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Find video protocols related to scientific articles indexed in Pubmed.
Modeling interactions between Human Equilibrative Nucleoside Transporter-1 and other factors involved in the response to gemcitabine treatment to predict clinical outcomes in pancreatic ductal adenocarcinoma patients.
J Transl Med
PUBLISHED: 05-06-2014
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BackgroundPancreatic ductal adenocarcinoma (PDAC) is an extremely aggressive malignancy, characterized by largely unsatisfactory responses to the currently available therapeutic strategies. In this study we evaluated the expression of genes involved in gemcitabine uptake in a selected cohort of patients with PDAC, with well-defined clinical-pathological features.MethodsmRNA levels of hENT1, CHOP, MRP1 and DCK were evaluated by means of qRT-PCR in matched pairs of tumor and adjacent normal tissue samples collected from PDAC patients treated with gemcitabine after surgical tumor resection. To detect possible interaction between gene expression levels and to identify subgroups of patients at different mortality/progression risk, the RECursive Partitioning and Amalgamation (RECPAM) method was used.ResultsRECPAM analysis showed that DCK and CHOP were most relevant variables for the identification of patients with different mortality risk, while hENT1 and CHOP were able to identify subgroups of patients with different disease progression risk. Conclusion: hENT1, CHOP, MRP1 and DCK appear correlated to PDAC, and this interaction might influence disease behavior.
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Influence of preoperative biliary drainage on surgical outcome after pancreaticoduodenectomy: single centre experience.
Langenbecks Arch Surg
PUBLISHED: 03-16-2014
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Controversy prevails on the impact of preoperative biliary drainage (PBD) on postoperative complications and clinical outcome of pancreatic cancer. We determined whether PBD is associated with increased morbidity and mortality rates after pancreaticoduodenectomy.
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A tumour score with multidetector spiral CT for venous infiltration in pancreatic cancer: influence on borderline resectable.
Radiol Med
PUBLISHED: 03-12-2014
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A tumour score for venous invasion in patients with pancreatic adenocarcinoma was evaluated by means of computed tomography (CT), in order to improve the assessment of medical treatment and clinical outcome with special attention to borderline resectable disease.
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Interplay between SOX9, ?-catenin and PPAR? activation in colorectal cancer.
Biochim. Biophys. Acta
PUBLISHED: 04-03-2013
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Colorectal carcinogenesis relies on loss of homeostasic mechanisms regulating cell proliferation, differentiation and survival. These cell processes have been reported to be influenced independently by transcription factors activated downstream of the Wnt pathway, such as SOX9 and ?-catenin, and by the nuclear receptor PPAR?. The purpose of this study was to explore the expression levels and functional link between SOX9, ?-catenin and PPAR? in the pathogenesis of colorectal cancer (CRC). We evaluated SOX9, ?-catenin and PPAR? expression levels on human CRC specimens by qPCR and immunoblot detection. We tested the hypothesis that PPAR? activation might affect SOX9 and ?-catenin expression using four colon cancer cell lines (CaCo2, SW480, HCT116, and HT29 cells). In CRC tissues SOX9 resulted up-regulated at both mRNA and protein levels when compared to matched normal mucosa, ?-catenin resulted up-regulated at protein levels, while PPARG mRNA and PPAR? protein levels were down-regulated. A significant relationship was observed between high PPARG and SOX9 expression levels in the tumor tissue and female gender (p=0.005 and p=0.04, respectively), and between high SOX9 expression in the tumor tissue and age (p=0.04) and microsatellite instability (MSI), in particular with MSI-H (p=0.0002). Moreover, treatment with the synthetic PPAR? ligand rosiglitazone induced different changes of SOX9 and ?-catenin expression and subcellular localization in the colon cancer cell lines examined. In conclusion, SOX9, ?-catenin and PPAR? expression levels are deregulated in the CRC tissue, and in colon cancer cell lines ligand-dependent PPAR? activation unevenly influences SOX9 and ?-catenin expression and subcellular localization, suggesting a variable mechanistic role in colon carcinogenesis.
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Chemokine receptor CXCR4: Role in gastrointestinal cancer.
Crit. Rev. Oncol. Hematol.
