Comparative analysis of the mutational landscape and evolutionary patterns of pancreatic ductal adenocarcinoma metastases in the liver or peritoneum.

Background: Pancreatic ductal adenocarcinoma (PDAC) often presents with liver or peritoneal metastases at diagnosis. Despite similar treatment approaches, patient outcomes vary between these metastatic sites. To improve targeted therapies for metastatic PDAC, a comprehensive analysis of the genetic profiles and evolutionary patterns at these distinct metastatic locations is essential. Methods: We performed whole exome sequencing on 44 tissue samples from 27 PDAC patients, including primary tumours and matched liver or peritoneal metastases. We analysed somatic mutation profiles, signatures, and affected pathways for each group, and examined clonal evolution using subclonal architectures and phylogenetic trees. Results: KRAS mutations remained the predominant driver alteration, with a prevalence of 89 % across all tumours. Notably, we observed site-specific differences in mutation frequencies, with KRAS alterations detected in 77.8 % (7/9) of peritoneal metastases and 87.5 % (7/8) of liver metastases. TP53 mutations exhibited a similar pattern, occurring in 55.6 % (5/9) of peritoneal and 37.5 % (3/8) of liver metastases. Intriguingly, we identified site-specific alterations in DNA repair pathway genes, including ATM and BRCA1, with distinct mutational profiles in liver versus peritoneal metastases. Furthermore, liver metastases demonstrated a significantly higher tumor mutational burden (TMB) compared to peritoneal metastases (median [IQR]: 2.14 [1.77-2.71] vs. 1.29 [1.21-1.69] mutations/Mb; P = 0.048). Conclusions: In conclusion, metastasis of pancreatic cancer may be influenced by variables other than KRAS mutations, such as TP53. PDAC peritoneal and liver metastases may differ in potential therapeutic biomarkers. Further inquiry is needed on the biological mechanisms underlying metastasis and the treatment of diverse metastases.

Immunoneoadjuvant therapy with immune checkpoint inhibitors of gastric cancer: an emerging exemplification : Immunoneoadjuvant therapy of gastric cancer.

Advances in immune checkpoint inhibitors (ICIs) have enabled more effective treatment for individuals with various types of solid tumors. Given the improved survival benefit and acceptable safety profile of ICIs in advanced gastric cancer, there is plenty of interest in the use of ICIs in the neoadjuvant setting with curative intent. Theoretically, immunoneoadjuvant with ICIs could boost the levels of endogenous tumor antigen present in the tumor to enhance T-cell priming and further enhance systemic immunity. This systemic immune response may improve the detection and elimination of the disseminated micrometastatic tumors beyond the resected tumor, which are sources of postsurgical relapse. Numerous clinical studies have begun to explore the application of ICIs in neoadjuvant treatment of gastric cancer. This article reviews the progress in the use of ICI monotherapy and in combination with alternative therapies for the treatment of gastric cancer to aid in the development of gastric cancer immunoneoadjuvant therapy and improve the overall therapeutic benefit.

Laparoscopic hepatopancreaticoduodenectomy for synchronous gallbladder cancer and extrahepatic cholangiocarcinoma: a case report.

BACKGROUND: Hepatopancreaticoduodenectomy (HPD) is one of the most complex procedures, and it is very rarely reported. Laparoscopic HPD (LHPD) is even rarer. To date, there are only 3 reports of LHPD for locally advanced gallbladder cancer (GBC) or extrahepatic cholangiocarcinoma (ECC). This is the first report of LHPD for synchronous GBC and ECC. CASE PRESENTATION: A 75-year-old female patient complained of jaundice for 2 weeks without fever or abdominal pain. She was diagnosed with synchronous GBC and ECC. After a comprehensive preparation, she underwent a laparoscopic pancreaticoduodenectomy and resection of hepatic segments of IVb and V, and her digestive tract reconstruction followed Child's methods. She was discharged on the 12th day postoperatively without pancreatic leakage, biliary leakage, or liver failure. CONCLUSIONS: LHPD is safe and feasible for selected cases of GBCs or ECCs.

Invaginated duct to mucosa pancreaticojejunostomy reduce postoperative pancreatic leakage: A matched case-controlled study.

