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Gou S.,Pancreatic Disease Institute | Yu J.,Union Hospital | Wang C.,Pancreatic Disease Institute | Liu T.,Pancreatic Disease Institute | And 2 more authors.
Pancreas | Year: 2013

Solid pseudopapillary tumors (SPTs) are a rare pancreatic neoplastic lesion. Familial aggregation has not been reported in this disease. The objectives of this study were to report the history, clinicopathological features, and gene mutations of 3 familial cases of SPT. Three female cases of SPT presented in 1 family. Eight family relatives, 5 healthy volunteers, and 8 patients with SPT acted as controls. Histological examination and immunohistochemistry were performed on the surgical tumor specimens. Polymerase chain reaction-single-strand conformation polymorphism and gene sequencing were performed on genomic DNA extracted from blood. All 3 patients underwent surgical treatment, 2 patients died (3 months and 5 months after surgery), whereas neither recurrence nor metastasis was observed in the other patient during 2-year follow-up. The tumors from the 3 cases had identical immunoreactivity to a series of molecular markers. A Leu104Val mutation of protease serine 1 (PRSS1) was observed in the familial patients and 2 healthy male family members; no β-catenin or adenomatous polyposis coli mutations were detected in the familial cases. This study indicates the possibility of genetic involvement in the pathogenesis of SPT. Family history may be a positive predictive factor for malignancy in SPT. Copyright © 2012 by Lippincott Williams & Wilkins.


Gou S.,Pancreatic Disease Institute | Xiong J.,Pancreatic Disease Institute | Wu H.,Pancreatic Disease Institute | Zhou F.,Pancreatic Disease Institute | And 3 more authors.
Journal of Gastrointestinal Surgery | Year: 2013

Introduction: Despite advances in the management of necrotizing pancreatitis, open necrosectomy remains an important management option for necrotizing pancreatitis, and patients undergoing necrosectomy suffer significant morbidity and mortality. The aim of this study was to report the outcomes of open necrosectomy from a recent large cohort of patients with necrotizing pancreatitis. Methods: Data are reported from a cohort of 276 consecutive patients with necrotizing pancreatitis who underwent open surgical debridement. Nutritional status, nutritional methods, bleeding, infection, demarcation of necrotic tissues, and time from onset of disease were scored. Scores ≥ 10 were considered as an indication for debridement. Results: One hundred sixty-two (58.7 %) and 52 (18.8 %) patients underwent minimally invasive peritoneal and retroperitoneal drainage, respectively, before necrosectomy. Median delay from disease onset to debridement was 48 days. Fifty-five patients (19.9 %) underwent more than one operation; 352 operations were performed in total. There were 17 deaths (6.2 %) postoperatively. Conclusion: This study demonstrated the results for open debridement in a recent large cohort of patients. Although minimally invasive necrosectomy has been developed in recent years, open necrosectomy remains an important approach for the debridement of necrotizing pancreatitis effectively and safely. © 2013 The Society for Surgery of the Alimentary Tract.


He H.,Pancreatic Disease Institute | Di Y.,Pancreatic Disease Institute | Liang M.,Fudan University | Yang F.,Pancreatic Disease Institute | And 6 more authors.
Oncology Reports | Year: 2013