PUBLISHED: 03-31-2013
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Chemokines (CK)s, small proinflammatory chemoattractant cytokines that bind to specific G-protein coupled seven-span transmembrane receptors, are major regulators of cell trafficking and adhesion. The CXCL12 [stromal cell-derived factor-1 (SDF-1)] binds primarily to CXC receptor 4 (CXCR4; CD184). The binding of CXCL12 to CXCR4 induces intracellular signaling through several divergent pathways initiating signals related to chemotaxis, cell survival and/or proliferation, increase in intracellular calcium, and gene transcription. CXCR4 is expressed on multiple cell types including lymphocytes, hematopoietic stem cells, endothelial and epithelial cells, and cancer cells. One of the most intriguing and perhaps important roles that CKs and the CK receptors have is in regulating metastasis. Here, CK receptors may potentially facilitate tumor dissemination at each of the key steps of metastasis, including adherence of tumor cells to endothelium, extravasation from blood vessels, metastatic colonization, angiogenesis, proliferation, and protection from the host response via activation of key survival pathways such as ERK/MAPK, PI-3K/Akt/mTOR, or Jak/STAT, etc. In addition, it is increasingly recognized that CKs play an important role in facilitating communication between cancer cells and non-neoplatic cells in the tumor microenvironment (TME), including endothelial cells and fibroblasts, promoting the infiltration, activation of neutrophils, and tumor-associated macrophages within the TME. In this review, we mainly focus on the roles of chemokines CXCL12 and its cognate receptors CXCR4 as they pertain to cancer progression. In particular, we summarizes our current understanding regarding the contribution of CXCR4 and SDF-1 to gastrointestinal tumor behavior and its role in local progression, dissemination, and immune evasion of tumor cells. Also, describes recent therapeutic approaches that target these receptors or their ligands.
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Neoadjuvant/preoperative gemcitabine for patients with localized pancreatic cancer: a meta-analysis of prospective studies.
Ann. Surg. Oncol.
PUBLISHED: 07-14-2011
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Long-term prognosis for localized pancreatic cancer remains poor. We sought to assess the benefit of neoadjuvant/preoperative chemotherapy with or without radiotherapy.
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Key role of phosphoinositide 3-kinase class IB in pancreatic cancer.
Clin. Cancer Res.
PUBLISHED: 09-28-2010
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Phosphoinositide 3-kinase (PI3K) signaling is well established as important in cancer. To date most studies have been focused on the PI3K/p110? isoform, which has been found to be mutated in several different cancers. The aim of our study was to determine which specific PI3K isoforms are involved in pancreatic ductal adenocarcinoma (PDAC) and investigate the effects of these isoforms on proliferation, survival, and induction of Akt activation in pancreatic cancer cells.
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Surgical aspects in management of hepato-pancreatico-biliary tumours in the elderly.
Best Pract Res Clin Gastroenterol
PUBLISHED: 05-13-2009
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Hepato-pancreatico-biliary (HPB) surgery encompasses major hepatic resection and pancreatic surgery, both procedures of high complexity with a potentially high complication rate. The establishment of centres of excellence with a high patient volume has lowered the complication and increased the resection rate. Besides this, increased life expectancy and improved general health status have increased the number of elderly patients eligible for major surgery. Because elderly patients have more co-morbidities and decreased life expectancy, the benefit of these procedures must be critically evaluated in such patients. Analysis of the literature on this subject demonstrated that pancreatico-duodenectomy can be performed safely in selected elderly patients (80 years of age or older), with morbidity and mortality rates approaching those observed in younger patients. This aspect was also confirmed by cost analysis studies that reported similar data in both groups. Similar findings are also reported for major hepatic resection in elderly patients with either hepatocellular carcinoma (HCC), Klatskin tumour or gallbladder carcinoma. Nevertheless, those elderly patients who will benefit from surgery must be critically selected.
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Genetic susceptibility to pancreatic cancer and its functional characterisation: the PANcreatic Disease ReseArch (PANDoRA) consortium.
