Prediction of subsolid pulmonary nodule growth rate using radiomics.

BACKGROUND: Pulmonary nodule growth rate assessment is critical in the management of subsolid pulmonary nodules (SSNs) during clinical follow-up. The present study aimed to develop a model to predict the growth rate of SSNs. METHODS: A total of 273 growing SSNs with clinical information and 857 computed tomography (CT) scans were retrospectively analyzed. The images were randomly divided into training and validation sets. All images were categorized into fast-growth (volume doubling time (VDT) ≤ 400 days) and slow-growth (VDT > 400 days) groups. Models for predicting the growth rate of SSNs were developed using radiomics and clinical features. The models' performance was evaluated using the area under the curve (AUC) values for the receiver operating characteristic curve. RESULTS: The fast- and slow-growth groups included 108 and 749 scans, respectively, and 10 radiomics features and three radiographic features (nodule density, presence of spiculation, and presence of vascular changes) were selected to predict the growth rate of SSNs. The nomogram integrating radiomics and radiographic features (AUC = 0.928 and AUC = 0.905, respectively) performed better than the radiographic (AUC = 0.668 and AUC = 0.689, respectively) and radiomics (AUC = 0.888 and AUC = 0.816, respectively) models alone in both the training and validation sets. CONCLUSION: The nomogram model developed by combining radiomics with radiographic features can predict the growth rate of SSNs more accurately than traditional radiographic models. It can also optimize clinical treatment decisions for patients with SSNs and improve their long-term management.

Signature of gene aberrant alternative splicing events in pancreatic adenocarcinoma prognosis.

Alternative splicing (AS), as an effective and universal mechanism of transcriptional regulation, is involved in the development and progression of cancer. Therefore, systematic analysis of alternative splicing in pancreatic adenocarcinoma (PAAD) is warranted. The corresponding clinical information of the RNA-Seq data and PAAD cohort was downloaded from the TCGA data portal. Then, a java application, SpliceSeq, was used to evaluate the RNA splicing pattern and calculate the splicing percentage index (PSI). Differentially expressed AS events (DEAS) were identified based on PSI values between PAAD cancer samples and normal samples of adjacent tissues. Kaplan-Meier and Cox regression analyses were used to assess the association between DEAS and patient clinical characteristics. Unsupervised cluster analysis used to reveal four clusters with different survival patterns. At the same time, GEO and TCGA combined with GTEx to verify the differential expression of AS gene and splicing factor. After rigorous filtering, a total of 45,313 AS events were identified, 1,546 of which were differentially expressed AS events. Nineteen DEAS were found to be associated with OS with a five-year overall survival rate of 0.946. And the subtype clusters results indicate that there are differences in the nature of individual AS that affect clinical outcomes. Results also identified 15 splicing factors associated with the prognosis of PAAD. And the splicing factors ESRP1 and RBM5 played an important role in the PAAD-associated AS events. The PAAD-associated AS events, splicing networks, and clusters identified in this study are valuable for deciphering the underlying mechanisms of AS in PAAD and may facilitate the establishment of therapeutic goals for further validation.

Preoperative Colonic Decompression With Decompression Tube Insertion Versus Stent Insertion in Patients With Malignant Left Colonic Obstruction.

PURPOSE: To compare the clinical effectiveness of preoperative colonic decompression (PCD) performed with stent or decompression tube insertion in patients with malignant left colonic obstruction (MLCO). MATERIALS AND METHODS: Between September 2014 and September 2018, 63 patients with MLCO underwent PCD (decompression tube: 35; stent: 28) in our center. Elective surgery was performed for patients with clinical success of PCD. RESULTS: The rates of technical success for PCD with tube and stent insertion were 91.4% (32/35) and 96.4% (27/28), respectively (P=0.773). Clinical success rates for PCD with tube and stent insertion were 90.6% (29/32) and 85.2% (23/27), respectively (P=0.811). Tumor resection with primary anastomosis was performed in all patients with clinical success in both groups. No significant differences were found between 2 groups regarding the duration of surgery and rates of postoperative complications. CONCLUSION: Decompression tube and stent insertion had similar effectiveness for PCD in patients with MLCO.

