Gastric Cancer Surgery

Le cancer de l’estomac est l’une des principales causes de mortalité par cancer dans le monde. Même si des progrès dans les traitements non chirurgicaux ont été réalisés, avec l’avènement de la chimiothérapie périopératoire, la chirurgie reste au centre de la prise en charge de ces tumeurs, représentant la seule option curative à l’heure actuelle, si une résection complète dite « R0 » peut être obtenue. Des recommandations ont ainsi été émises par la Société Française de Chirurgie Digestive (SFCD) et l’Association de Chirurgie Hépato-Biliaire et Transplantation (ACHBT), recommandations labellisées par l’Institut National du Cancer (INCa). Le but de cet article est de discuter de l’étendue de la résection digestive et du curage ganglionnaire ainsi que de la technique de reconstruction digestive à effectuer, et de préciser la place de la chimiohyperthermie intrapéritonéale et de la chirurgie palliative dans la prise en charge des adénocarcinomes gastriques

Open versus laparoscopically-assisted oesophagectomy for cancer: a multicentre randomised controlled phase III trial - the MIRO trial

<p>Abstract</p> <p>Background</p> <p>Open transthoracic oesophagectomy is the standard treatment for infracarinal resectable oesophageal carcinomas, although it is associated with high mortality and morbidity rates of 2 to 10% and 30 to 50%, respectively, for both the abdominal and thoracic approaches. The worldwide popularity of laparoscopic techniques is based on promising results, including lower postoperative morbidity rates, which are related to the reduced postoperative trauma. We hypothesise that the laparoscopic abdominal approach (laparoscopic gastric mobilisation) in oesophageal cancer surgery will decrease the major postoperative complication rate due to the reduced surgical trauma.</p> <p>Methods/Design</p> <p>The MIRO trial is an open, controlled, prospective, randomised multicentre phase III trial. Patients in study arm A will receive laparoscopic-assisted oesophagectomy, i.e., a transthoracic oesophagectomy with two-field lymphadenectomy and laparoscopic gastric mobilisation. Patients in study arm B will receive the same procedure, but with the conventional open abdominal approach. The primary objective of the study is to evaluate the major postoperative 30-day morbidity. Secondary objectives are to assess the overall 30-day morbidity, 30-day mortality, 30-day pulmonary morbidity, disease-free survival, overall survival as well as quality of life and to perform medico-economic analysis. A total of 200 patients will be enrolled, and two safety analyses will be performed using 25 and 50 patients included in arm A.</p> <p>Discussion</p> <p>Postoperative morbidity remains high after oesophageal cancer surgery, especially due to major pulmonary complications, which are responsible for 50% of the postoperative deaths. This study represents the first randomised controlled phase III trial to evaluate the benefits of the minimally invasive approach with respect to the postoperative course and oncological outcomes in oesophageal cancer surgery.</p> <p>Trial Registration</p> <p><a href="http://www.clinicaltrials.gov/ct2/show/NCT00937456">NCT00937456</a> (ClinicalTrials.gov)</p

Impact de la chirurgie mini-invasive sur la diminution des complications pulmonaires majeures après oesophagectomie pour cancer (étude cas-témoins)

LILLE2-BU Santé-Recherche (593502101) / SudocSudocFranceF

Lecture d'une lettre des représentants Bellegarde, Briez et Haussmann, lors de la séance du 24 fructidor an II (10 septembre 1794)

Haussmann Nicolas, Dubois de Bellegarde, Briez Philippe Constant Joseph, Bentabole Pierre Louis. Lecture d'une lettre des représentants Bellegarde, Briez et Haussmann, lors de la séance du 24 fructidor an II (10 septembre 1794). In: Archives Parlementaires de 1787 à 1860 - Première série (1787-1799) Tome XCVII - Du 23 fructidor an II au 2 vendémiaire an III (9 au 23 septembre 1794) Paris : CNRS éditions, 1993. pp. 67-68

Lecture d'une lettre des représentants Bellegarde, Briez et Haussmann, lors de la séance du 24 fructidor an II (10 septembre 1794)

