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Yiyang Gong,1,2,* Minqin Zhou,2,* Yanting Zhu,2,* Jingying Pan,2 Xuanrui Zhou,2 Yike Jiang,2 Hong Zeng,2 Hao Zheng,2 Xitong Geng,2 Da Huang1 1Department of Thyroid Surgery; Second Affiliated Hospital of Nanchang University, Nanchang, People’s Republic of China; 2Second College of Clinical Medicine, Nanchang University, Nanchang, People’s Republic of China*These authors contributed equally to this workCorrespondence: Da Huang, Department of Thyroid Surgery, Second Affiliated Hospital of Nanchang University, 1 Minde Road, Nanchang, Jiangxi Province, 330000, People’s Republic of China, Tel +13576113993, Email danmo0904@163.comPurpose: Hepatocellular carcinoma is the most common primary liver cancer, with poor prognosis. Complex immune microenvironment of the liver is linked to the development of HCC. PVALB is a calcium-binding protein which has been described as a cancer suppressor gene in thyroid cancer and glioma. Nevertheless, the role of PVALB in HCC is unknown.Materials and Methods: We obtained data from TCGA and GSE54236 datasets. MCP-counter, WGCNA and LASSO model were applied to identify PVALB. With UALCAN, MethSurv, and other websites, we probed the expression, methylation and survival of PVALB. LinkedOmics and GSEA were adopted for functional analysis, while TIMER, TISIDB, Kaplan-Meier plotter, TIDE databases were utilized to evaluate the relevance of PVALB to the tumor immune microenvironment and predict immunotherapy efficacy. TargetScan, DIANA, LncRNASNP2 databases and relevant experiments were employed to construct ceRNA network. Finally, molecular docking and drug sensitivity of PVALB were characterized by GeneMANIA, CTD, and so on.Results: PVALB was recognized as a gene associated with HCC and NK cell. Its expression was down-regulated in HCC tissue, which lead to adverse prognosis. Besides, the hypomethylation of PVALB was related to its reduced expression. Notably, PVALB was tightly linked to immune, and its reduced expression attenuated the anticancer effect of NK cells via the Fas/FasL pathway, leading to a adverse outcome. The lnc-YY1AP1-3/hsa-miR-6735-5p/PVALB axis may regulate the PVALB expression. Finally, we found immunotherapy might be a viable treatment option.Conclusion: In a word, PVALB is a prognostic indicator, whose low expression facilitates HCC progression by impacting NK cell infiltration.Keywords: PVALB, hepatocellular carcinoma, immune, ceRNA, bioinformatics, prognostic factor

Jiaxin Zhao,1 Cheng Wang,1 Liang Zhao,1 Huiying Zhou,1 Rui Wu,1 Tao Zhang,1 Jiawei Ding,1 Junjie Zhou,2 Huilin Zheng,3 Lei Zhang,3 Tianci Kong,3 Jie Zhou,4 Zhenhua Hu1,4 1Department of Hepatobiliary and Pancreatic Surgery, Department of Surgery, Fourth Affiliated Hospital, School of Medicine, Zhejiang University, Yiwu, Zhejiang Province, People’s Republic of China; 2Department of Radiology, Fourth Affiliated Hospital, School of Medicine, Zhejiang University, Yiwu, Zhejiang Province, People’s Republic of China; 3Zhejiang Provincial Collaborative Innovation Center of Agricultural Biological Resource Biochemical Manufacturing, School of Biological and Chemical Engineering, Zhejiang University of Science and Technology, Hangzhou, Zhejiang Province, People’s Republic of China; 4Department of Hepatobiliary and Pancreatic Surgery, Department of Surgery, First Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, Zhejiang Province, People’s Republic of ChinaCorrespondence: Zhenhua Hu, Department of Hepatobiliary and Pancreatic Surgery, Department of Surgery, Fourth Affiliated Hospital, School of Medicine, Zhejiang University, Yiwu, Zhejiang Province, People’s Republic of China, Tel/Fax +86-570-89935878, Email huzhenh@zju.edu.cn Jie Zhou, Department of Hepatobiliary and Pancreatic Surgery, Department of Surgery, First Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, Zhejiang Province, People’s Republic of China, Tel +86-13429661721, Email jzhou329@zju.edu.cnPurpose: Nonsense-mediated RNA decay (NMD), a surveillance pathway for selective degradation of aberrant mRNAs, is associated with cancer progression. Its potential as a predictor for aggressive hepatocellular carcinoma (HCC) is unclear. Here, we present an innovative NMD risk model for predicting HCC prognosis.Methods: The Cancer Genome Atlas (TCGA) data of 374 liver HCC (LIHC) and 50 normal liver samples were extracted. A risk model based on NMD-related genes was developed through least absolute shrinkage and selection operator Cox (LASSO-Cox) regression of the LIHC-TCGA data. Prognostic validation was done using GSE54236, GSE116174, and GSE76427 data. Univariate and multivariate Cox regression analyses were conducted to assess the prognostic value of the model. We also constructed nomograms for survival prediction. Tumor immune infiltration was evaluated using the CIBERSORT algorithm, and the tumor cell phenotype was assessed. Finally, mouse experiments verified UPF3B knockdown effects on HCC tumor characteristics.Results: We developed a risk model based on four NMD-related genes (PABPC1, RPL8, SMG5, and UPF3B) and validated it using GSE54236, GSE116174, and GSE76427 data. The model effectively distinguished high- and low-risk groups corresponding to unfavorable and favorable HCC outcomes. Its prognostic prediction accuracy was confirmed through time-dependent ROC analysis, and clinical-use nomograms with calibration curves were developed. Single-cell RNA sequencing results indicated significantly higher expression of SMG5 and UPF3B in tumor cells. Knockdown of SMG5 and UPF3B inhibited HCC cell proliferation, invasion, and migration, while affecting cell-cycle progression and apoptosis. In vivo, UPF3B knockdown delayed tumor growth and increased immune cell infiltration.Conclusion: Our NMD-related gene-based risk model can help identify therapeutic targets and biomarkers for HCC. Additionally, it assists clinicians in predicting the prognosis of HCC patients.Keywords: nonsense-mediated RNA decay, hepatocellular carcinoma, biomarker, LASSO, survival, tumor immunity

