staging system based on the C-index calculation and ROC analysis. Conclusions: Our nomogram-based immunoprofile can provide more accurate prognosis prediction and is an important complement to the TNM staging system for operable ESCC patients.
Objective To evaluate the technique of finger palpation in thoracoscopic localization in patients with pulmonary nodules,and to summarize its technical details,especially with exploit of chest computed tomography (CT) facilitating it.Methods 95 patients with total amount of 109 pulmonary nodes 20 mm or smaller in size shown with lung window of CT,were reviewed.They were located subpleurally,with a median depth of 8.2 mm and a median size of 10.0 mm.The value of their depth over their size (D/d value) could be used as the extent of localizing difficulty.Each node had its own radiographic fealures for being localized,which was built preoperatively.Under thoracoscopic vision,nodules were finger-palpated by index finger via the 4th or 5th intercostal space on anterior axillary line,followed by wedgectomy or lobectomy for instant histopathological diagnosis to further decide the final surgical type.The distance between the nodule and the origin of segmental bronchus (L value) were also calculated out,as it might be relevant to the way the nodule could be biopsied.Results All nodules were successfully localized and resected for biopsy goal,105 by wedgectomy,4 by lobectomy.After intraoperative diagnosis was made by the pathologist,VATS lobectomy and lymph node dissection were further performed in 55 patients.L value of 4 cases being biopsied by lobectomy ranged from 18.3 to 30.3 mm,averaging 26.1 mm.Conclusion Finger palpation is viable in any cases of pulmonary nodules.Detailed reference of CT digital information,and enough detachment of mediastinal pleura,can greatly facilitate thoracoscopic localization by finger palpation.Lobectomy or segementectomy is preferable when L value is less than 30 mm.