A Panel of Three Biomarkers Identified by iTRAQ for the Early Diagnosis of Pancreatic Cancer.

PURPOSE: Due to a lack of early diagnostic markers, pancreatic cancer (PC) remains a lethal disease. Proteomic approaches are now being applied to identify novel PC biomarkers. EXPERIMENTAL DESIGN: In this study, iTRAQ and LC-MS/MS are used to perform comparative analyses of serum from PC patients and healthy controls (HC), to identify specific serum biomarkers for PC. Serum levels of candidate proteins are determined using ELISA. RESULTS: Among 869 proteins identified, 55 are potential biomarkers; Vitamin K-dependent protein Z (PROZ) and tumor necrosis factor receptor superfamily member 6b (TNFRSF6B) are selected for further analysis. Serum levels of PROZ and TNFRSF6B are significantly higher in PC patients than in HC or pancreatic benign controls (BC) (p < 0.01). The AUCs range from 0.816 to 0.971 for PROZ, TNFRSF6B, and carbohydrate antigen 19-9, either individually or in combination, in PC versus HC+BC, and from 0.711 to 0.932 in PC Stage I versus HC+BC. CONCLUSIONS AND CLINICAL RELEVANCE: It is demonstrated that PROZ and TNFRSF6B are novel serum biomarkers for detecting early stage PC, and for distinguishing PC from pancreatic benign tumor and healthy individuals. Additional large cohort studies are needed to develop PROZ and TNFRSF6B as clinical PC biomarkers.

miR-557 inhibits the proliferation and invasion of pancreatic cancer cells by targeting EGFR.

Deregulation of microRNA has been suggested as a critical event in pancreatic cancer development and progression. Thus far, very little is known about the role of miR-557; therefore, the goal of this study was to investigate the potential role of miR-557 in pancreatic cancer. In the present study, we discovered that miR-557 expression was lowered in cancerous pancreatic tissue samples relative to non-cancerous adjacent controls, and when miR-557 was overexpressed we found that this promoted the apoptotic death of pancreatic cancer cells, suppressing their proliferation, invasion, and migration. Using western blotting and luciferase reporter assays, we further found evidence that this miRNA may directly suppress expression of the epidermal growth factor receptor via suppressing its translation through 3'-UTR binding. When EGFR was overexpressed in our pancreatic cancer cells, this was sufficient to reverse the effects of miR-557 inhibition. In summary, miR-557 acts as a tumor suppressor in pancreatic cancer cells, impairing their ability to grow and invade surrounding tissues due at least in part to EGFR inhibition. Harnessing this targeting of EGFR via this miRNA may therefore be a viable strategy useful for patient suffering from this deadly disease.

DNM1L, a key prognostic predictor for gastric adenocarcinoma, is involved in cell proliferation, invasion, and apoptosis.

Dynamin-1-like protein (DNM1L) encodes a member of the dynamin superfamily of GTPases. It mediates mitochondrial and peroxisomal division and is involved in the regulation of apoptosis. However, its role in gastric cancer remains unclear. MKN-45 gastric cancer cells were transfected with short hairpin RNA (shRNA) to suppress DNM1L expression. MTT, flow cytometry, and Transwell assays were used to detect the changes in cell proliferation, apoptosis, and invasion, respectively. Immunohistochemistry was used to detect DNM1L expression in gastric adenocarcinoma specimens, and the association of DNM1L expression with clinicopathological features and prognosis was analyzed. After the suppression of endogenous DNM1L expression in MKN-45 cells with shRNA, cell proliferation and invasion rates were significantly reduced, whereas apoptosis was significantly increased (all P<0.01). The expression of DNM1L was significantly higher in gastric adenocarcinoma specimens compared with that in pericarcinoma tissues (P<0.001). The expression of DNM1L increased with increasing infiltration depth, lymphatic metastasis, and higher tumor node metastasis stage (P<0.05). The expression of DNM1L associated negatively with prognosis (P<0.01). DNM1L plays a critical role in the proliferation, invasion and apoptosis of human gastric adenocarcinoma. DNM1L expression has prognostic significance for the survival of patients with gastric adenocarcinoma.