Simiao Yu,1,* Jingxiao Wang,2,* Haocheng Zheng,3,* Ruilin Wang,4,* Nadia Johnson,1 Tao Li,3 Ping Li,1 Jie Lin,5 Yuan Li,5 Jin Yan,6 Ying Zhang,6 Zhenyu Zhu,6 Xia Ding3,7 1Dongzhimen Hospital, Beijing University of Chinese Medicine, Beijing, 100700, People’s Republic of China; 2School of Life Sciences, Beijing University of Chinese Medicine, Beijing, 100029, People’s Republic of China; 3School of Traditional Chinese Medicine, Beijing University of Chinese Medicine, Beijing, 100029, People’s Republic of China; 4Department of Hepatology of Traditional Chinese Medicine, The Fifth Medical Center of PLA General Hospital, Beijing, 100039, People’s Republic of China; 5National Institute of Traditional Chinese Medicine Constitution and Preventive Medicine, Beijing University of Chinese Medicine, Beijing, 100029, People’s Republic of China; 6Department of Hepatobiliary Surgery, The Fifth Medical Center of PLA General Hospital, Beijing, 100039, People’s Republic of China; 7Centre of Research for Traditional Chinese Medicine Digestive, Beijing University of Chinese Medicine, Beijing, 100029, People’s Republic of China*These authors contributed equally to this workCorrespondence: Xia Ding, School of Traditional Chinese Medicine, Beijing University of Chinese Medicine, Email dingx@bucm.edu.cn Zhenyu Zhu, Department of Hepatobiliary Surgery, The Fifth Medical Center of PLA General Hospital, Email zhuzy302@163.comAbstract: Hepatocellular carcinoma (HCC) is the most common type of primary liver cancer and one of the deadliest cancers worldwide. As opposed to the majority of patients with HCC, approximately 20– 30% of cases of non-alcoholic steatohepatitis (NASH)-derived HCC develop malignant tumours in the absence of liver cirrhosis. NASH is characterized by metabolic dysregulation, chronic inflammation and cell death in the liver, which provide a favorable setting for the transformation of inflammation into cancer. This review aims to describe the pathogenesis and the underlying mechanism of the transition from inflammation to cancer in NASH.Keywords: non-alcoholic steatohepatitis, hepatocellular carcinoma, inflammation to cancer transition, metabolic dysregulation, immune microenvironment

Yinjie Fan,1,2 Hang Xue,2 Huachuan Zheng2 1College of Integrated Chinese and Western Medicine, Liaoning University of Traditional Chinese Medicine, Shenyang, Liaoning, 110847, People’s Republic of China; 2Department of Oncology and Experimental Center, the Affiliated Hospital of Chengde Medical University, Chengde, Hebei, 067000, People’s Republic of ChinaCorrespondence: Huachuan Zheng, Department of Oncology and Experimental Center, the Affiliated Hospital of Chengde Medical University, Chengde, Hebei, 067000, People’s Republic of China, Tel +86-0314-2279458, Fax +86-0314-2279458, Email zheng_huachuan@hotmail.comAbstract: Hepatocellular carcinoma (HCC) has emerged the culprit of cancer-related mortality worldwide with its dismal prognosis climbing. In recent years, ground-breaking progress has been made in systemic therapy for HCC. Targeted therapy based on specific signaling molecules, including sorafenib, lenvatinib, regorafenib, cabozantinib, and ramucirumab, has been widely used for advanced HCC (aHCC). Immunotherapies such as pembrolizumab and nivolumab greatly improve the survival of aHCC patients. More recently, synergistic combination therapy has boosted first-line (atezolizumab in combination with bevacizumab) and second-line (ipilimumab in combination with nivolumab) therapeutic modalities for aHCC. This review aims to summarize recent updates of systemic therapy relying on the biological mechanisms of HCC, particularly highlighting the approved agents for aHCC. Adjuvant and neoadjuvant therapy, as well as a combination with locoregional therapies (LRTs), are also discussed. Additionally, we describe the promising effect of traditional Chinese medicine (TCM) as systemic therapy on HCC. In this setting, the challenges and future directions of systemic therapy for HCC are also explored.Keywords: hepatocellular carcinoma, targeted therapy, immunotherapy, traditional Chinese medicine, locoregional therapies, adjuvant therapy, neoadjuvant therapy

Yumin Ke,1,* Shuiling Zu,2,* Lijun Chen,3,* Meizhi Liu,4 Haijun Yang,5 Fuqiang Wang,5 Huanhuan Zheng,6 Fangjie He7,8 1Department of Obstetrics and Gynecology, The Second Affiliated Hospital of Fujian Medical University, Quanzhou, 362000, People’s Republic of China; 2Nursing Department, The Third Affiliated People’s Hospital of Fujian University of Traditional Chinese Medicine, Fuzhou, 350100, People’s Republic of China; 3Department of Gynecological Oncology, Fujian Cancer Hospital, Fujian Medical University Cancer Hospital, Fuzhou, 350014, People’s Republic of China; 4Department of Gynecology, The Third Affiliated People’s Hospital of Fujian University of Traditional Chinese Medicine, Fuzhou, 350100, People’s Republic of China; 5Department of Pathology, The Anyang Tumor Hospital, Anyang, 455000, People’s Republic of China; 6Department of Endocrinology, Ji’an Central People’s Hospital, Ji’an, 343000, People’s Republic of China; 7Department of Obstetrics and Gynecology, The First People’s Hospital of Foshan, Foshan, 528000, People’s Republic of China; 8State Key Laboratory of Oncology in South China, Sun Yat-sen University Cancer Center, Guangzhou, 510060, People’s Republic of China*These authors contributed equally to this workCorrespondence: Fangjie HeDepartment of Obstetrics and Gynecology, The First People’s Hospital of Foshan, Foshan, People’s Republic of China; State Key Laboratory of Oncology in South China, Sun Yat-sen University Cancer Center, Guangzhou, 510060, People’s Republic of China, Tel +86-18038864533, Fax +86 757-83162610, Email hfj5362@fsyyy.com; dr_hefangjie@163.comObjective: This study aimed to identify a subset of patients with stage IA2 to IIA2 cervical cancer who are at low risk of lymph node metastasis (LNM) using pathological parameters including estrogen receptor alpha (ERα) and progesterone receptor (PR).Methods: The clinical data of patients with stage IA2 to IIA2 cervical cancer who underwent radical surgery between 2014 and 2015 were retrospectively reviewed. Immunohistochemical staining was used to determine the expression of ERα and PR. A low-risk criterion for LNM was identified using logistic regression analysis, and its performance was estimated through receiver-operating characteristic curve analysis.Results: Of 263 patients, 57 (21.7%) had pathological LNM. ERα (adjusted odds ratio [aOR], 7.582; 95% confidence interval [CI], 2.991– 19.222; P < 0.001) and squamous cell carcinoma (aOR, 3.520; 95% CI, 1.887– 6.568; P < 0.001) were identified as independent predictors for no LNM by multivariate logistic regression analysis, while PR had no effect on LNM. The rate of LNM was 1.4% for low-risk patients (n = 73) identified as ERα positive with squamous cell carcinoma. The 5-year disease-free survival in low-risk patients was significantly greater than in those negative for ERα and/or those with non-squamous cell carcinoma (96.9% vs 80.1%, P = 0.002).Conclusion: ERα positivity and squamous cell carcinoma are associated with a low risk of LNM in patients with stage IA2 to IIA2 cervical cancer. Hence, those patients without a low risk of LNM could be considered for definitive chemoradiotherapy to avoid unnecessary surgery.Keywords: cervical cancer, lymph node, estrogen receptor alpha, progesterone receptor, squamous cell carcinoma