ABSTRACT: Postoperative pancreatic leakage is an obstacle in pancreaticoduodenectomy, which always follows pancreaticojejunostomy (PJ) failure. Dozens of PJ procedures have been reported, and none have shown superiority over others. Therefore, the present study is conducted to assess the potential advantages of invaginated duct-to-mucosa (D-M) PJ.We retrospectively analyze the related data from patients who underwent pancreaticodedunostomy due to malignant tumors at the First Affiliated Hospital of Henan University of Science and Technology from January 2017 to August 2019. According to the different PJ procedures, the patients are divided into custom D-M group and invaginated D-M group. Matching by sex, age, pancreatic duct size, and pancreatic texture is performed. Pancreatic leakage and other complications are compared, and SPSS 16.0 is employed for analysis.A total of 48 pairs of patients are included. Patients in both groups has almost the same baseline characteristics in terms of sex (P = 1.000), age (P = .897), American Society of Anesthesiologists status (P = .575), body mass index (P = .873), pancreatic duct size (P = .932), pancreatic texture (P = 1.000) and tumor origin (P = .686). No significant difference is observed in operative outcomes, such as operative duration (P = .632), PJ duration (P = .748), blood loss (P = .617) and number of required transfusions (P = .523). Pancreatic leakage is significantly decreased in the invaginated D-M group (P = .005). The differences in other complications, such as bleeding (P = .617), biliary leakage (P = .646), pneumonia (P = .594) and thrombosis (P = .714), do not reach statistical significance. The postoperative hospitalization duration is almost the same for both groups (P = .764).Invaginated D-M PJ may reduce pancreatic leakage following pancreaticoduodenectomy.

Interpretation of Electrocardiogram Heartbeat by CNN and GRU.

The diagnosis of electrocardiogram (ECG) is extremely onerous and inefficient, so it is necessary to use a computer-aided diagnosis of ECG signals. However, it is still a challenging problem to design high-accuracy ECG algorithms suitable for the medical field. In this paper, a classification method is proposed to classify ECG signals. Firstly, wavelet transform is used to denoise the original data, and data enhancement technology is used to overcome the problem of an unbalanced dataset. Secondly, an integrated convolutional neural network (CNN) and gated recurrent unit (GRU) classifier is proposed. The proposed network consists of a convolution layer, followed by 6 local feature extraction modules (LFEM), a GRU, and a Dense layer and a Softmax layer. Finally, the processed data were input into the CNN-GRU network into five categories: nonectopic beats, supraventricular ectopic beats, ventricular ectopic beats, fusion beats, and unknown beats. The MIT-BIH arrhythmia database was used to evaluate the approach, and the average sensitivity, accuracy, and F1-score of the network for 5 types of ECG were 99.33%, 99.61%, and 99.42%. The evaluation criteria of the proposed method are superior to other state-of-the-art methods, and this model can be applied to wearable devices to achieve high-precision monitoring of ECG.

Safety analysis of application of mediastinal CO2 aeration in mediastinal esophagectomy.

BACKGROUND: In recent years, minimally invasive esophagectomy (MIE) has been used gradually in esophageal surgery. The application of CO2 aeration in minimally invasive surgeries, especially in laparoscopic surgery, has been very mature. However, the application of CO2 aeration in mediastinal esophagectomy is still in the exploration stage. This study was designed to investigate the safety of mediastinal CO2 aeration in the mediastinal esophagectomy. METHODS: A total of 15 pigs were used to construct an experimental animal model of mediastinal CO2 aeration. The effects of different inflation pressures on the circulatory respiratory function of pigs were studied by detecting the relevant physiological parameters. Heart rate (HR), mean arterial pressure (MAP) and central venous pressure (CVP) were monitored before ventilating CO2 (T0), and also monitored at 30 (T1), 60 (T2), 90 (T3) min after inflation and 30 min after deflation (T4). Arterial blood was collected for PaCO2, blood lactate concentration (cLac), PaO2/FiO2, SaO2, pH value, and cardiac output (CO) was measured by esophageal ultrasound. RESULTS: The results of animal experiments showed that under 5-10 mmHg CO2 inflation pressure, circulation function indicators (CVP, MAP, HR, CO) and respiratory function indicators (PaCO2, cLac, PaO2/FiO2, SaO2, pH value) in pigs had no significant difference compared with the indicators before inflation; and under 15 mmHg CO2 inflation pressure, CVP, HR, PaCO2 and blood cLac increased, while MAP, CO, PaO2, SaO2 and pH values decreased. The visual field using mediastinoscopy under 15 and 10 mmHg CO2 inflation pressure was better than that under 5 mmHg CO2 inflation pressure. CONCLUSIONS: Mediastinal esophagectomy with 5-10 mmHg CO2 inflation pressure has no significant effect on the circulation and respiratory function of the body. Compared with the conventional non-inflated transseptal esophageal cancer (EC) surgery, it can provide a better surgical vision and reduce the difficulty of the surgery.