SP1 reduces autophagic flux through activating p62 in gastric cancer cells.

Gastric cancer is the most common type of gastrointestinal cancer, causing mortality worldwide. However, the underlying molecular mechanism in gastric cancer progression remains unclear. The autophagic flux was determined in gastric cancer cells overexpressing or inhibiting Sp1 transcription factor (SP1) using western blotting, reverse transcription­polymerase chain reaction and immunofluorescence staining. Luciferase and ChIP assays were performed to detect the potential underlying mechanism of SP1 in gastric cancer cells. Lastly, immunohistochemistry was also performed on SP1 and p62 expression levels in human gastric cancer specimens. It was demonstrated that SP1 diminished autophagic flux via activating p62 in gastric cancer. Moreover, SP1 deficiency increased the rate of autophagy of gastric cancer cells. Notably, it was observed that SP1 enhanced the expression levels of p62 by directly binding to the promoter of p62. Analysis of gastric cancer specimen staining established that p62 expression levels were increased in SP1­positve gastric tissues. The present study provided evidence for a novel mechanism regulating autophagy in gastric cancer cells.

HIF-2α promotes the formation of vasculogenic mimicry in pancreatic cancer by regulating the binding of Twist1 to the VE-cadherin promoter.

Vasculogenic mimicry (VM) is a blood supply modality that occurs independently of endothelial cell angiogenesis. Hypoxia and the epithelial-mesenchymal transition (EMT) induce VM formation by remodeling the extracellular matrix. Our previous study demonstrated that hypoxia-inducible factor-2 alpha (HIF-2α) promotes the progress of EMT in pancreatic cancer; however, whether HIF-2α promotes VM formation in pancreatic cancer remains unknown. In this study, we investigated HIF-2α expression and VM by immunohistochemistry in 70 pancreatic cancer patients as well as the role of Twist1and Twist2 in HIF-2α-induced VM in vitro and in vivo. We found that the overexpression of HIF-2α and VM were correlated with poor tumor differentiation, late clinical stage and lymph node metastasis, and a poor prognosis in pancreatic cancer. Moreover, the upregulation of HIF-2α in SW1990 cells induced VM formation, whereas the opposite results were found after silencing HIF-2α in AsPC-1 cells. A mechanistic study indicated that HIF-2α might regulate the binding of twist1 to vascular endothelial cadherin (VE-cadherin) to promote VM formation in pancreatic cancer cells, and that the P1 (-421bp) and P4 (-2110bp) regions of the Twist1 binding sequences are positive regulatory elements for VE-cadherin. In addition, we confirmed that the overexpression of HIF-2α increased Twist1 expression and promoted tumor growth and VM formation in pancreatic cancer xenografts in nude mice. These findings indicated that HIF-2α might play a critical role in VM and that HIF-2α and the pathway of HIF-2α inducing VM formation are potential therapeutic targets for pancreatic cancer.

Expression and clinical significance of glucose transporter-1 in pancreatic cancer.

Increasing evidence has demonstrated that malignant cells exhibit increased glucose uptake, which facilitates survival and growth in a hypoxic environment. The glucose transporter-1 (GLUT-1) is overexpressed in a variety of malignant tumors. However, the association between GLUT-1 expression and clinicopathological factors, 18F-fluorodeoxyglucose uptake and tumor proliferation in pancreatic cancer has not been investigated to date. In the present study, the expression of GLUT-1 in 53 pancreatic cancer tissues was analyzed, which revealed that GLUT-1 was overexpressed in pancreatic tissue and correlated with poor prognosis and clinicopathological characteristics, including increased tumor size, clinical stage and lymph node metastasis, maximum standardized uptake value (SUVmax) and Ki-67 expression. The receiver operating characteristic curve analysis indicated that a cut-off SUVmax value of 4.830 was associated with optimal sensitivity (88%) and specificity (71.4%) for the detection of strong positive GLUT-1 expression. In addition, as the expression of GLUT-1 was found to correlate with Ki-67 expression, GLUT-1 may exhibit a significant effect on cell proliferation in pancreatic cancer. Overall, these findings indicate that GLUT-1 may represent a prognostic indicator, and a potential therapeutic target for pancreatic cancer.