Hu Zhou,1,2,&ast; Yuan Yuan,1– 3,&ast; Haorun Wang,1,2 Wei Xiang,1,2 shenjie Li,1,2 Haowen Zheng,1,2 Yuqi Wen,1,2 Yang Ming,1,2 Ligang Chen,1,2,4,5 Jie Zhou1,2,4,5 1Department of Neurosurgery, Affiliated Hospital of Southwest Medical University, Luzhou, Sichuan, People’s Republic of China; 2Sichuan Clinical Research Center for Neurosurgery, Luzhou, Sichuan, People’s Republic of China; 3Department of Operation and Anaesthesia, Yibin First People’s Hospital, Yibin, Sichuan, People’s Republic of China; 4Academician (Expert) Workstation of Sichuan Province, Luzhou, Sichuan, People’s Republic of China; 5Neurological Diseases and Brain Function Laboratory, Luzhou, Sichuan, People’s Republic of China&ast;These authors contributed equally to this workCorrespondence: Jie Zhou Email zj000718@yeah.netAbstract: The gut microbiota plays a crucial role in many physiological processes in the human body. Dysbiosis can disrupt the intestinal barrier and alter metabolism and immune responses, leading to the development of diseases. Over the past few decades, evidence has accumulated linking changes in the composition of the gut microbiota to dozens of seemingly unrelated conditions, including cancer. Overall, the gut microbiota mainly affects the occurrence and development of cancer by damaging host DNA, forming and maintaining a pro-inflammatory environment, and affecting host immune responses. In addition, the gut microbiota can also affect the efficacy and toxicity of chemotherapy, radiotherapy, and immunotherapy. Scientists attempt to improve the efficacy and decrease the toxicity of these treatment modalities by fine-tuning the gut microbiota. The aim of this review is to assist researchers and clinicians in developing new strategies for the detection and treatment of tumors by providing the latest information on the intestinal microbiome and cancer, as well as exploring potential application prospects and mechanisms of action.Keywords: intestinal flora, carcinogenesis, mechanism, therapy, fecal bacteria transplantation

Ning Guan,1,&ast; Haiying Zheng,2,&ast; Xiaoling Wu,3 Longfei Xie,4 Xiaojing Tong5 1Department of Physical Examination Center, Cancer Hospital of China Medical University, Liaoning Cancer Hospital & Institute, Liaoning, 110042, People’s Republic of China; 2Department of the Traditional and Modern Treatment Center, The Affiliated Shenben Hospital of Liaoning University of Traditional Chinese Medicine, Liaoning, 110031, People’s Republic of China; 3Department of Gynecology, The Second People’s Hospital of Baise, Guangxi, 533100, People’s Republic of China; 4Department of Physics and Integrative Biology, University of California, Berkeley, CA, 94720, USA; 5Department of Gynecology, Cancer Hospital of China Medical University, Liaoning Cancer Hospital & Institute, Liaoning, 110042, People’s Republic of China&ast;These authors contributed equally to this workCorrespondence: Xiaojing TongDepartment of Gynecology, Cancer Hospital of China Medical University, Liaoning Cancer Hospital & Institute, Liaoning, 110042, People’s Republic of ChinaTel +86 24 15542 253448Email adnikenike@sina.comObjectives: Long non-coding RNAs (lncRNAs) play a crucial part in cancer progression. However, in epithelial ovarian carcinoma (EOC), the role of SNHG22 needs to be further explained.Methods: Quantitative real-time PCR was used to detect the expression of SNHG22. EOC cells were stably transfected with lentivirus approach and cell proliferation, glycolysis and cell apoptosis, as well as tumorigenesis in animal were performed to assess the effects of SNHG22 in EOC. Chromatin immunoprecipitation (ChIP) and luciferase reporter assay were conducted to confirm the relationship between SP1 and SNHG22.Results: Higher expressed SNHG22 was associated with a poor prognosis in EOC tissues. SNHG22 facilitated glycolysis and proliferation. Mechanistically, LDHA deficiency and glycolysis inhibitor (2-DG, 3-BG) partly rescued proliferation. SP1 mediated SNHG22 expression at the transcriptional level and the SNHG22 promoter region (− 900∼ − 600) was necessary for SP1 binding. Hypoxia and HIF-1α also upregulated SNHG22 expression.Conclusion: SNHG22 is an independent prognostic biomarker for EOC. SNHG22 promotes EOC progression and is a prospective therapeutic target.Keywords: hypoxia, SNHG22, SP1, epithelial ovarian carcinoma, glycolysis