Circular RNA Expression Profiles and the Pro-tumorigenic Function of CircRNA_10156 in Hepatitis B Virus-Related Liver Cancer.

Liver cancer is one of the most common malignant tumors in the world. Circular RNAs (circRNAs) perform important functions in cancer progression and are regarded as prospective biomarkers for cancer diagnosis and therapy. Here, we used the high-throughput RNA sequencing technology in conjunction with bioinformatics tools to profile circRNA expression in patients with HBV-related liver cancer. A total of 13,124 circRNAs were identified in HBV-related liver cancer, approximately 86.25% of which were sense-overlapping circRNAs. Moreover, 2,996 circRNAs exhibited different expression patterns between liver cancer tissues and matched pericancerous tissues. Function annotation indicated that these aberrantly expressed circRNAs were primarily engaged in cellular processes and cancer-associated pathways. Notably, the circRNA-miRNA interaction networks showed that 6,020 circRNAs were predicted to target 1,654 miRNAs. Quantitative RT-PCR (qRT-PCR) assay indicated that ten randomly selected circRNAs displayed consistent expression patterns with the sequencing results. We further predicted that circRNA_10156 might work as a molecular sponge of miR-149-3p, which served an important function in tumor development. Consequently, our results demonstrated that depletion of circRNA_10156 upregulated miR-149-3p, reduced Akt1 expression, and suppressed liver cancer cell proliferation. The present study will facilitate the elucidation of biological functions of circRNAs in the progression of HBV-related liver cancer providing prospective biomarkers and therapeutic targets for this disease. Our findings also reveal that circRNA_10156 might represent a promising therapeutic target for liver cancer management.

IL-32 expression indicates unfavorable prognosis in patients with colon cancer.

Recently, interleukin (IL)-32 has been demonstrated to represent a novel biomarker for evaluating the prognosis of patients with gastric and lung cancer; however, its clinical significance in colon cancer remains unknown. In the present study, the IL-32 expression in 60 patients with colon cancer was examined with an immunohistochemistry assay. IL-32 expression was determined in 37 (61.67%) patients with colon cancer. Additionally, IL-32 was associated with tumor size and Dukes' stage. By using the Kaplan-Meier method, patients with positive IL-32 expression had shorter overall survival time, compared with those with negative IL-32 expression. Multivariate analysis indicated that IL-32 could be an independent prognostic factor in patients with colon cancer; therefore, IL-32 may be a novel prognostic biomarker and therapeutic target for colon cancer.

LncRNA FTX Promotes Proliferation and Invasion of Gastric Cancer via miR-144/ZFX Axis.

BACKGROUND: Long non-coding RNAs are important regulators in cancer cell tumorigenesis. We have demonstrated in a prior study that lncRNA FTX is dysregulated in gastric cancer (GC). In this study, we aim to report gastric cancer-related lncRNA FTX as a main regulator in GC development and progression. METHODS: In vitro and in vivo assays of FTX alterations have been performed to reveal a complex integrated phenotype affecting cell growth, migration, and invasion. lncRNA FTX expression levels in gastric cancer cells and normal cells were measured by RT-PCR. Luciferase reporter assays, Western blotting, and many immune, microscopy technologies were utilized to investigate the expressions of FTX- related proteins and RNAs. The functional role of FTX in cell growth, migration, and invasion were observed in vitro and in vivo. RESULTS: We explored the underlying mechanisms of FTX in GC development, and the microRNAs' relationship with FTX. We found that FTX promoted cell proliferation, migration, and invasion, as well as tumor growth, and this effect could latterly be attenuated by miR-144. ZFX attenuated the effects of FTX/miR-144 axis by sponging with miR-144. CONCLUSION: In summary, the above results support a model in which the FTX/miR-144/ZFX act as important effectors in GC tumorigenesis and progression, indicating new therapeutic methods in GC.

Circ_0056618 and CXCR4 act as competing endogenous in gastric cancer by regulating miR-206.

