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Pancreatic Neoplasms: HELP
Articles by Jean-François Emile
Based on 6 articles published since 2010
(Why 6 articles?)
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Between 2010 and 2020, J. Emile wrote the following 6 articles about Pancreatic Neoplasms.
 
+ Citations + Abstracts
1 Clinical Trial Asparagine Synthetase Expression and Phase I Study With L-Asparaginase Encapsulated in Red Blood Cells in Patients With Pancreatic Adenocarcinoma. 2015

Bachet, Jean-Baptiste / Gay, Fabien / Maréchal, Raphaël / Galais, Marie-Pierre / Adenis, Antoine / MsC, David Salako / Cros, Jerome / Demetter, Pieter / Svrcek, Magali / Bardier-Dupas, Armelle / Emile, Jean-François / Hammel, Pascal / Ebenezer, Christelle / Berlier, Willy / Godfrin, Yann / André, Thierry. ·From the *Department of Hepato-Gastroenterology, Pitié Salpêtrière Hospital, Paris; and †Erytech Pharma, Lyon, France; ‡Department of Gastroenterology, Erasme University Hospital, Brussels, Belgium; §Department of Oncology, Centre François Baclesse, Caen; ∥Department of Oncology, Centre Oscar Lambret, Lille; and ¶Pathology Department, Beaujon Hospital, Paris, France; #Department of Pathology, Erasme Hospital, Brussels, Belgium; **Department of Pathology, Saint Antoine Hospital; and ††Department of Pathology, Pitié Salpêtrière Hospital, Paris; ‡‡Department of Pathology, Ambroise Paré Hospital, Boulogne-Billancourt; and §§Department of Gastroenterology, Beaujon Hospital; and Departments of ∥∥Medical Oncology and ¶¶Oncology, Saint-Antoine Hospital, Paris, France. ·Pancreas · Pubmed #26355551.

ABSTRACT: OBJECTIVES: Asparaginase encapsulated in erythrocytes (ERY-ASP) is a potentially effective drug in patients with pancreatic adenocarcinoma (PAC) with null/low asparagine synthetase (ASNS) expression. Our aims were to assess ASNS expression in PAC from a large cohort and its prognostic and/or predictive value and to conduct a phase I trial with ERY-ASP in patients with metastatic PAC. METHODS: Asparagine synthetase expression was evaluated using immunohistochemistry in resected PAC (471 patients) and in pairs of primary tumor and metastases (55 patients). Twelve patients were included in the phase I trial and received a single administration of ERY-ASP (25-150 IU/kg). RESULTS: Null/low ASNS expression was found in 79.4% of the resected PAC with a high concordance between primary tumor and metastases. Asparagine synthetase expression was significantly correlated with sex and CXCR4 expression. In the phase I trial, ERY-ASP was well tolerated by patients with metastatic PAC. No patient had DLTs, and 6 patients had at least 1 ERY-ASP causally related adverse event out of the 12 adverse events reported. CONCLUSIONS: Given the high rate of PAC with null/low ASNS expression and the good tolerability profile of ERY-ASP, ERY-ASP should be evaluated in further clinical studies in metastatic PAC.

