Diagnosis of Inverted Meckel's diverticulum by double-balloon enteroscopy: a case report.

Background: Meckel's diverticulum (MD) is the most common congenital defect of the gastrointestinal tract, occurring in about 1% to 2% of population. Most MD are rarely symptomatic, with presenting symptoms including diverticulitis, digestive tract hemorrhage and intestinal obstruction. The semblance of symptoms to enteritis and appendicitis makes preoperative diagnosis challenging. Current diagnosis of MD includes technetium-99m pertechnate scan, laparoscopic or intraoperative findings and examining surgical specimens. Here, we report that a double-balloon enteroscopy (DBE) improves the diagnosis accuracy of MD and presents high clinical application value. Case Description: A 12-year-old male patient was admitted to our hospital due to recurrent abdominal pain and black stools for more than half a year, recurrence for 2 days, accompanied by vomiting. The boy had anemic appearance, with periumbilical tenderness, and no mass was detected upon palpations. Past medical records revealed recurrent abdominal pain episodes thrice. Pre-surgery 99TcmO4-single-photon emission computed tomography/computed tomography (SPECT/CT) imaging was performed but did not reach the condition for diagnosis of MD. DBE was then performed and identified an upper ileum mass. After surgery, it was confirmed that the patient was an inverted MD, and the pathology showed gastric mucosa and pancreatic tissue. The patient recovered well after surgery and was discharged. Conclusions: DBE is not widely used in the diagnosis of MD, but its accuracy is higher than that of radionuclide scanning imaging. In addition, several advantages such as hemostasis treatment, direct detection and observation of the diverticulum, and demarcation of the site and scope of the lesion prior to surgery brings high clinical application value.

iTRAQ-Based Proteomics Screen identifies LIPOCALIN-2 (LCN-2) as a potential biomarker for colonic lateral-spreading tumors.

The improvement and implementation of a colonoscopy technique has led to increased detection of laterally spreading tumors (LSTs), which are presumed to constitute an aggressive type of colonic neoplasm. Early diagnosis and treatment of LSTs is clinically challenging. To overcome this problem, we employed iTRAQ to identify LST-specific protein biomarkers potentially involved in LST progression. In this study, we identified 2,001 differentially expressed proteins in LSTs using iTRAQ-based proteomics technology. Lipocalin-2 (LCN-2) was the most up-regulated protein. LSTs expression levels of LCN-2 and matrix metallopeptidase-9 (MMP-9) showed positive correlation with worse pathological grading, and up-regulation of these proteins in LSTs was also reflected in serum. Furthermore, LCN-2 protein overexpression was positively correlated with MMP-9 protein up-regulation in the tumor tissue and serum of LST patients (former rs = 0.631, P = 0.000; latter rs = 0.815, P = 0.000). Our results suggest that LCN-2 constitutes a potential biomarker for LST disease progression and might be a novel therapeutic target in LSTs.

Decreased expression of PBLD correlates with poor prognosis and functions as a tumor suppressor in human hepatocellular carcinoma.

Recent accumulating genomic and proteomic data suggested that decreased expression of phenazine biosynthesis-like domain-containing protein (PBLD) was frequently involved in hepatocellular carcinoma (HCC). However, there is lack of systematical investigation focusing on its expression pattern, clinical relevance, and biological function. Here, we found that PBLD was frequently decreased in HCC tissues relative to adjacent non-tumorigenic liver tissues. This decreased expression was significantly associated with poor tumor differentiation and advanced tumor stage. Kaplan-Meier analysis further showed that recurrence-free survival and overall survival were significantly worse among patients with low PBLD expression. Moreover, multivariate analyses revealed that PBLD was an independent predictor of OS and RFS. This prognostic value of PBLD was further validated in another independent cohort. We also found PBLD inhibited HCC cell growth and invasion in vitro and tumor growth in vivo. Furthermore, forced expression of PBLD influenced multiple downstream genes related to MAPK, NF-κB, EMT, and angiogenesis signaling pathways. PBLD deletion was an independent predictor of poor prognosis in patients with HCC. Elevated PBLD expression may reduce HCC cell growth and invasion via inactivation of several tumorigenesis-related signaling pathways.