Mei Zhan,1– 3 Hanrui Zheng,1– 3 Yu Yang,2,4 Zhiyao He,1 Ting Xu,1,3 Qiu Li2,4 1Department of Pharmacy, West China Hospital, Sichuan University, Chengdu, People’s Republic of China; 2West China Biomedical Big Data Center, Sichuan University, Chengdu, People’s Republic of China; 3West China School of Pharmacy, Sichuan University, Chengdu, People’s Republic of China; 4Department of Medical Oncology, Cancer Center, West China Hospital, Sichuan University, Chengdu, People’s Republic of ChinaCorrespondence: Ting XuDepartment of Pharmacy, West China Hospital, Sichuan University, Chengdu, Sichuan 610041, People’s Republic of ChinaEmail tingx2009@163.comQiu LiDepartment of Medical Oncology, Cancer Center, West China Hospital, Sichuan University, Chengdu, Sichuan 610041, People’s Republic of ChinaEmail fbqiu9@163.comObjective: The phase III POLO trial demonstrated that olaparib as maintenance therapy for metastatic pancreatic cancer patients with a germline BRCA mutation had greater efficacy than placebo, but maintenance olaparib places an economic burden on patients. This study evaluated the cost-effectiveness of olaparib as maintenance therapy based on the POLO trial (NCT02184195).Methods: A three-state Markov model (progression-free survival [PFS], progressive disease [PD] and death) based on data from the POLO trial was used to estimate the incremental cost-effectiveness ratio (ICER) of maintenance olaparib versus placebo for metastatic pancreatic cancer patients with a germline BRCA mutation. The cost was evaluated from the Chinese society’s perspective, and health outcomes were assessed in terms of quality-adjusted life years (QALYs). The primary outcome was the ICER gained in terms of 2019 US$ per QALY. Model robustness was explored with one-way and probabilistic sensitivity analyses.Results: Compared with placebo, maintenance olaparib increased costs by $23,544.35 while gaining 0.69 QALYs, resulting in an ICER of $34,122.25 per QALY. The ICER was far higher than the commonly accepted willingness-to-pay threshold ($28,255.55 per QALY).Conclusion: Compared with placebo, maintenance olaparib for metastatic pancreatic cancer patients with a germline BRCA mutation is not cost-effective in China.Keywords: cost effectiveness, pancreatic cancer, olaparib, BRCA, Markov model

Hao Long,1 Hui Zheng,2 Long Ai,1 Kamil Osman,1 Zhigang Liu3 1Department of Pain Management, The Sixth Affiliated Hospital of Xinjiang Medical University, Urumqi, People’s Republic of China; 2Orthopedics Department, The Sixth Affiliated Hospital of Xinjiang Medical University, Urumqi, People’s Republic of China; 3Department of Pain Management, The Second Hospital of Jilin University, Changchun, Jilin, People’s Republic of ChinaCorrespondence: Zhigang Liu Department of Pain ManagementThe Second Hospital of Jilin University, No. 218, Ziqiang Street, Nanguan District, Changchun, Jilin 130041, People’s Republic of ChinaEmail liuzhigang_82@163.comIntroduction: Cancer-induced bone pain (CIBP) is very common in patients with advanced cancer. Recent studies have shown that reactive oxygen species (ROS) can sense and regulate pain response process through spinal cord mechanism, and play a role in CIBP. NADPH oxidase (NOX) is a group of protease complexes that produce ROS. In the current study, we investigated the expression of NOX4 in the spinal dorsal horn of rats with CIBP and its related role and molecular mechanism.Materials and Methods: A rat CIBP model was established by injecting Walker-256 cells into the tibia medullary cavity, and the expression of NOX4 in spinal dorsal horn was down-regulated by injecting lentivirus into spinal cord. RT-PCR, Western blot and immunofluorescence staining were used to detect the expression of NOX4 in CIBP rats, cell localization and its effect on CIBP rats, and the effect of down-regulating the expression of NOX4 on the expression of H2O2, nitric oxide synthase nNO, antioxidant enzyme SOD, and the activity of neuro-receptor in spinal dorsal horn of rats.Results: In rats with CIBP, the expression of NOX4 was significantly increased, and immunofluorescence showed that NOX4 was mainly expressed in microglia in the dorsal horn of spinal cord. Down-regulating the expression of NOX4 in rats can reduce the level of H2O2 and nNO in dorsal horn tissue, and increase the expression of SOD to reduce the oxidative stress response. At the same time, down-regulating NOX4 can reduce the sensitivity of spinal cord and relieve the pain of bone cancer by inhibiting the expression of NMDAR and GABAA-γ 2 in dorsal horn tissue.Conclusion: NOX4 is a promising therapeutic target in CIBP, and down-regulation of NOX4 expression can alleviate CIBP in rats by reducing oxidative stress and weakening spinal cord sensitization.Keywords: cancer-induced bone pain, NOX4, reactive oxygen species, spinal cord sensitization

Xiao Lu,1,* Quan-Xing Liu,1,* Jiao Zhang,1 Dong Zhou,1 Gui-Xue Yang,1 Man-Yuan Li,1 Yuan Qiu,2 Qian Chen,3 Hong Zheng,1 Ji-Gang Dai1 1Department of Thoracic Surgery, Xinqiao Hospital, Army Medical University, Chongqing 400037, People’s Republic of China; 2Department of General Surgery, Xinqiao Hospital, Army Medical University, Chongqing 400037, People’s Republic of China; 3Cancer Center of Daping Hospital, Army Medical University, Chongqing 400042, People’s Republic of China*These authors contributed equally to this workCorrespondence: Ji-Gang Dai; Hong Zheng Email daijigang@tmmu.edu.cn; ziecoe@163.comBackground: Lung cancer remains the leading cause of cancer-related death worldwide. The human PINK1 gene (PTEN induced kinase 1, Park6), an important gene for Parkinson’s disease, was found to be associated with tumor development although the molecular mechanisms underlying this relationship remain largely unknown.Objective: To analyze the clinical value and molecular mechanism of PINK1 in non-small cell lung cancer (NSCLC).Materials and Methods: Western blot, qRT-PCR and Immunohistochemistry were employed to determine the levels of PINK1 in 87 paired NSCLC tissues, Oncomine and TCGA databases were also used for the evaluation of expression and prognosis of PINK1. The mitophagy, proliferation, migration, invasion, and apoptosis abilities of A549 and H1975 cells were detected, and the autophagy-related proteins in the cells were also determined.Results: Immunohistochemical staining revealed higher PINK1 expression in tumor tissues, which was strongly linked to the tumor-node-metastasis classification. Survival analysis of 1085 NSCLC patients also revealed that low PINK1 expression levels were associated with significantly longer overall survival. Univariate and multivariate analyses indicated that PINK1 expression was an independent predictor of overall survival among patients with NSCLC. We also evaluated the influence of PINK1 deficiency in NSCLC cell lines (A549 and H1975), which revealed significant suppression of migration capability and cell viability, as well as a significantly elevated apoptosis ratio. In cells with stable interference of PINK1 expression, dysfunctional mitochondria accumulated while autophagy was inhibited, which indicated that cell activity suppression was mediated by the accumulation of dysfunctional mitochondria. The suppression of migration and autophagy was reversed in cells that overexpressed PINK1.Conclusion: Our results suggest that PINK1 may be a potential therapeutic target and prognostic biomarker in NSCLC.Keywords: PINK1, NSCLC, mitochondria, autophagy, migration, proliferation