Endovascular Repair of Celiac Artery Aneurysm with the Use of Stent Grafts.

PURPOSE: To determine the feasibility, safety, and long-term outcome of stent-graft insertion for endovascular repair of celiac artery aneurysm (CAA). MATERIALS AND METHODS: From January 2010 to April 2015, 10 patients (three men and seven women; mean age, 51.6 y ± 12.1; age range, 39-81 y) with CAAs underwent endovascular repair via stent-graft insertion in a single center. During treatment, the stent graft was placed at the celiac and common hepatic arteries. Standard follow-up protocol included abdominal CT angiography and clinical examinations at 1, 3, 6, and 12 months and annually thereafter. Follow-up was performed every 2-3 months via telephone for the duration of the follow-up period to confirm patients' general condition. Data on patient characteristics, technical success, procedure-related complications, and follow-up were collected and analyzed retrospectively. RESULTS: CAA was successfully sealed by the stent graft in all patients. The common hepatic artery was patent after stent insertion in all patients, and no procedure-related complication occurred. All patients were followed up for 1-64 months (mean, 19.3 mo ± 18.9). Abdominal CT angiography demonstrated no endoleak, stent obstruction, or splenic infarction during follow-up. All patients experienced CAA shrinkage with formation of thrombi or increase in the quantity of thrombi in the CAA sac. CONCLUSIONS: Stent-graft insertion is a safe and effective method for endovascular repair of CAA.

Percutaneous recanalization for hepatic vein-type Budd-Chiari syndrome: long-term patency and survival.

OBJECTIVE: To determine the long-term patency and survival of percutaneous recanalization for hepatic vein (HV)-type Budd-Chiari syndrome (BCS). METHODS: From March 2009 to November 2014, consecutive symptomatic HV-type BCS patients were treated by percutaneous recanalization in our centers. These patients underwent main HV (MHV) or accessory HV (AHV) recanalization. Data on patient characteristics, technical success, clinical success, long-term patency, and survival were collected and analyzed. RESULTS: During the enrolled periods, a total of 143 symptomatic HV-type BCS patients were treated by percutaneous recanalization in our centers. Technical success was achieved in 140 of 143 patients. One hundred eleven patients underwent MHV recanalization, and 29 underwent AHV recanalization. Clinical success was achieved in 136 of 140 patients. The mean MHV/AHV pressure decreased from 33.5 ± 4.1 mmHg before treatment to 12.5 ± 3.1 mmHg after treatment (p = 0.000). The 136 patients were followed for 7-75 months (mean 33.9 ± 15.3 months). Twenty-eight patients experienced re-obstruction of MHV (n = 24) or AHV (n = 4) at 3 to 36 months (mean 18.0 ± 11.5 months) after treatment. The cumulative 1-, 3-, and 6-year primary patency rates were 91.1, 77.4, and 74.0%, respectively. The cumulative 1-, 3-, and 6-year secondary patency rates were 97.0, 92.4, and 88.8%, respectively. The cumulative 1-, 3-, and 6-year survival rates were 97.7, 92.2, and 90.0%, respectively. CONCLUSION: Percutaneous recanalization can provide good long-term patency and survival in HV-type BCS patients.

Expression of HIP/PAP in hepatocellular carcinoma and effect of siRNA on migration and invasion in HCC cells.

