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| 1 | Gut microbiota imbalance and colorectal cancer显示文摘The gut microbiota acts as a real organ. The symbiotic interactions between resident micro-organisms and the digestive tract highly contribute to maintain the gut homeostasis. However, alterations to the microbiome caused by environmental changes(e.g., infection, diet and/or lifestyle) can disturb this symbiotic relationship and promote disease, such as inflammatory bowel diseases and cancer. Colorectal cancer is a complex association of tumoral cells, non-neoplastic cells and a large amount of micro-organisms, and the involvement of the microbiota in colorectal carcinogenesis is becoming increasingly clear. Indeed, many changes in the bacterial composition of the gut microbiota have been reported in colorectal cancer, suggesting a major role of dysbiosis in colorectal carcinogenesis. Some bacterial species have been identified and suspected to play a role in colorectal carcinogenesis, such as Streptococcus bovis, Helicobacter pylori, Bacteroides fragilis, Enterococcus faecalis, Clostridium septicum, Fusobacterium spp. and Escherichia coli. The potential pro-carcinogenic effects of these bacteria are now better understood. In this review, we discuss the possible links between the bacterial microbiota and colorectal carcinogenesis, focusing on dysbiosis and the potential pro-carcinogenic properties of bacteria, such as genotoxicity and other virulence factors, inflammation, host defenses modulation, bacterial derived metabolism, oxidative stress and anti-oxidative defenses modulation. We lastly describe how bacterial microbiota modifications could represent novel prognosis markers and/or targets for innovative therapeutic strategies. | Johan Gagnière Jennifer Raisch Julie Veziant Nicolas Barnich Richard Bonnet Emmanuel Buc Marie-Agnès Bringer Denis Pezet Mathilde Bonnet | 2016 | World Journal of Gastroenterology2016,22,2: | 76 |
| 2 | Colon cancer-associated B2 Escherichia coli colonize gut mucosa and promote cell proliferation显示文摘AIM:To provide further insight into the characterization of mucosa-associated Escherichia coli(E.coli)isolated from the colonic mucosa of cancer patients.METHODS:Phylogroups and the presence of cyclomodulin-encoding genes of mucosa-associated E.coli from colon cancer and diverticulosis specimens weredetermined by PCR.Adhesion and invasion experiments were performed with I-407 intestinal epithelial cells using gentamicin protection assay.Carcinoembryonic antigen-related cell adhesion molecule 6(CEACAM6)expression in T84 intestinal epithelial cells was measured by enzyme-linked immunosorbent assay and by Western Blot.Gut colonization,inflammation and procarcinogenic potential were assessed in a chronic infection model using CEABAC10 transgenic mice.Cell proliferation was analyzed by real-time mRNA quantification of PCNA and immunohistochemistry staining of Ki67.RESULTS:Analysis of mucosa-associated E.coli from colon cancer and diverticulosis specimens showed that whatever the origin of the E.coli strains,86%of cyclomodulin-positive E.coli belonged to B2 phylogroup and most harbored polyketide synthase(pks)island,which encodes colibactin,and/or cytotoxic necrotizing factor(cnf)genes.In vitro assays using I-407 intestinal epithelial cells revealed that mucosa-associated B2 E.coli strains were poorly adherent and invasive.However,mucosa-associated B2 E.coli similarly to Crohn’s disease-associated E.coli are able to induce CEACAM6expression in T84 intestinal epithelial cells.In addition,in vivo experiments using a chronic infection model of CEACAM6 expressing mice showed that B2 E.coli strain11G5 isolated from colon cancer is able to highly persist in the gut,and to induce colon inflammation,epithelial damages and cell proliferation.CONCLUSION:In conclusion,these data bring new insights into the ability of E.coli isolated from patients with colon cancer to establish persistent colonization,exacerbate inflammation and trigger carcinogenesis. | Jennifer Raisch Emmanuel Buc Mathilde Bonnet Pierre Sauvanet Emilie Vazeille Amélie de Vallée Pierre Déchelotte Claude Darcha Denis Pezet Richard Bonnet Marie-Agnès Bringer Arlette Darfeuille-Michaud | 2014 | World Journal of Gastroenterology2014,20,21: | 12 |
| 3 | Peng’s Binding Pancreaticojejunostomy After Pancreaticoduodenectomy: A French Prospective Study显示文摘 | Emmanuel Buc Renaud Flamein Claudio Golffier Anne Dubois Ganesh Nagarajan Emmanuel Futier Denis Pezet | 2010 | Journal of Gastrointestinal Surgery2010,,4: | 1 |