Pancreatic cancer is known for its poor prognosis and early lymphatic metastasis is a notable characteristic. microRNAs (miRNAs) have been shown to be involved in the initiation and progression of pancreatic cancer. We, therefore, established a screening strategy to find miRNAs related to the lymphatic metastasis of pancreatic cancer and explored the target genes of miRNAs. miRNA array profiles were analyzed in tissue samples [pancreatic ductal adenocarcinoma (PDAC) and matched adjacent benign tissues (MAT)] and cell lines (BxPC-3-LN and BxPC-3). Combined analysis of profiling data from tissue samples and cell lines was used to identify miRNAs related to the lymphatic metastasis of pancreatic cancer. The expression levels of miRNAs were confirmed by real-time reverse transcription PCR (RT-PCR) in tissue samples and cell lines. The correlation between miRNAs and clinicopathological characteristics was investigated. The expression features of miRNAs in pancreatic cancer, precursor lesions and metastatic lymph nodes were characterized by in situ hybridization (ISH). Predicted target genes of miRNAs were validated by RT-PCR and the protein levels of target genes were revealed by western blotting. Seventy and 63 miRNAs were differentially expressed in pancreatic cancer and BxPC- 3-LN, compared to MAT and BxPC-3, respectively. Combined microarray analysis found 4 co-differentially expressed miRNAs (miRNA-663, miRNA-145, miRNA-218 and let-7) related to the lymphatic metastasis of pancreatic cancer. miRNA-218 was significantly downregulated in BxPC-3-LN (fold-change >10) and the expression levels of miRNA-218 were confirmed by RT-PCR. The group with lymph node metastasis and the elder group (age >64) showed lower expression of miRNA-218 (P=0.003 and 0.002), compared to patients without lymph nodes metastasis and patients in the younger group (age ≤64), respectively. The expression of miRNA-218 showed a decreasing trend from normal acinar/ductal epithelium, intraductal papillary mucinous neoplasm (IPMN), pancreatic cancer to metastatic lymph nodes by ISH. Among 8 predicted target genes of miRNA-218, rodent bone (ROBO-1) was confirmed to be upregulated in both mRNA and protein levels in pancreatic cancer. In conclusion, we established a screening strategy based on microarray results and found miRNA-218 to be a notable gene related to lymphatic metastasis of pancreatic cancer. Downregulation of miRNA-218 and upregulation of ROBO-1 were first demonstrated in pancreatic cancer. The miRNA-218 and ROBO-1 signaling axis may contribute to the lymphatic metastasis of pancreatic cancer.


Jiang Y.,Pancreatic Disease Institute | Jin C.,Pancreatic Disease Institute | Yang F.,Pancreatic Disease Institute | Yu X.,Pancreatic Disease Institute | And 6 more authors.
Journal of Nanoparticle Research | Year: 2011

Amino-carbon nanotubes (amino-CNTs) can conjugate with the DNA by electrostatic interactions and shuttle the DNA to the cell cytoplasm or even the nucleus. Here we report a new approach to produce amino-CNTs by cycloaddition of nitrenes. Fourier transform infrared spectroscopy was used to verify the success of the functionalization, and the functionalization degree was calculated by thermal gravity analysis. Transmission electron microscope (TEM) was used to observe the solubility of the CNTs and the interactions of the amino-CNTs with the plasmids. Cell ultrathin sections were made and observed under the TEM to confirm the amino-CNTs enter the cells. Transfection experiments ultimately verify the amino-CNTs produced through cycloadditions of nitrenes can serve as plasmid vector. © 2010 Springer Science+Business Media B.V.


Gou S.,Pancreatic Disease Institute | Cui P.,Pancreatic Disease Institute | Li X.,Pancreatic Disease Institute | Shi P.,Pancreatic Disease Institute | And 2 more authors.
PLoS ONE | Year: 2013

Pancreatic cancer is the fourth leading cause of cancer related deaths in the United States. The prognosis remains dismal with little advance in treatment. Metformin is a drug widely used for the treatment of type II diabetes. Recent epidemiologic data revealed that oral administration of metformin is associated with a reduced risk of pancreatic cancer, suggesting its potential as a novel drug for this disease. Many studies have demonstrated the in vitro anticancer action of metformin, but the typically used concentrations were much higher than the in vivo plasma and tissue concentrations achieved with recommended therapeutic doses of metformin, and low concentrations of metformin had little effect on the proliferation of pancreatic cancer cells. We examined the effect of low concentrations of metformin on different subpopulations of pancreatic cancer cells and found that these selectively inhibited the proliferation of CD133+ but not CD24+CD44+ESA+ cells. We also examined the effect of low concentrations of metformin on cell invasion and in vivo tumor formation, demonstrating in vitro and in vivo anticancer action. Metformin was associated with a reduction of phospho-Erk and phospho-mTOR independent of Akt and AMPK phosphorylation. CD133+ pancreatic cancer cells are considered to be cancer stem cells that contribute to recurrence, metastasis and resistance to adjuvant therapies in pancreatic cancer. Our results provide a basis for combination of metformin with current therapies to improve the prognosis of this disease. © 2013 Gou et al.

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