OBJECTIVE: To investigate the expression of HIP/PAP in hepatocellular carcinoma (HCC) patients and explore its role in migration and invasion of HCC. METHODS: The expression of HIP/PAP in HCC tissue and corresponding adjacent noncancerous tissue was assessed by IHC, RT-PCR and Western blot. The correlation between clinicopathological features and HIP/PAP expression was analyzed. The role of HIP/PAP on invasion and migration of HCC cells was observed by RNA interference, wound healing and Transwell assay. RESULTS: Both mRNA and protein expression of HIP/PAP was upregulated in HCC tissues compared to tumor-adjacent tissue and correlated with poor tumor differentiation, advanced tumor stage and vascular invasion. HIP/PAP expression was also upregulated in HCC cells, and silencing its expression by specific siRNA could inhibit the invasion and migration of HCC cells. CONCLUSIONS: HIP/APA is overexpressed in HCC and contributes to the migration and invasion of HCC cells.

Palliative Stent Insertion for Acute Malignant Colorectal Obstruction: Long-term Patency and Survival.

PURPOSE: To investigate the long-term outcome of palliative stent insertion for acute malignant colorectal obstruction. METHODS: From May 2009 to February 2015, consecutive patients with acute malignant colorectal obstruction underwent palliative stent insertion in our center. Technical success, clinical success, and long-term outcomes were analyzed retrospectively. RESULTS: A total of 45 patients with acute malignant colorectal obstruction underwent palliative stent insertion. Technical success was achieved in 42 of 45 patients. Clinical success was achieved in 41 of 42 patients. During a follow-up of 5 days to 25 months (mean, 6.9±4.5 mo), the cumulative 6- and 12-month patency rates were 88.6% and 72.7%, respectively. The cumulative 6- and 12-month survival rates were 60.1% and 14.3%, respectively. The independent predictor of prolonging survival was subsequent chemotherapy after stenting (P=0.017). CONCLUSION: Palliative colorectal stent insertion can provide a good long-term outcome in patients with malignant colorectal obstruction.

Placement of the Decompression Tube as a Bridge to Surgery for Acute Malignant Left-Sided Colonic Obstruction.

PURPOSE: The aim of this study is to investigate the feasibility, safety, and effectiveness of placing the decompression tube as a bridge to surgery for acute malignant left-sided colonic obstruction. METHODS: From January 2009 to August 2014, consecutive patients with acute malignant left-side colonic obstruction underwent placement of the decompression tube as a bridge to surgery in our center. The technical and clinical success of placing the decompression tube was evaluated. Clinical success was defined as relief of obstructive symptoms within 48 h after placing the decompression tube. Elective tumor resection was performed 7-9 days after colonic decompression. The types of surgery, primary anastomosis rate, and follow-up findings were analyzed. RESULTS: Twenty patients with acute malignant left-side colonic obstruction underwent placement of the decompression tube as a bridge to surgery. Placement of decompression tube was technically successful in all patients. No procedure-related complication occurred. Clinical success was achieved in 19 patients. Elective tumor resection and primary anastomosis were successfully performed in all 19 patients. The postoperative complications included wound infection (n = 2) and anastomotic stenosis (n = 1). CONCLUSION: Decompression tube can serve as an easy, safe, and effective bridge to subsequent surgery for patients with acute malignant left-sided colonic obstruction.

Percutaneous recanalization for combined-type Budd-Chiari syndrome: strategy and long-term outcome.

PURPOSE: To investigate the feasibility, strategy, and long-term outcome of percutaneous recanalization for combined-type Budd-Chiari syndrome (BCS). METHODS: From December 2007 to August 2014, consecutive symptomatic combined-type BCS patients were treated by percutaneous recanalization in our centers. Inferior vena cava (IVC) recanalization was the first-stage treatment for all patients. Recanalization of one hepatic vein (HV) was the second-stage treatment for the selected patients. If the patient had the compensatory and patent accessory HV (AHV), we observed this patient for 7 days after IVC recanalization. If the symptoms of portal hypertension improved, HV recanalization was not needed. Otherwise, HV recanalization was performed. If the patient had no patent AHV, HV recanalization was performed 3 days after IVC recanalization. Data on technical success, clinical success, and follow-up were analyzed, respectively. RESULTS: Sixty-two symptomatic combined-type BCS patients were enrolled. Technical success of percutaneous recanalization was achieved in 60 patients. Among them, 52 patients had the patent AHV and underwent single IVC recanalization, and 8 patients had no patent AHV and underwent combined IVC and HV recanalization. Clinical success was achieved in all of the 60 patients. Three patients died during the follow-up. The cumulative 1-, 2-, and 4-year survival rates were 98.3%, 96.5%, and 92.7%, respectively. CONCLUSION: Percutaneous recanalization is suitable for most combined-type BCS patients. Treatment strategy can be made according to the situation of AHV. If the patient has the patent AHV, single IVC recanalization is enough. Otherwise, combined IVC and HV recanalization should be performed.