Dig Liver Dis
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Pancreatic cancer is the fourth leading cause of cancer deaths in the European Union and in the USA, but little is known about its genetic susceptibility. The PANcreatic Disease ReseArch (PANDoRA) consortium was established to unite the efforts of different research groups; its aim is to create a large bio-database to uncover new genetic factors for pancreatic cancer risk, response to treatment, and patient survival. So far 2220 cases of pancreatic adenocarcinoma, a smaller number of cases of endocrine pancreatic tumours (n=86), chronic pancreatitis (n=272) and 3847 healthy controls have been collected. As a collective effort of the consortium, SNPs associated with pancreatic adenocarcinoma risk from a genome-wide association study performed in Caucasians were replicated. The possibility that the same genetic polymorphisms may influence patient survival as well was also addressed. This collective effort is particularly important for pancreatic cancer because it is a relatively rare disease for which little is known about aetiopathogenesis and risk factors. The recruitment of additional collaborators and partner institutions is continuously on-going.
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Cathepsins and pancreatic cancer: the 2012 update.
Pancreatology
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Pancreatic cancer is the result of distinctive genetic and epigenetic disturbances. This multistep process is in part well-defined and includes alterations in oncogenes and suppressor genes that control proliferation, apoptosis, angiogenesis, invasion and cell migration. Cathepsins are proteolytic enzymes and represent potential therapeutic targets in human tumors. Cathepsins predominantly function as endopeptidases within endolysosomal vesicles of normal cells and they are involved in physiological processes such as protein turnover, differentiation and apoptosis. In various types of malignancies, cathepsins have been associated with tumor progression and metastasis. Growing evidence and direct proofs suggest that cathepsins are highly up-regulated in pancreatic cancer and contribute to the development and progression of the cancer phenotype. In this review, the role of cathepsins in pancreatic cancer tumorigenesis is reported and discussed. Some critical aspects will be underlined such as specificity of cathepsin activity in pancreatic cancer and in its precursor lesions; the genetic perturbation and the intracellular signaling pathway activated by cathepsins as reported in preclinical models and in human tissues; the preliminary results and the oncological effects of cathepsin inhibitors currently tested on pancreatic cancer cells; the role of combined therapy based on chemotherapeutic agents and cathepsin inhibition. Although mounting evidences indicate that cysteine cathepsins are potential therapeutic targets in pancreatic cancer, as suggested by their functional role in controlling invasiveness and metastasis, it remains to be seen whether the promising benefits of pharmacological inhibitors observed in preclinical study might be translated to the current clinical practice.
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Time-Qualified Patterns of Variation of PPAR?, DNMT1, and DNMT3B Expression in Pancreatic Cancer Cell Lines.
PPAR Res
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Carcinogenesis is related to the loss of homeostatic control of cellular processes regulated by transcriptional circuits and epigenetic mechanisms. Among these, the activities of peroxisome proliferator-activated receptors (PPARs) and DNA methyltransferases (DNMTs) are crucial and intertwined. PPAR? is a key regulator of cell fate, linking nutrient sensing to transcription processes, and its expression oscillates with circadian rhythmicity. Aim of our study was to assess the periodicity of PPAR? and DNMTs in pancreatic cancer (PC). We investigated the time-related patterns of PPARG, DNMT1, and DNMT3B expression monitoring their mRNA levels by qRT-PCR at different time points over a 28-hour span in BxPC-3, CFPAC-1, PANC-1, and MIAPaCa-2 PC cells after synchronization with serum shock. PPARG and DNMT1 expression in PANC-1 cells and PPARG expression in MIAPaCa-2 cells were characterized by a 24?h period oscillation, and a borderline significant rhythm was observed for the PPARG, DNMT1, and DNMT3B expression profiles in the other cell lines. The time-qualified profiles of gene expression showed different shapes and phase relationships in the PC cell lines examined. In conclusion, PPARG and DNMTs expression is characterized by different time-qualified patterns in cell lines derived from human PC, and this heterogeneity could influence cell phenotype and human disease behaviour.
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Expression of the antiapoptotic protein BAG3 is a feature of pancreatic adenocarcinoma and its overexpression is associated with poorer survival.
Am. J. Pathol.