Na Li,1,2,* Huanrui Zheng,1,2,* Bin Zheng,1,2 Chaoxin Chen,1,2 Hongfu Cai,1,2 Maobai Liu1,2 1Department of Pharmacy, Fujian Medical University Union Hospital, Fuzhou, Fujian Province, People’s Republic of China; 2School of Pharmacy, Fujian Medical University, Fuzhou, Fujian Province, People’s Republic of China*These authors contributed equally to this workCorrespondence: Maobai LiuDepartment of Pharmacy, Fujian Medical University Union Hospital, Fuzhou, Fujian Province, People’s Republic of ChinaEmail liumaobai@163.comObjective: This review aimed to assess the quality of available evidence on the economic evaluations of immune checkpoint inhibitors in patients with non-small cell lung cancer (NSCLC) and provide evidence to improve the efficiency of healthcare resources.Materials and Methods: Literature search was performed using some electronic databases (PubMed, Embase and Cochrane Central Register of Controlled Trials). Final search was performed in December 2019. Study characteristics and results were recorded and compared. The quality of the studies was assessed using the Consolidated Health Economic Evaluation Reporting Standards (CHEERS) checklists. We did not elaborate the restrictions on the target population. We included patients with squamous or non-squamous NSCLC and metastatic or advanced cancer.Results: Of 98 papers considered, 21 were chosen for this review. Most of them are cost-effectiveness analysis. Comparative regimens consisted of either immune checkpoint inhibitor monotherapy, immune checkpoint inhibitor plus chemotherapy, or chemotherapy alone. Fourteen, four, and three studies were about pembrolizumab, nivolumab, and atezolizumab, respectively. The methods mostly used in these studies were modeling and sensitivity analysis. All studies used quality-adjusted life year (QALY) and life years (LY) as outcomes. Most studies were conducted in high-income countries. Based on the willingness to pay threshold, atezolizumab, and pembrolizumab were found to be cost-effective in one and 10 studies, respectively. None of the studies concluded that nivolumab was cost-effective. For quality assessment, all studies fulfilled more than 50% of the CHEERS checklist.Conclusion: The included studies indicated that pembrolizumab regimens are cost-effective as first-line treatment for patients with NSCLC in developed countries. Nivolumab and atezolizumab are likely to be cost-effective as second-line treatment but not as first-line treatment.Keywords: non-small cell lung cancer, economic analyses, immune checkpoint inhibitors, systematic review, PD-L1 positive

Xiao Zhang,1,* Chenli Zhang,1,* Zhiheng Ren,1 Fangfang Zhang,1 Jinyu Xu,1 Xu Zhang,1 Haixue Zheng2 1Department of Pathology, School of Basic Medicine, Lanzhou University, Lanzhou, Gansu 730000, People’s Republic of China; 2National Foot and Mouth Diseases Reference Laboratory, Lanzhou Veterinary Research Institute, Chinese Academy of Agricultural Sciences, Lanzhou, Gansu 730000, People’s Republic of China*These authors contributed equally to this workCorrespondence: Xu ZhangDepartment of Pathology, School of Basic Medicine, Lanzhou University, 222 Tianshui Road, Lanzhou, Gansu 730000, People’s Republic of ChinaEmail zhangxu64@163.comHaixue ZhengNational Foot and Mouth Diseases Reference Laboratory, Lanzhou Veterinary Research Institute, Chinese Academy of Agricultural Sciences, 1 Yanchang Road, Lanzhou, Gansu 730000, People’s Republic of ChinaEmail haixuezheng@163.comPurpose: The function of curcumin on the gastric cancer cell line, SGC-7901 is unknown. The present study aimed to observe the effects of curcumin on gastric cancer cells through the Shh and Wnt signaling pathways.Methods: SGC-7901 cells were transfected with si-Gli1 and si-β-catenin siRNA, then cells were stimulated with curcumin and its effects on cell migration, invasion, cytoskeleton remodeling, EMT, apoptosis and cell cycle were investigated by transwell assays, immunofluorescence and flow cytometry assays. The interaction between Gli1 and β-catenin was observed by co-immunoprecipitation.Results: We show that curcumin suppressed the expression of Shh, Gli1 and Foxm1 in the Shh signaling pathway, and the expression of β-catenin in the Wnt signaling pathway in SGC-7901 cells, both in mRNA and protein. As a result, cellular migration, invasion and cytoskeletal remodeling ability decreased. Our results revealed that when stimulated with curcumin, cells showed decreased cellular migration and invasion, while enhanced apoptosis. In addition, curcumin induced cytoskeletal remodeling and S phase cell cycle arrest. The inhibition of Shh and Wnt signaling pathway and the addition of curcumin also inhibited the epithelial–mesenchymal transition process. Furthermore, a physical interaction was observed between Gli1 of the Shh signaling and β-catenin of the Wnt signaling in these cells, but curcumin inhibited the interaction of these two proteins.Conclusion: The present study indicated that curcumin plays an anti-tumor role through Gli1-β-catenin pathway in gastric cancer SGC-7901 cells.Keywords: curcumin, Gli1, β-catenin, migration, invasion, cytoskeleton