Suppression of the Epidermal Growth Factor-like Domain 7 and Inhibition of Migration and Epithelial-Mesenchymal Transition in Human Pancreatic Cancer PANC-1 Cells.

BACKGROUND: Epidermal growth factor-like domain multiple 7 (EGFL7), a secreted protein specifically expressed by endothelial cells during embryogenesis, recently was identified as a critical gene in tumor metastasis. Epithelial-mesenchymal transition (EMT) was found to be closely related with tumor progression. Accordingly, it is important to investigate the migration and EMT change after knock-down of EGFL7 gene expression in human pancreatic cancer cells. MATERIALS AND METHODS: EGFL7 expression was firstly testified in 4 pancreatic cancer cell lines by real-time polymerase chain reaction (Real-time PCR) and western blot, and the highest expression of EGFL7 was found in PANC-1 cell line. Then, PANC-1 cells transfected with small interference RNA (siRNA) of EGFL7 using plasmid vector were named si-PANC-1, while transfected with negative control plasmid vector were called NC-PANC-1. Transwell assay was used to analyze the migration of PANC-1 cells. Real-time PCR and western blotting were used to detect the expression change of EGFL7 gene, EMT markers like E-Cadherin, N-Cadherin, Vimentin, Fibronectin and transcription factors like snail, slug in PANC-1, NC- PANC-1, and si-PANC-1 cells, respectively. RESULTS: After successful plasmid transfection, EGFL7 gene were dramatically knock-down by RNA interference in si-PANC-1 group. Meanwhile, migration ability decreased significantly, compared with PANC-1 and NC-PANC-1 group. Meanwhile, the expression of epithelial phenotype marker E-Cadherin increased and that of mesenchymal phenotype markers N-Cadherin, Vimentin, Fibronectin dramatically decreased in si-PANC-1 group, indicating a reversion of EMT. Also, transcription factors snail and slug decreased significantly after RNA interference. CONCLUSIONS: Current study suggested that highly-expressed EGFL7 promotes migration of PANC-1 cells and acts through transcription factors snail and slug to induce EMT, and further study is needed to confirm this issue.

Clinicopathological significance of cytoplasmic transducer of ErbB2. 1 expression in gastric cancer.

The aim of the present study was to investigate the expression of transducer of ErbB2. 1 (TOB1) in gastric carcinoma and to clarify the association between TOB1 expression and the clinical significance of this expression in patients with gastric carcinoma. Western blot analysis was performed to confirm the expression of TOB1 in gastric cancer. Immunohistochemistry (IHC) was performed on a tissue microarray containing 90 pairs of primary gastric cancer and adjacent normal tissue samples. TOB1 expression was evaluated separately with cytoplasmic and nuclear staining. Western blot analysis revealed significantly lower expression levels of TOB1 in gastric cancer tissues than those in adjacent normal tissues in 91.7% of cases. This was confirmed by IHC, which revealed decreased cytoplasmic TOB1 expression in cancer tissues compared with those of normal tissue samples in 84.4% of cases. The IHC data also revealed low cytoplasmic expression of TOB1 in 67.8% of human gastric cancer samples. Nuclear TOB1 expression exhibited no significant association with specific pathological features. However, a significant association was identified between cytoplasmic expression levels of TOB1 and clinicopathological characteristics, including the depth of invasion (P=0.017), differentiation grade (P=0.034) and tumor-node-metastasis stage (P<0.000). In conclusion, cytoplasmic TOB1 expression was suggested to be significant in angiogenesis and cell differentiation in gastric cancer tissues and may be used as a potential prognostic marker.