Haussmann Nicolas, Dubois de Bellegarde, Briez Philippe-Constant-Joseph, Bentabole Pierre-Louis. Lecture d'une lettre des représentants Bellegarde, Briez et Haussmann, lors de la séance du 24 fructidor an II (10 septembre 1794). In: Archives Parlementaires de 1787 à 1860 - Première série (1787-1799) Tome XCVII - Du 23 fructidor an II au 2 vendémiaire an III (9 au 23 septembre 1794) Paris : CNRS éditions, 1993. pp. 67-68

MUC1, a New Hypoxia Inducible Factor Target Gene, Is an Actor in Clear Renal Cell Carcinoma Tumor Progression

International audienceThe hypoxia inducible factor (HIF) signaling pathway is known as the main renal carcinogenetic pathway. MUC1, an O-glycoprotein membrane-bound mucin, is overexpressed in clear renal cell carcinomas (cRCC) with correlation to two major prognostic factors: tumor-node-metastasis stage and nuclear Fürhman grade. We questioned whether there is a direct link between the HIF pathway and MUC1 overexpression in renal tumors. Interestingly, we observed concomitant increase of HIF-1α and MUC1 in metastatic cRCC group versus nonmetastatic cRCC group. Using different renal cell models and small interfering RNA assays targeting either HIF-1α or YC-1, a HIF-1 pharmacologic inhibitor, we showed induction of MUC1 expression under hypoxia by a HIF-dependent mechanism. Chromatin immunoprecipitation assay showed a direct binding of HIF-1α at the MUC1 promoter. In addition, combined site-directed mutagenesis and gel shift assay allowed the identification of two functional putative hypoxia responsive elements at −1488/−1485 and at −1510/−1507 in the promoter. Using a rat kidney model of ischemia/reperfusion, we confirmed in vivo that clamping renal pedicle for 1 hour followed by 2 hours of reperfusion induced increased MUC1 expression. Furthermore, MUC1 knockdown induced significant reduction of invasive and migration properties of renal cancer cells under hypoxia. Altogether, these results show that MUC1 is directly regulated by HIF-1α and affects the invasive and migration properties of renal cancer cells. Thus, MUC1 could serve as a potential therapeutic target in cRCC

Operatively induced chronic reflux in rats: A suitable model for studying esophageal carcinogenesis?

International audienceBackground. The mechanisms of esophageal reflux leading to esophageal adenocarcinoma (EA) remain poorly understood. This study appraises critically an operatively induced chronic reflux rat model. Methods. We randomized 108 Sprague-Dawley rats into 2 experimental groups; one was performing esophagoduodenal (ED) anastomosis with or without gastrectomy to induce duodeno-esophageal reflux (DER group; n = 63), and the other involved duodeno-gastro-esophageal reflux (DGER group; n = 45). Control groups included (i) Roux-en-Y esophagojejunal anastomosis, (ii) laparotomy alone, (iii) subtotal gastrectomy to induce duodenogastric reflux (DGR group), and (iv) the same procedure as in the DGER group plus proton pump inhibition (PPI group). The esophagus underwent histologic and molecular analyses. Results. The prevalence of Barrett's esophagus (BE), dysplasia, and EA in the experimental groups was 41%, 7%, and 11%, respectively. Histologic and molecular analyses in groups DER, DGER, and DGR suggested that BE occurred through de novo intestinal metaplasia and proximal migration of duodenal cells. No distant metastases were identified. The molecular characteristics of both BE and EA were similar to humans. BE was more common, and dysplasia and EA less frequent in the DER group when compared with the DGER group (44% vs 24% [ P = .038] and 7% vs 25% [ P = .012], respectively). Compared with the DGER group, carcinogenic sequence occurred less frequently in the PPI-treated group (P = .019). Conclusion. Despite pathophysiologic differences with humans, the rat model of esophagoduodenostomy reproduces accurately histologic and molecular lesions in the carcinogenetic sequence of BE and allowed us to identify novel, tumor-associated proteins that may be potential biomarkers and new therapeutic targets in EA