Simin Liu,1,* Jianhao Xie,2,* Fei Yu,1 Haidong Cai,1 Fengyu Wu,3 Hui Zheng,1 Chao Ma,1 Zhongwei Lv,1 Hui Wang4 1Department of Nuclear Medicine, Tenth People’s Hospital of Tongji University, Shanghai, People’s Republic of China; 2Medical School of Soochow University, Suzhou, People’s Republic of China; 3Department of Nuclear Medicine, Affiliated Hospital of Qingdao University, Qingdao, People’s Republic of China; 4Department of Nuclear Medicine, Xinhua Hospital, School of Medicine, Shanghai Jiaotong University, Shanghai, People’s Republic of China*These authors contributed equally to this workCorrespondence: Chao Ma; Zhongwei LvDepartment of Nuclear Medicine, Tenth People’s Hospital of Tongji University, Yanchangzhong Road 301, Shanghai 200072, People’s Republic of ChinaTel +8621-66302075Email mc_7419@hotmail.com; shtjnmd@163.comObjective: To analyze the difference in 99mTc-methylene diphosphonate (MDP) uptake on bone scintigraphy in extraosseous soft tissue tumors between children and adults and the correlation between tracer uptake and tumor differentiation and histopathology.Methods: Patients with neoplasms with MDP uptake were retrospectively identified. Based on histopathology, tumors were categorized as epithelial malignant tumors, mesenchymal tumors, blastomas and germ cell tumors. The degree of radioactivity accumulation in lesions relative to the uptake in ribs and sternum or spine was classified as “+”, “++” and “+++”. The results were compared between children and adults. The correlations between MDP uptake in soft tumors and tumor differentiation and pathology were investigated.Results: Extraosseous soft tissue tumors that accumulated MDP were found in 33 children and 31 adults. In children, neuroblastoma was the most common extraosseous soft tissue tumor that accumulated MDP; in adults, MDP uptake was mostly found in lung cancer. MDP uptake in pediatric soft tissue tumors was higher than that in adults. MDP uptake in extraosseous soft tissue tumors with different histopathologic classifications was significantly different among 64 patients. In 41 patients with available tumor differentiation data from histopathology, MDP uptake in low or poorly differentiated soft tumors was higher than that in the moderately or well-differentiated lesions. Necrosis and/or calcifications were showed in most of pediatric and adult neoplasms.Conclusion: Significant elevations in MDP uptake in extraosseous soft tissue tumors are associated with poorly differentiated tumors in both children and adults. The mechanism of bone tracer uptake in pediatric and adult neoplasms was mostly related to necrosis and/or necrosis and calcification. The extraosseous soft tissue tumors with MDP uptake in pediatric patients were different from those in adults. In addition, consistent with the inherent degree of tumor malignancy, MDP uptake in children was higher than that in adults.Keywords: pediatric, adult, extraosseous soft tissue tumor, differentiation, bone scintigraphy, MDP

Xin Wang,1,* Ziwei Feng,1,* Yubei Huang,1 Haixin Li,1,2 Ping Cui,1 Dezheng Wang,3 Hongji Dai,1 Fangfang Song,1 Hong Zheng,1 Peishan Wang,1 Xuchen Cao,4 Lin Gu,5 Jin Zhang,6 Fengju Song,1 Kexin Chen1 1Department of Epidemiology and Biostatistics, National Clinical Research Center for Cancer，Key Laboratory of Cancer Prevention and Therapy, Tianjin Medical University Cancer Institute and Hospital, Tianjin 300060, People’s Republic of China; 2Department of Cancer Biobank, Tianjin Medical University Cancer Institute and Hospital, Tianjin 300060, People’s Republic of China; 3Center for Non-Communicable Disease Control and Prevention, Tianjin Centers for Disease Control and Prevention, Tianjin 300011, People’s Republic of China; 4The First Department of Breast Cancer, National Clinical Research Center for Cancer, Key Laboratory of Cancer Prevention and Therapy, Tianjin Medical University Cancer Institute and Hospital, Tianjin 300060, People’s Republic of China; 5The Second Department of Breast Cancer, National Clinical Research Center for Cancer, Key Laboratory of Cancer Prevention and Therapy, Tianjin Medical University Cancer Institute and Hospital, Tianjin 300060, People’s Republic of China; 6The Third Department of Breast Cancer, National Clinical Research Center for Cancer, Key Laboratory of Cancer Prevention and Therapy, Tianjin Medical University Cancer Institute and Hospital, Tianjin 300060, People’s Republic of China*These authors contributed equally to this workCorrespondence: Fengju Song; Kexin ChenTianjin Medical University Cancer Institute and Hospital, Huanhu Xi Road, Tiyuan Bei, Hexi District, Tianjin 300060, People’s Republic of ChinaTel/Fax +86-22-23372231Email songfengju@163.com; chenkexin@tjmuch.comPurpose: We aim to construct a nomogram to predict breast cancer survival and guide postoperative adjuvant chemotherapy in China.Patients and methods: A total of 5,504 breast cancer patients from the Tianjin Breast Cancer Cases Cohort were included. Multivariable Cox regression was used to investigate the factors associated with overall survival (OS) and a nomogram was constructed based on these prognostic factors. The nomogram was internal and external validated and the performance was evaluated by area under the curve (AUC) and calibration curve. The partial score was also constructed and stratified them into low, moderate and high-risk subgroups for death according to the tripartite grouping method. Multivariate Cox regression analysis and the propensity score matching method were respectively used to test the association between adjuvant chemotherapy and OS in different risk subgroups.Results: Age, diameter, histological differentiation, lymph node metastasis, estrogen, and progesterone receptor were incorporated into the nomogram and validation results showed this nomogram was well-calibrated to predict the 3-year [AUC =74.1%; 95% confidence interval (CI): 70.1–78.0%] and 5-year overall survival [AUC =72.3%; 95% CI: 69.6–75.1%]. Adjuvant chemotherapy was negatively associated with death in high risk subgroup [Hazard Ratio (HR) = 0.54; 95% CI: 0.37–0.77; P

Juan Feng,1,2 Yuting Zhan,1 Yuting Zhang,1 Hongmei Zheng,1 Weiyuan Wang,3 Songqing Fan1 1Department of Pathology, The Second Xiangya Hospital, Central South University, Changsha, Hunan, People’s Republic of China; 2Clinical Laboratory of Hunan Prevention and Treatment Institute for Occupational Diseases, Changsha, Hunan, People’s Republic of China; 3Department of Pathology, Xiangya Hospital, Central South University, Changsha, Hunan, People’s Republic of ChinaCorrespondence: Songqing FanDepartment of Pathology, The Second Xiangya Hospital, Central South University, 139 Renmin Middle Road, Changsha, Hunan 410011, People’s Republic of ChinaEmail songqingfan@csu.edu.cnBackground: Heat shock proteins (HSPs) are a large family of chaperones implicating in occurrence and progression of tumor. In our previous study, we found HSP10 correlates with poor prognosis of oral squamous cell carcinoma and astrocytoma. HSP70 is also an important part of this family and whether the alterations of HSP10 and HSP70 expression and their common expression correlates with carcinogenesis and progression of nasopharyngeal carcinoma (NPC) has not been reported.Method: In this study, we investigate the correlation between the expression of HSP10 and HSP70 and clinicopathological characteristics in NPC by immunohistochemistry (IHC).Results: Results indicated that positive expression of HSP10 and HSP70 was higher in NPC tissues (both P