Endoscopic submucosal dissection for the treatment of rectal carcinoid tumors 7-16 mm in diameter.

OBJECTIVE: Small rectal carcinoid tumors (<10 mm) are often removed via endoscopic submucosal dissection (ESD). However, the use of ESD for tumors of an intermediate size (7-16 mm) is less well documented. This study aimed to evaluate the efficacy and safety of ESD compared with endoscopic mucosal resection using a cap (EMR-C) for the treatment of 7-16-mm rectal carcinoids. MATERIAL AND METHODS: From September 2007 to August 2012, 55 patients with large rectal carcinoid tumors were treated by EMR-C (30 cases) or ESD (25 cases). The en bloc resection rate, pathological complete response (pCR) rate, procedure time, and incidence rates of complications, local recurrence, and distant metastasis were evaluated. RESULTS: The basic and clinical characteristics of the patients in the two groups did not differ significantly (p > 0.05). The mean procedure time was longer for ESD than EMR-C (24.79 ± 4.89 vs. 9.52 ± 2.14 min, p < 0.001). The rates of en bloc resection and pCR were higher with ESD than with EMR-C (100 vs. 83.33 %, and 100 vs. 70.00 %, respectively). No patients in the EMR-C group experienced complications. However, in the ESD group, two cases of perforation occurred, and one patient experienced delayed bleeding. These complications were successfully managed via endoscopical therapy. Five cases of local recurrence were detected after EMR-C, whereas no patients experienced recurrence after ESD. CONCLUSIONS: Compared with EMR-C, ESD appears to be a more favorable therapeutic option for the treatment of rectal carcinoid tumors less than 16 mm in diameter based on improved rates of pCR and local recurrence.

ZNF703 acts as an oncogene that promotes progression in gastric cancer.

ZNF703, a member of the NET/Nlz family of zinc finger transcription factors, contributes to aspects of developmental growth and patterning across evolutionarily diverse species. ZNF703 has been identified as a novel oncogene in human breast cancer. In the present study, we investigated the expression of ZNF703 in gastric carcinoma and attempted to determine, using cell line models, its biological actions. Using immunohistochemistry, we analyzed the ZNF703 protein expression in 120 clinicopathologically characterized gastric cancer cases. Using RNA interference, we investigated the effects of ZNF703 depletion on tumor proliferation and metastasis in vitro. We found that ZNF703 was overexpressed in invasive gastric carcinoma tissues, and its expression levels were closely correlated with the depth of invasion, node metastasis and venous invasion. RNA interference-mediated silencing of the ZNF703 gene in SGC7901 cells inhibited cell proliferation and migration significantly. The results showed that ZNF703 acts as a gastric cancer oncogene and should be considered a therapeutic target for metastatic gastric cancer.

Interleukin-11 induces the expression of matrix metalloproteinase 13 in gastric cancer SCH cells partly via the PI3K-AKT and JAK-STAT3 pathways.

Interleukin (IL)-11 is expressed in the majority of gastric carcinomas and has been associated with an aggressive phenotype and poor prognosis of gastric adenocarcinoma. Matrix metalloproteinase (MMP)-13 has been detected in numerous invasive malignant tumor types and exhibits a broad spectrum of activities on connective tissue components. In this study, we investigated whether IL-11 affects the expression of MMP-13 in human gastric cancer cells, as well as the underlying mechanism. Using western blot assays, we investigated the effect of recombinant human (rh) IL-11 on the expression of MMP-13 in gastric carcinoma cell lines. Using the PI3K inhibitor wortmannin and RNA interference to target the STAT3 gene, we investigated the effects of PI3K inhibition and/or STAT3 depletion on the expression of the MMP-13 protein. Results showed that IL-11 induced MMP-13 expression in a time- and concentration-dependent manner in SCH cells. IL-11 activated PI3K-AKT and JAK-STAT3 signal transduction. Wortmannin and depletion of STAT3 by means of small interfering RNA (siRNA) synergistically reduced the expression of MMP-13. These findings suggested that IL-11 induces the expression of MMP-13 in gastric cancer SCH cells partly via the PI3K-AKT and JAK-STAT3 pathways.