Circular RNAs (circRNAs) have proved to play an important role in gastric cancer. In this study, we found that circ_0056618 took part in gastric cancer cell proliferation and survival. The real-time polymerase chain reaction result showed that circ_0056618 was overexpressed in tumor tissues or cells compared with adjacent normal tissues or normal cells and had a negative relationship to gastric cancer patients' survival time. Meanwhile, the inhibition of circ_0056618 suppressed the proliferation and metastasis of gastric cancer cells. Further bioinformatical analysis indicated that circ_0056618 sponged miR-206 to regulate CXCR4 according to the prediction of TargetScan and miRanda. Dual-luciferase reporter assay and Western blot analysis revealed the underlying relationship of circ_0056618, miR-206, and CXCR4. Hence, circ_0056618 negatively regulated miR-206 expression promoting CXCR4 expression. Altogether, circ_0056618 is a potential gastric cancer prognostic marker, as well as a potential therapeutic target to inhibit gastric cancer metastasis.

ZNF280B promotes the growth of gastric cancer in vitro and in vivo.

Zinc finger protein 280B (ZNF280B) mediates pro-survival and pro-growth functions in prostate cancer. However, in gastric cancer, its clinical significance remains poorly characterized. In the present study, the expression levels of ZNF280B in 60 patients with gastric cancer were examined using immunohistochemistry. The association between ZNF280B expression and clinicopathological features was assessed. Positive ZNF280B staining was demonstrated for 38 (63.3%) samples out of 60 gastric cancer cases in immunohistochemical analysis. ZNF280B expression was significantly associated with tumor size (P=0.017) and TNM stage (P=0.001). Furthermore, the proliferation index in the positive ZNF280B expression group was significantly higher (38.8±6.2) compared with that of the negative ZNF280B expression group (16.9±8.9; P<0.01). These results suggest that ZNF280B expression may be associated with the proliferation of gastric cancer cells. The role of ZNF280B in the growth of gastric cancer cells (MGC-803) was also investigated in vitro and in vivo by enhancing the expression of ZNF280B. A colony formation assay indicated that the number of colonies in the MGC-803 cells with enhanced ZNF280B (146±5.8) was significantly higher than that of the MGC-803 control group (97±5.1) and the negative control group (101±6.5; P<0.05). An MTT assay demonstrated that ZNF280B significantly promoted the proliferation of MGC-803 cells at days 3 and 4 (P<0.05). It was observed that the overexpression of ZNF280B may promote the growth of gastric cancer in vivo in xenograft studies. These findings indicate that ZNF280B may be a novel therapeutic target for gastric cancer.

The long non-coding RNA AK001796 contributes to tumor growth via regulating expression of p53 in esophageal squamous cell carcinoma.

BACKGROUND: Esophageal squamous cell carcinoma (ESCC) is one of the prevalent and deadly cancers worldwide, especially in China. Considering the poor prognosis of ESCC, the aim of this study is to dissect the effects of long non-coding RNA (lncRNA) AK001796 on cell proliferation and cell cycle in vitro and tumorigenicity in vivo, providing therapeutic targets for ESCC. METHODS: We conducted quantitative real time PCR to detect the expression level of lncRNA AK001796 in human ESCC tumor and adjacent non-tumor tissues, and analyzed the correlation between lncRNA AK001796 expression and clinicopathologic feature of ESCC patients. Then we knocked down the expression of lncRNA AK001796 in human ESCC cell lines Eca-109 and TE-1, and next inspected cell cycle and apoptosis condition in these cells using flow cytometry. Subsequently, we used CCK-8 assay to test proliferation ability of the lncRNA AK001796-silenced ESCC cells, and the MDM2/p53 signaling pathway in these cells was analyzed by western blot analysis. At last, the ESCC xenograft models were established to verify the role of lncRNA AK001796 on the occurrence and development of ESCC. RESULTS: In this study, we demonstrated that lncRNA AK001796 was significantly upregulated in ESCC tumor tissues compared to adjacent non-tumor tissues. Knockdown of lncRNA AK001796 inhibited ESCC cell growth, cell cycle, and tumor growth in a xenograft mouse model via regulating MDM2/p53 signal pathway. The expression of lncRNA AK001796 was positively correlated with MDM2 levels in human ESCC samples. CONCLUSIONS: Overall, lncRNA AK001796 regulates cell proliferation and cell cycle via modulating MDM2/p53 signaling in ESCC, which provides a new insight into the treatment targets for ESCC.Trial registration This study was registrated in the Ethics Committee of the First Affiliated Hospital of Nanjing Medical University (Trial registration: 2012-SR-127, Registered 20 January 2012).