Hongmei Zheng, Yuting Zhang, Yuting Zhan, Sile Liu, Junmi Lu, Juan Feng, Xia Wu, Qiuyuan Wen, Songqing FanDepartment of Pathology, The Second Xiangya Hospital, Central South University, Changsha, Hunan 410011, People’s Republic of ChinaPurpose: The purpose of this study was to investigate the relationship between epidermal growth factor receptor (EGFR) gene mutation and clinicopathological features of lung adenocarcinoma, and the prognostic and therapeutic value of EGFR.Methods: EGFR gene mutations were detected in 424 patients with lung adenocarcinoma by amplification refractory mutation system (ARMS).Results: The total EGFR gene mutation rate was 55.2% (234/424) and EGFR gene mutation rates were statistically different in gender, smoking status, and pathological degree (P0.05). Among 424 cases of lung adenocarcinoma, multivariate analysis showed that EGFR gene mutation, age, gender, clinical stages, and pathological degree (P

Tao Yan,1* Guo-Hua Zhang,1* Yao-Zhong Cheng,1* Lin-Xin Wu,1 Xiao-Yan Liu,1 Yu-Lin Sun,2 Hui Zheng*,1 Li Sun31Department of Anesthesiology, National Cancer Center/National Clinical Research Center for Cancer/Cancer Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100021, People’s Republic of China; 2State Key Laboratory of Molecular Oncology, National Cancer Center/National Clinical Research Center for Cancer/Cancer Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100021, People’s Republic of China; 3Department of Anesthesiology, National Cancer Center/National Clinical Research Center for Cancer/Cancer Hospital & Shenzhen Hospital,Chinese Academy of Medical Sciences and Peking Union Medical College, Shenzhen 518116, People’s Republic of China*These authors contributed equally to this work Background: Surgery and anesthesia-induced immunosuppression may play a critical role in tumor progression and metastasis. Myeloid-derived suppressor cells (MDSCs) are highly immunosuppressive myeloid cells, closely linked with tumor staging, clinical therapeutic efficacy and prognosis. This study aims to investigate the effect of anesthetic technique and surgery on the expression of MDSCs and prognosis in women who received breast cancer surgery.Methods: From March 2016 to January 2017, a total of 80 patients with breast cancer were prospectively enrolled and randomized into two anesthetic groups: sevoflurane-based anesthetic group (SEV; n=38) and propofol-based total intravenous anesthetic group (TIVA; n=42). The expression of MDSCs and prognosis between different anesthetic techniques and stresses of surgical methods were compared. The primary endpoint is the postoperative expression of MDSCs and prognosis between SEV and TIVA groups. The secondary endpoint is the VAS scores at 24 hr post-operation between SEV and TIVA groups.Results: There was no significant difference in postoperative expression of MDSCs (P=0.202) and prognosis (P=0.138) between SEV and TIVA groups. Compared to breast-conserving surgery (BCS), patients who underwent breast mastectomy had significantly fewer MDSCs (P=0.040) and lower VAS score at 24 hr post-operation (P=0.044), while no significant difference in prognosis was found (P=0.953). When MDSCs were classified as subtypes of granulocytic/polymorphonuclear (PMN)-MDSCs and monocytic (Mo)-MDSCs, it showed higher ratio of Mo-MDSCs (P=0.018) or lower ratio of (PMN)-MDSCs (P=0.022) correlates to later tumor stage.Conclusion: Sevoflurane and propofol-based anesthesia do not show significant difference in MDSCs expression and prognosis after breast cancer surgery. Compared to BCS, although mastectomy with high extent of surgical stress exhibits lower levels of MDSCs, there is no significant difference in prognosis. The ratio of MDSCs subtype correlates to tumor stage.Keywords: breast cancer, anesthesia, surgery, propofol, sevoflurane, MDSCs

Huifei Zheng,1,* Tengfei Chen,2,* Chang Li,2 Chun Xu,2 Cheng Ding,2 Jun Chen,2 Sheng Ju,2 Zhiwei Zhang,2 Zhipan Liang,2 Zihan Cui,2 Jun Zhao2 1National Center for Liver Cancer, Eastern Hepatobiliary Surgery Hospital, Second Military Medical University, Shanghai, China; 2Department of Thoracic and Cardiovascular Surgery, The First Affiliated Hospital of Soochow University, Soochow University, Suzhou, Jiangsu, China *These authors contributed equally to this work Purpose: Most recently, circular RNAs (circRNAs) were considered playing regulatory roles in tumor initiation and development. The specific function of circRNAs in hepatocellular carcinoma (HCC) remains unknown. This study was designed to detect specific roles of a circRNA hsa_circ_0079299 in HCC.Methods: The expression of hsa_circ_0079299 in HCC and tumor cell lines was detected using quantitative PCR (qPCR). Cell proliferation, migration, cell cycle and apoptosis after overexpression of the circRNA were measured using cell counting kit-8 (CCK8) assay, colony formation, 5-ethynyl-2′-deoxyuridine (EdU) assay, wound healing assay, transwell culture system and flow cytometry. Western blotting assay detected the protein expression of PI3K/AKT/mTOR signaling pathway and cyclin B1 (CCNB1). Overexpression of the circRNA in vivo was measured by nude mice tumorigenesis.Results: The expression of hsa_circ_0079299 was lower in HCC tissues. Overexpression of hsa_circ_0079299 suppressed tumor growth in vitro and in vivo, retarded cell cycle progression while had no effect on cell migration and apoptosis. The inhibitory effect of hsa_circ_0079299 was partly mediated by PI3K/AKT/mTOR signaling pathway.Conclusion: Our study shows that tumor suppressive role of hsa_circ_0079299 in HCC provides new recognition of circRNAs in cancers. Keywords: cell proliferation, cell cycle, cyclin B1, liver cancer