| 4 | The liver hanging manoeuvre 显示文摘 | Guido Liddo Emmanuel Buc Ganesh Nagarajan | 2009 | International Hepato- Pancreato-Biliary Association2009,11,: | 1 |
| 5 | Massive hepatic necrosis with toxic liver syndrome following portal vein ligation显示文摘Right portal vein ligation (PVL) is a safe and widespread procedure to induce controlateral liver hypertrophy for the treatment of bilobar colorectal liver metastases. We report a case of a 60-year-old man treated by both right PVL and ligation of the glissonian branches of segment 4 for colorectal liver metastases surrounding the right and median hepatic veins. After surgery, the patient developed massive hepatic necrosis with secondary pulmonary and renal insufficiency requiring transfer to the intensive care unit. This so-called toxic liver syndrome finally regressed after hemofiltration and positive oxygen therapy. Diagnosis of acute congestion of the ligated lobe was suspected. The mechanism suspected was an increase in arterial inflow secondary to portal vein ligation concomitant with a decrease in venous outflow due to liver metastases encircling the right and median hepatic vein. This is the first documented case of toxic liver syndrome in a non-cirrhotic patient with favorable issue, and a rare complication of PVL. | Aurélien Dupré Johan Gagnière Lucie Tixier David Da Ines Sébastien Perbet Denis Pezet Emmanuel Buc | 2013 | World Journal of Gastroenterology2013,19,18: | 1 |
| 6 | Peng’s Binding Pancreaticojejunostomy After Pancreaticoduodenectomy: A French Prospective Study显示文摘 | Emmanuel Buc Renaud Flamein Claudio Golffier Anne Dubois Ganesh Nagarajan Emmanuel Futier Denis Pezet | 2010 | Journal of Gastrointestinal Surgery2010,,4: | 1 |
| 7 | Tobacco Smoking: A Factor of Early Onset of Colorectal Cancer显示文摘 | Emmanuel Buc M.D. Fabrice Kwiatkowski Ph.D. Arnaud Alves M.D. Yves Panis M.D. Ph.D. Georges Mantion M.D. Ph.D. Karem Slim M.D | 2006 | Diseases of the Colon & Rectum2006,,12: | 1 |
| 8 | Epidural versus Continuous Preperitoneal Analgesia during Fast-track Open Colorectal Surgery: A Randomized Controlled Trial显示文摘 | Philippe Jouve Jean-Etienne Bazin Antoine Petit Vincent Minville Adeline Gerard Emmanuel Buc Aurelien Dupre Fabrice Kwiatkowski Jean-Michel Constantin Emmanuel Futier | 2013 | Anesthesiology2013,,3: | 1 |
| 9 | Giant mucinous cystic adenoma with pancreatic atrophy mimicking dorsal agenesis of the pancreas显示文摘Mucinous cystic adenoma(MCA) of the pancreas is a rare benign cystic tumor with ovarian-like stroma and lack of communication with the pancreatic ductal sys-tem. The ovarian tissue is incorporated from the left gonad within the dorsal pancreas during embryogen-esis. Consequently, congenital dorsal agenesis of the pancreas(DAP) cannot be associated with MCA. We report the case of a giant MCA associated with atro-phy of the dorsal pancreas mimicking complete DAP. Pancreato-magnetic resonance imaging failed to iden-tify the dorsal pancreas but the absence of diabetes mellitus and compression of the splenic vein with major tributaries rectified the diagnosis of secondary atrophy of the distal pancreas. Unusual proximal location of the cyst in the pancreas may have induced chronic obstruc-tion of both the dorsal pancreatic duct and the splenic vein, with secondary atrophy of the distal pancreas. | Johan Gagnière Aurélien Dupré David Da Ines Lucie Tixier Denis Pezet Emmanuel Buc | 2014 | World Journal of Gastrointestinal Surgery2014,6,3: | 0 |
| 10 | Hepatic veins as a site of clot formation following liver resection显示文摘Pulmonary embolism occurs more frequently after hepatectomy than previously thought but is infrequently associated with peripheral deep vein thrombosis. In this paper, we report 2 cases of postoperative hepatic vein thrombosis after liver resection. Both patients had undergone major hepatectomy of a non-cirrhotic liver largely exposing the middle hepatic vein. Clots were incidentally found in the middle hepatic vein 4 and 17 d after surgery despite routine systemic thrombo-prophylaxis with low molecular weight heparin. Coagulation of the transition plan in a context of mutation of the prothrombin gene and inflammation induced biloma were the likely predisposing conditions. Clots disappeared following curative anticoagulation. We conclude that thrombosis of hepatic veins may occur after liver resection and is a potential source of pulmonary embolism. | Emmanuel Buc Safi Dokmak Magaly Zappa Marie Helene Denninger Dominique Charles Valla Jacques Belghiti Olivier Farges | 2011 | World Journal of Gastroenterology2011,17,3: | 0 |