Rapamycin enhances lytic replication of Epstein-Barr virus in gastric carcinoma cells by increasing the transcriptional activities of immediate-early lytic promoters.

Epstein-Barr virus (EBV), a human herpesvirus, is linked to both epithelial and lymphoid malignancies. Induction of EBV reactivation is a potential therapeutic strategy for EBV-associated tumors. In this study, we assessed the effects of rapamycin on EBV reactivation in gastric carcinoma cells. We found that rapamycin upregulated expression of EBV lytic proteins and increased the viral proliferation triggered by the EBV lytic inducer sodium butyrate. Reverse transcription-qPCR, luciferase activity assays, chromatin immunoprecipitation and western blotting were employed to explore the mechanism by which rapamycin promotes EBV reactivation. Our results showed that rapamycin treatment resulted in increased mRNA levels of EBV immediate-early genes. Rapamycin also enhanced the transcriptional activities of the EBV immediate-early lytic promoters Zp and Rp by strengthening Sp1 binding. Repression of the cellular ataxia telangiectasia-mutated/p53 pathway by siRNA-mediated knockdown of the ataxia telangiectasia-mutated gene significantly abrogated virus reactivation by rapamycin/sodium butyrate treatment, indicating that the ataxia telangiectasia-mutated/p53 pathway is involved in rapamycin-promoted EBV reactivation. Taken together, these findings demonstrate that rapamycin might have the potential to enhance the effectiveness of oncolytic viral therapies developed for EBV-associated malignancies.

MiR-106b-5p Promotes Proliferation and Inhibits Apoptosis by Regulating BTG3 in Non-Small Cell Lung Cancer.

BACKGROUND/AIMS: MicroRNAs have been validated to play a crucial role in tumorigenesis of non-small cell lung cancer (NSCLC). Although miR-106b-5p has been reported to play a vital role in various malignancies the physiological function of miR-106b-5p in NSCLC still remain unknown. In this study, we investigated the role of miR-106b-5p in NSCLC. METHODS: Quantitative real-time polymerase chain reaction was conducted to estimate the expression of miR-106b-5p and BTG3 in both NSCLC tissues and cell lines. The effects of miR-106b-5p on proliferation were determined in vitro using CCK-8 proliferation assays, 5-ethynyl-2'-deoxyuridine (EdU) incorporation, colony formation assays and cell-cycle assays and the in vivo effects were evaluated by a mouse tumorigenicity model. Cell apoptosis and cell cycle was investigated by flow cytometric analysis in vitro. The molecular mechanism underlying the relevance between miR-106b-5p and BTG3 was confirmed by luciferase assay and western blot. RESULTS: In current study, we found a relatively higher miR-106b-5p and lower BTG3 expression in NSCLC specimens and cell lines. BTG3 was verified as a direct target of miR-106b-5p by luciferase assay. In vitro, over-expression of miR-106b-5p promoted proliferation and inhibited apoptosis by down-regulating BTG3 expression. In vivo, miR-106b-5p promoted xenograft tumor formation. CONCLUSION: Our findings revealed for the first time that miR-106b-5p plays a tumorigenesis role in NSCLC progression by down-regulating BTG3 expression, which may lead to a novel insight to the potential biomarker and novel therapeutic strategies for NSCLC patients.

Long non­coding RNA AK001796 contributes to cisplatin resistance of non­small cell lung cancer.