Hong Zheng,1,* Chao Zhou,2,* Xiao Lu,1 Quanxing Liu,1 Minqiang Liu,2 Guoqing Chen,2 Weigang Chen,2 Shuai Wang,2 Yuan Qiu2 1Department of Thoracic Surgery of Xinqiao Hospital, The Third Military Medical University, Shapingba, 400037, Chongqing, People’s Republic of China; 2Department of General Surgery of Xinqiao Hospital, The Third Military Medical University, Shapingba, 400037, Chongqing, People’s Republic of China *These authors contributed equally to this work Background: Protein/nucleic acid deglycase (DJ-1) and hypoxia-inducible factor-1α (HIF-1α) play significant roles in the progression of various types of cancer and are associated with the phosphatidylinositol 3-kinase (PI3K) pathway. However, their functions in colorectal cancer (CRC) have not been identified. The aim of this study was to analyze the putative signaling pathway encompassing DJ-1, PI3K, and HIF-1α in a series of CRC tissues and cell lines.Purpose: This study aimed at exploring the expression status of DJ-1 in colon cancer and its role in survival of cancer cell lines.Methods: The expression and localization of DJ-1, PI3K-p110α, phosphorylated Akt (p-AKT), and HIF-1α were determined by immunohistochemistry in 73 resected CRC tissues. The effect of DJ-1 on cell activity was explored by in vitro knockdown and overexpression experiments in SW480 and HT-29 cells. The cells were treated with a PI3K inhibitor (LY294002 or wortmannin), and p-AKT and HIF-1α protein expression were then analyzed. Apoptosis was analyzed by flow cytometry. The expression levels of several HIF-1 target genes were assessed under hypoxic conditions by reverse transcription-PCR and Western blot. Xenograft tumor growth studies were conducted in DJ-1 knockdown or overexpression cells.Results: High DJ-1 expression was found in 68.49% (50/73) of CRC tissues and associated with larger tumor size and advanced clinical stages. DJ-1 expression was positively associated with PI3K-p110α, p-AKT, and HIF-1α expression in CRC. HIF-1α and p-AKT protein levels were lower in SW480 and HT-29 cells with stable DJ-1 knockdown than in those with DJ-1 overexpression. PI3K inhibitors almost completely blocked DJ-1-induced AKT phosphorylation. However, the expression of HIF-1α was partially preserved after treatment with PI3K inhibitors. We also show that DJ-1 is necessary for the transcriptional ability of HIF-1α and CRC cell survival after hypoxic stress. Moreover, DJ-1 promoted the growth of established tumor xenografts in nude mice.Conclusion: Our findings are the first to show that DJ-1 is overexpressed in CRC. We suggest a model in which DJ-1 mediates CRC cell survival by regulating the PI3K-AKT-HIF-1α pathway. Keywords: DJ-1, hypoxia-inducible factor-1α, phosphatidylinositol 3-kinase, phosphorylated Akt, colorectal cancer

Xiao Lu,1,* Dong Zhou,1,* Bing Hou,1 Quan-Xing Liu,1 Qian Chen,2 Xu-Feng Deng,1,3 Zu-Bin Yu,1 Ji-Gang Dai,1 Hong Zheng1 1Department of Thoracic Surgery, Xinqiao Hospital, Third Military Medical University, Chongqing, People’s Republic of China; 2Institute of Pathology and Southwest Cancer Center, Southwest Hospital, Third Military Medical University, Chongqing, People’s Republic of China; 3Department of Cardiothoracic Surgery, First People’s Hospital of Zunyi, Guizhou, People’s Republic of China *These authors contributed equally to this work Background: Chemotherapy is still the primary adjuvant strategy of cancer therapy; however, the emergence of multi-drug resistance has been a cause for concern. Autophagy has been demonstrated to have a protective role against chemotherapeutic drugs in cancer cells, and autophagy inhibition is generally considered to be a promising therapeutic strategy. However, the paucity of effective and specific autophagy inhibitors limits its application. Purpose: The objective of this study was to explore the effect of DCA, small molecular antitumor agent, on the autophagy regulation and chemosensitization in NSCLC cells. Methods: We investigated the autophagy regulation of dichloroacetate (DCA) by laser confocal microscopy and western blotting in A549 and H1975 cell lines. The MTT assay and flow cytometry was performed for explore the chemosensitization effectiveness of DCA. The results were verified with subcutaneous tumor model in nude mice and the immunohistochemistry was applied for assessing the level of cell apoptosis and autophagy in vivo post treatment. Results: We found that DCA, which exhibited antitumor properties in various carcinoma models, induced apoptosis of non-small cell lung cancer cells (NSCLC) by inhibiting cancer cell autophagy. Furthermore, Perifosine, an AKT inhibitor, can greatly weaken the capacity of inducing apoptosis by DCA. The results indicate that the AKT-mTOR pathway, a main negative regulator of autophagy, is involved in the DCA-induced inhibition of autophagy. Then, we detected the effectiveness of autophagy inhibition by DCA. When used in co-treatment with the chemotherapeutic drug paclitaxel (PTX), DCA markedly decreased cell autophagy, enhanced apoptosis and inhibited proliferation in A549 and H1975 cells. The results of the xenograft experiment demonstrate that co-treatment of PTX and DCA can significantly decrease cell proliferation in vivo and prolong the survival of mice. Conclusion: Our results suggest that DCA can inhibit cell autophagy induced by chemotherapeutics, providing a new avenue for cancer chemotherapy sensitization. Keywords: DCA, autophagy, multi-drug resistance, non-small-cell lung cancer, paclitaxel, xenograft nude mice, chemosensitization

Dong Zhou, Quan-Xing Liu, Xu-Feng Deng, Hong Zheng, Xiao Lu, Ji-Gang Dai, Li Jiang Department of Thoracic Surgery, Xinqiao Hospital, Third Military Medical University, Chongqing, People’s Republic of China Purpose: Anastomotic leakage is the most feared postoperative complication after esophagectomy. Omentoplasty, wrapping the omentum around the alimentary tract anastomosis, is thought to decrease the anastomotic leakage rate. The purpose of this clinical study is to investigate the use of omentoplasty to reinforce cervical esophagogastrostomy after minimally invasive esophagectomy (MIE).Patients and methods: In this retrospective study, the data of 160 consecutive patients who underwent cervical esophagogastrostomy after MIE between September 2012 and May 2015 were analyzed, 87 who underwent omentoplasty (group A) and 73 who did not undergo omentoplasty (group B). The primary outcome was the incidence of anastomotic leakage and anastomotic strictures after the operation. Secondary outcomes were other complications and mortality rate. Univariate and multivariate analysis of variables associated with an increased risk for anastomotic leak was performed.Results: The median age was 61 years (range, 37–82 years). The anastomotic leakage rates were 4.6% (4/87) in group A and 15.1% (11/73) in group B (P = 0.023). There was no statistical significance in anastomotic stricture rates between group A (6.9%) and group B (9.6%; P = 0.535). No difference was noted in other complications between the groups. There was a trend toward lower leak-associated mortality rates for group A (0%) compared with that for group B (4.1%).Conclusion: Cervical esophagogastrostomy with omentoplasty is more effective than esophagogastrostomy without omentoplasty for the prevention of anastomotic leakage in MIE with cervical anastomosis. Omentoplasty could be used as an adjunct technique to reduce the incidence of anastomotic leakage in cervical esophagogastrostomy following MIE. Keywords: omentoplasty, cervical esophagogastrostomy, minimally invasive esophagectomy, anastomosis leakage, stricture