Diagnosis of Small Bowel Obstruction using Targeted Enterography During Nasointestinal Decompression.

The aim of the study is to investigate the efficacy of using targeted enterography during intestinal decompression in the diagnosis of small bowel obstruction (SBO). Thirty-five patients with SBO and who had neither strangulation nor other contradictions received intestinal decompression, under the guidance of X-ray, using a 300-cm-long nasointestinal tube which reached the upper jejunum. Contrast radiography of intestines was performed when the tip of the decompression tube reached the obstruction by administering double-contrast medium, containing 20-100 ml 76 % gastrografin and 50-200 ml air, through the nasointestinal tube. Serial erect and supine plain abdominal radiographs were obtained. Intubation procedure was successful in all 35 patients. SBO was resolved in 20 patients, alleviated in 15 patients and 10 patients received surgery. Selective enterographies showed clear and high quality images. Imaging findings demonstrated no significant abnormality in six patients and adhesive SBO in 15. Furthermore, intestinal tumours were identified in four patients of which three were metastatic tumours and one was an original intestinal cancer; Crohn's disease was confirmed in three patients; radiation enteritis in three (one of them was misdiagnosed and was then confirmed as metastatic tumour during surgery); enteric intussusception was found in two patients; polyps in one patient and carcinoma of the ascending colon in one. Targeted enterography during nasointestinal decompression allows confirmation of pathology of SBO by direct identification of the location, the extent and aetiology of obstruction, thereby providing evidence for the choice of timing and strategy of surgery.

Radiophotographically Controlled Nasointestinal Intubation to Treat Recurrent Postoperative Adhesive Ileus.

This study describes clinical experience and curative effect of radiophotographically controlled nasointestinal intubation in the treatment of small intestine arrangement in recurrent postoperative adhesive ileus. A 300-cm-long nasointestinal tube was installed into the jejunum through the nasal cavity under radiophotographic observation in 25 patients with recurrent postoperative adhesive ileus. The tube was advanced into the ileum by enterokinesia to relieve adhesive ileus and conduct small bowel arrangement. Duration of tube installation was 13 ± 11 min (range of 9-36 min). The success rate was 88 %. In 3 patients, assistance by a gastroscope was required. Twenty-one out of 25 patients were cured, making the cure rate of 84 %. The time for intestinal arrangement was 18.5 ± 3 days. The patients were followed up for 6 months to 2 years; there was 1 case of recurrence, while other patients recovered smoothly with no recurrence. A non-surgical nasointestinal intubation under radiophotography is a simple, safe, and effective management with few complications and beneficial outcome in recurrent postoperative adhesive ileus.

Inhibition of EZH2 expression is associated with the proliferation, apoptosis, and migration of SW620 colorectal cancer cells in vitro.

Epigenetic changes have been recently recognized as important in many human cancers. Enhancer of zeste homologue 2 (EZH2)gene has shown overexpression in various human cancers, consistent with a straightforward role of EZH2 as an oncogene, but its function in carcinogenesis is partly contradictory. The role of EZH2 in development of human colorectal cancer (CRC) has not yet been clarified. In present study, we observed up-regulation of EZH2 expression in tumor tissues from CRC patients [corrected]. The expression of EZH2 in CRC cell lines is consistent with the trend in cancer tissues using RT-PCR. We showed that TNM stage and lymph node metastasis in CRC patients are significantly correlated with EZH2 expression levels [corrected]. EZH2 level of transcription and protein was inhibited by small interfering RNA (siRNA). More importantly, EZH2-siRNA inhibited the proliferation and migration of SW620 cells while promoting their apoptosis, and inducing G0/G1 cell cycle arrest of CRC cells. Collectively, our results suggest that upregulated EZH2 expression may contribute to the progression of the patients with CRC. A comprehensive study of epigenetic mechanisms and the relevance of EZH2 in CRC is important for fully understanding this disease and as a basis for developing new treatment options in patients with CRC [corrected].