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Pancreatic ductal adenocarcinoma (PDAC) is one of the most deadly cancers, being the fourth leading cause of cancer-related deaths. Long-term survival reaching 15% is achieved in less than 5% of patients who undergo surgery, and median survival is only 6 months in those with inoperable lesions. A deeper understanding of PDAC biologic characteristics as well as novel prognostic markers are therefore required to improve outcomes. Herein we report that BAG3, a protein with recognized anti-apoptotic activity, was expressed in 346 PDACs analyzed, but was not expressed in the surrounding nonneoplastic tissue. In a cohort of 66 patients who underwent radical resection (R0), survival was significantly shorter in patients with high BAG3 expression (median, 12 months) than in those with low BAG3 expression (median, 23 months) (P = 0.001). Furthermore, we report that BAG3 expression in PDAC-derived cell lines protects from apoptosis and confers resistance to gemcitabine, offering a partial explanation for the survival data. Our results indicate that BAG3 has a relevant role in PDAC biology, and suggest that BAG3 expression level might be a potential marker for prediction of patient outcome.
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Correlations among PPAR?, DNMT1, and DNMT3B Expression Levels and Pancreatic Cancer.
PPAR Res
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Emerging evidence indicates that peroxisome proliferator-activated receptor ? (PPAR?) and DNA methyltransferases (DNMTs) play a role in carcinogenesis. In this study we aimed to evaluate the expression of PPAR?, DNMT1, and DNMT3B and their correlation with clinical-pathological features in patients with pancreatic cancer (PC), and to define the effect of PPAR? activation on DNMTs expression in PC cell lines. qRT-PCR analysis showed that DNMT3B expression was downregulated in tumors compared to normal tissues (P = 0.03), whereas PPAR? and DNMT1 levels did not show significant alterations in PC patients. Expression levels between PPAR? and DNMT1 and between DNMT1 and DNMT3B were highly correlated (P = 0.008 and P = 0.05 resp.). DNMT3B overexpression in tumor tissue was positively correlated with both lymph nodes spreading (P = 0.046) and resection margin status (P = 0.04), and a borderline association with perineural invasion (P = 0.06) was found. Furthermore, high levels of DNMT3B expression were significantly associated with a lower mortality in the whole population (HR = 0.485; 95%CI = 0.262-0.895, P = 0.02) and in the subgroup of patients without perineural invasion (HR = 0.314; 95%CI = 0.130-0.758; P = 0.01), while such association was not observed in patients with tumor invasion into perineural structures (P = 0.70). In conclusion, in vitro and in vivo PPAR? and DNMTs appear interrelated in PC, and this interaction might influence cell phenotype and disease behavior.
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Changes in miR-143 and miR-21 expression and clinicopathological correlations in pancreatic cancers.
Pancreas
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Despite advances in clinical management of pancreatic cancer (PC), there is still room for improvement in early detection, diagnosis, and treatment strategies. The role of microRNAs (miRNAs) in tumor biology might pinpoint an alteration in expression of miRNAs as new diagnostic/prognostic biomarkers.
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Mirna expression profiles identify drivers in colorectal and pancreatic cancers.
PLoS ONE
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Altered expression of microRNAs (miRNAs) hallmarks many cancer types. The study of the associations of miRNA expression profile and cancer phenotype could help identify the links between deregulation of miRNA expression and oncogenic pathways.
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Combined modality treatments in pancreatic cancer.
Expert Opin. Ther. Targets
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Of all the carcinomas, pancreatic carcinoma (PC) has the highest mortality rate, with a 1- and 5-year survival rate of 25% and less than 5% respectively. This is regardless of the stage at diagnosis.
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What is Visualize?

JoVE Visualize is a tool created to match the last 5 years of PubMed publications to methods in JoVE's video library.

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We use abstracts found on PubMed and match them to JoVE videos to create a list of 10 to 30 related methods videos.

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In developing our video relationships, we compare around 5 million PubMed articles to our library of over 4,500 methods videos. In some cases the language used in the PubMed abstracts makes matching that content to a JoVE video difficult. In other cases, there happens not to be any content in our video library that is relevant to the topic of a given abstract. In these cases, our algorithms are trying their best to display videos with relevant content, which can sometimes result in matched videos with only a slight relation.