Cisplatin (DDP)­based chemotherapy is the most widely used therapy for non­small cell lung cancer (NSCLC). However, the existence of chemoresistance has become a major limitation in its efficacy. Long non­coding RNAs (lncRNAs) have been shown to be involved in chemotherapy drug resistance. The aim of the present study was to investigate the biological role of lncRNA AK001796 in cisplatin­resistant NSCLC A549/DDP cells. Reverse transcription­quantitative polymerase chain reaction (RT­qPCR) analysis was performed to monitor the differences in the expression of AK001796 in cisplatin-resistant (A549/DDP) cells and parental A549 cells. Cellular sensitivity to cisplatin and cell viability were examined using an MTT assay. Cell apoptosis and cell cycle distribution were measured using flow cytometry. The expression levels of cell cycle proteins cyclin C (CCNC), baculoviral IAP repeat containing 5 (BIRC5), cyclin­dependent kinase 1 (CDK1) and G2 and S phase­expressed 1 (GTSE1) were assessed using RT­qPCR and western blot analyses. It was found that the expression of AK001796 was increased in A549/DDP cells, compared with that in A549 cells. The knockdown of AK001796 by small interfering RNA reduced cellular cisplatin resistance and cell viability, and resulted in cell­cycle arrest, with a marked increase in the proportion of A549/DDP cells in the G0/G1 phase. By contrast, the knockdown of AK001796 increased the number of apoptotic cancer cells during cisplatin treatment. It was also shown that the knockdown of AK001796 positively induced the expression of cell apoptosis­associated factors, CCNC and BIRC5, and suppressed the expression of cell cycle­associated factors, CDK1 and GTSE5. Taken together, these findings indicated that lncRNA AK001796 increased the resistance of NSCLC cells to cisplatin through regulating cell apoptosis and cell proliferation, and thus provides an attractive therapeutic target for NSCLC.

Long Noncoding RNA FAL1 Promotes Cell Proliferation, Invasion and Epithelial-Mesenchymal Transition Through the PTEN/AKT Signaling Axis in Non-Small Cell Lung Cancer.

BACKGROUND/AIMS: Recently, long non-coding RNAs (lncRNAs) have been found to have many biological effects in different cancer stages. Several studies have revealed that focally amplified lncRNA on chromosome 1 (FAL1) regulates cancer progression via p21. However, the expression and mechanism of FAL1 in non-small cell lung cancer (NSCLC) still remain unclear. METHODS: We detected the FAL1 level in NSCLC tissues and in established cell lines using quantitative real-time PCR and evaluated the clinical significance. FAL1 was silenced or overexpressed using siRNA or lentivirus to study whether FAL1 affected cell proliferation, invasion and migration. Xenograft growth and pulmonary metastasis were observed using nude mouse models. The mechanisms were explored with western blotting and immunohistochemistry. RESULTS: FAL1 was significantly overexpressed in NSCLC compared with adjacent normal tissues, and a high level of FAL1 correlated with poor histological grade, increased lymph node metastasis and advanced TNM stage. Loss- and gain-of-function experiments in vitro verified that knockdown of FAL1 inhibited cell proliferation, invasion, migration and EMT via the PTEN/AKT pathway. Furthermore, an in vivo assay confirmed that overexpression of FAL1 facilitated tumor growth and metastasis. CONCLUSION: FAL1 may promote tumorigenesis and progression of NSCLC through the PTEN/AKT axis, which could lead to lncRNA-related diagnostics and therapeutics in NSCLC.

Long noncoding RNA RP11-766N7.4 functions as a tumor suppressor by regulating epithelial-mesenchymal transition in esophageal squamous cell carcinoma.

BACKGROUND: Numerous studies have proved that long non-coding RNAs participate in the initiation and metastasis of various cancers including esophageal squamous cell carcinoma (ESCC). Recently, a novel long non-coding RNA RP11-766N7.4 was discovered in a variety of human tissues. However, its role in oncogenesis and tumor metastasis remains unknown. METHODS: To investigate the function of long noncoding RNA RP11-766N7.4 in ESCC, RT-qPCR was used to monitor the expression level of long non-coding RNA RP11-766N7.4 in ESCC cell lines and 50 paired ESCC tissues. Moreover, the association between long non-coding RNA RP11-766N7.4 expression level and clinicopathological characteristics as well as 5-year survival rate of ESCC patients was evaluated. Furthermore, function assays containing cell proliferation assay, flow cytometry, Colony Formation, wound healing assay and Transwell assays were conducted to investigate the role of long noncoding RNA RP11-766N7.4 in ESCC. Western blotting assay were used to explore the regulation mechanism. RESULTS: In this study, we found that long noncoding RNA RP11-766N7.4 was downregulated in ESCC tissues and cell lines and correlated with lymph node metastasis, tumor stage and survival rate. Results also revealed that long noncoding RNA RP11-766N7.4 had no significant effect on cell proliferation, cell cycle or cell apoptosis of ESCC cells. In addition, long noncoding RNA RP11-766N7.4 knockdown promoted cellular migration and invasion via inducing EMT process, and overexpression of long noncoding RNA RP11-766N7.4 inhibited cellular migration and invasion by suppressing EMT process. CONCLUSION: Our study suggested that long noncoding RNA RP11-766N7.4 acts as a tumor suppressor in ESCC carcinogenesis and metastasis, and may be a potential prognostic mark and a therapeutic target for ESCC.

The associations between MDM4 gene polymorphisms and cancer risk.

Considerable studies have investigated the associations between MDM4 gene polymorphisms and cancer risk recently, but with contradictory results. The aim of this meta-analysis was to evaluate the associations between MDM4 gene polymorphisms and cancer risk. Relevant studies were identified by a systematic search of PubMed, Embase, and CNKI databases. Crude odds ratios (ORs) and 95% confidence intervals (CIs) were used to describe the strength of the associations. Fifty-six studies published in 11 publications involving 18,910 cases and 51,609 controls were included in this meta-analysis. Five MDM4 gene polymorphisms were evaluated: rs4245739, rs1563828, rs11801299, rs10900598, and rs1380576. Our analyses suggested that the rs4245739 polymorphism was significantly associated with overall cancer risk. Furthermore, stratification analyses of ethnicity indicated that rs4245739 decreased the risk of cancer among the Asian population, and stratification analyses of smoking status indicated that rs4245739 decreased the risk of cancer among nonsmokers. However, stratification analyses of cancer type and sex suggested that rs4245739 was not related to cancer risk. There were no associations of rs1563828, rs11801299, rs10900598, or rs1380576 with overall cancer risk. In conclusion, our analyses indicated that rs4245739 polymorphism in the MDM4 gene may play an important role in the etiology of cancer.

MYO9B gene polymorphisms are associated with the risk of inflammatory bowel diseases.

Myosin IXB (MYO9B) gene polymorphisms have been extensively investigated in terms of their associations with inflammatory bowel disease (IBD), with contradictory results. The aim of this meta-analysis was to evaluate associations between MY09B gene polymorphisms and the risk of IBD, Crohn's disease (CD) and ulcerative colitis (UC). Eligible studies from PubMed, Embase, and CNKI databases were identified. Pooled odds ratios (ORs) and 95% confidence intervals (95% CIs) were calculated. Ten studies published in eight papers reporting 8,975 cases and 9,482 controls were included in this meta-analysis. Five MY09B gene polymorphisms were evaluated: rs1545620, rs962917, rs1457092, rs2305764, and rs2305767. Our data suggested that the rs1545620 polymorphism was associated with a decreased risk of IBD. A similar result was found for rs2305767 and UC. The rs962917 single nucleotide polymorphism (SNP) increased the risk of IBD, CD and UC. Moreover, rs1457092 increased the risk of IBD and UC. Rs2305764 was also associated with an increased risk of IBD. Furthermore, stratification analyses indicated that rs1545620 decreased the risk of IBD, while rs962917 increased the risk of IBD, CD and UC in Caucasian populations. To sum up, our data indicate that these five SNPs in MY09B are significantly associated with the risk of IBD.

Continuous suturing with two anterior layers reduces post-operative complications and hospitalization time in pancreaticoenterostomy.

BACKGROUND: Most complications after pancreaticoduodenectomy (PD) were relation to pancreaticoenterostomy. We improved a new method of pancreaticoenterostomy that included the continuous suturing of the jejunum and the stump of the pancreas end-to-side with one layer posteriorly and two layers anteriorly. To evaluate the safety and efficiency of this new method, we introduced this retrospectively compared trial. METHODS: We compared 45 patients who had undergone pancreaticoduodenectomy with either the regular interrupted suturing method or the new continuous mattress suturing method in our hospital from September 2011 to March 2014. RESULTS: Although the total operation times were not reduced, the suturing time for the pancreaticoenterostomies in the continuous suture group (11.3 ± 1.8 min) was greatly reduced compared with that for the interrupted suture group (14.1 ± 2.9 min, p = 0.045). Importantly, the continuous mattress suturing method significantly decreased short-term post-operative complications, including pancreatic leakage (p = 0.042). Furthermore, shorter hospitalization times were observed in the continuous mattress suture group (12.3 ± 5.0 d) than in the interrupted suture group (24.2 ± 11.6 d, p = 0.000). CONCLUSIONS: Continuous mattress suturing is a safe and effective pancreaticoenterostomy method that leads to reduced complications and hospitalization times.