2 Article Prevalence of Microsatellite Instability in Intraductal Papillary Mucinous Neoplasms of the Pancreas. 2018

Lupinacci, Renato M / Goloudina, Anastasia / Buhard, Olivier / Bachet, Jean-Baptiste / Maréchal, Raphaël / Demetter, Pieter / Cros, Jérôme / Bardier-Dupas, Armelle / Collura, Ada / Cervera, Pascale / Scriva, Aurélie / Dumont, Sylvie / Hammel, Pascal / Sauvanet, Alain / Louvet, Christophe / Delpéro, Jean-Robert / Paye, François / Vaillant, Jean-Christophe / André, Thierry / Closset, Jean / Emile, Jean-François / Van Laethem, Jean-Luc / Jonchère, Vincent / Abd Alsamad, Issam / Antoine, Martine / Rodenas, Anita / Fléjou, Jean-François / Dusetti, Nelson / Iovanna, Juan / Duval, Alex / Svrcek, Magali. ·INSERM, UMR S 938 - Centre de Recherche Saint-Antoine, Equipe Instabilité des Microsatellites et Cancers, Equipe labellisée par la Ligue Nationale contre le Cancer, F-75012, Paris, France; Sorbonne Université, Université Pierre et Marie Curie - Paris 6, Paris, France; Groupe Hospitalier Diaconesses - Croix Saint-Simon, Service de Chirurgie Digestive, Viscérale et Endocrinienne, Paris, France. · INSERM, UMR S 938 - Centre de Recherche Saint-Antoine, Equipe Instabilité des Microsatellites et Cancers, Equipe labellisée par la Ligue Nationale contre le Cancer, F-75012, Paris, France; Inovarion F - 75013, Paris, France. · INSERM, UMR S 938 - Centre de Recherche Saint-Antoine, Equipe Instabilité des Microsatellites et Cancers, Equipe labellisée par la Ligue Nationale contre le Cancer, F-75012, Paris, France. · Sorbonne Université, Université Pierre et Marie Curie - Paris 6, Paris, France; AP-HP, Groupe Hospitalier Pitié-Salpêtrière, Service d'Hépato-Gastro-Entérologie, Paris, France. · Department of Gastroenterology and Digestive Oncology, Erasme Hospital, Brussels, Belgium. · Department of Pathology, Erasme Hospital, Brussels, Belgium. · AP-HP, Service d'Anatomie et Cytologie Pathologiques, Hôpital Beaujon, Clichy, France; Université Paris Diderot - Paris 7, Paris, France. · AP-HP, Groupe Hospitalier Pitié-Salpêtrière, Service d'Anatomie et Cytologie Pathologiques, Paris, France. · INSERM, UMR S 938 - Centre de Recherche Saint-Antoine, Equipe Instabilité des Microsatellites et Cancers, Equipe labellisée par la Ligue Nationale contre le Cancer, F-75012, Paris, France; Sorbonne Université, Université Pierre et Marie Curie - Paris 6, Paris, France. · INSERM, UMR S 938 - Centre de Recherche Saint-Antoine, Equipe Instabilité des Microsatellites et Cancers, Equipe labellisée par la Ligue Nationale contre le Cancer, F-75012, Paris, France; Sorbonne Université, Université Pierre et Marie Curie - Paris 6, Paris, France; AP-HP, Hôpitaux Universitaires Est Parisien, Hôpital Saint-Antoine, Service d'Anatomie et Cytologie Pathologiques, Paris, France. · AP-HP, Hôpitaux Universitaires Est Parisien, Hôpital Saint-Antoine, Service d'Anatomie et Cytologie Pathologiques, Paris, France. · Sorbonne Université, Université Pierre et Marie Curie - Paris 6, Paris, France. · Université Paris Diderot - Paris 7, Paris, France; AP-HP, Hôpital Beaujon, Department of Gastroenterology, Pôle des Maladies de l'Appareil Digestif (PMAD), Clichy, France. · Université Paris Diderot - Paris 7, Paris, France; AP-HP, Hôpital Beaujon, Department of Hepato-Pancreato-Biliary Surgery, Pôle des Maladies de l'Appareil Digestif (PMAD), Clichy, France. · Department of Oncology, Institut Mutualiste Montsouris, Paris, France. · Department of Digestive Surgical Oncology, Paoli Calmettes Institute, Comprehensive Cancer Centre, Marseille, France. · Sorbonne Université, Université Pierre et Marie Curie - Paris 6, Paris, France; AP-HP, Hôpitaux Universitaires Est Parisien, Hôpital Saint-Antoine, Service de Chirurgie Générale et Digestive, Paris, France. · Sorbonne Université, Université Pierre et Marie Curie - Paris 6, Paris, France; AP-HP, Groupe Hospitalier Pitié-Salpêtrière, Service de Chirurgie Digestive et Hépato-bilio-pancréatique, Paris, France. · Sorbonne Université, Université Pierre et Marie Curie - Paris 6, Paris, France; Department of Oncology, Hôpital Saint Antoine, Paris, France. · EA4340 and Service d'Anatomie et Cytologie Pathologiques, Hôpital Ambroise Paré, AP-HP and Versailles University, Boulogne, France. · Hôpital Intercommunal de Créteil, Service d'Anatomie et Cytologie Pathologiques, Créteil, France. · Sorbonne Université, Université Pierre et Marie Curie - Paris 6, Paris, France; AP-HP, Hôpitaux Universitaires Est Parisien, Hôpital Tenon, Service d'Anatomie et Cytologie Pathologiques, Paris, France. · Centre de Recherche en Cancérologie de Marseille (CRCM), INSERM U1068, CNRS UMR 7258, Parc Scientifique et Technologique de Luminy, Aix-Marseille Université and Institut Paoli-Calmettes, Marseille, France. · INSERM, UMR S 938 - Centre de Recherche Saint-Antoine, Equipe Instabilité des Microsatellites et Cancers, Equipe labellisée par la Ligue Nationale contre le Cancer, F-75012, Paris, France; Sorbonne Université, Université Pierre et Marie Curie - Paris 6, Paris, France. Electronic address: alex.duval@inserm.fr. · INSERM, UMR S 938 - Centre de Recherche Saint-Antoine, Equipe Instabilité des Microsatellites et Cancers, Equipe labellisée par la Ligue Nationale contre le Cancer, F-75012, Paris, France; Sorbonne Université, Université Pierre et Marie Curie - Paris 6, Paris, France; AP-HP, Hôpitaux Universitaires Est Parisien, Hôpital Saint-Antoine, Service d'Anatomie et Cytologie Pathologiques, Paris, France. Electronic address: magali.svrcek@aphp.fr. ·Gastroenterology · Pubmed #29158190.

ABSTRACT: Microsatellite instability (MSI) caused by mismatch repair deficiency (dMMR) is detected in a small proportion of pancreatic ductal adenocarcinomas (PDACs). dMMR and MSI have been associated with responses of metastatic tumors, including PDACs, to immune checkpoint inhibitor therapy. We performed immunohistochemical analyses of a 445 PDAC specimens, collected from consecutive patients at multiple centers, to identify those with dMMR, based on loss of mismatch repair proteins MLH1, MSH2, MSH6, and/or PMS2. We detected dMMR in 1.6% of tumor samples; we found dMMR in a larger proportion of intraductal papillary mucinous neoplasms-related tumors (4/58, 6.9%) than non- intraductal papillary mucinous neoplasms PDAC (5/385, 1.3%) (P = .02). PDACs with dMMR contained potentially immunogenic mutations because of MSI in coding repeat sequences. PDACs with dMMR or MSI had a higher density of CD8+ T cells at the invasive front than PDACs without dMMR or MSI (P = .08; Fisher exact test). A higher proportion of PDACs with dMMR or MSI expressed the CD274 molecule (PD-L1, 8/9) than PDACs without dMMR or MSI (4/10) (P = .05). Times of disease-free survival and overall survival did not differ significantly between patients with PDACs with dMMR or MSI vs without dMMR or MSI. Studies are needed to determine whether these features of PDACs with dMMR or MSI might serve as prognostic factors.

3 Article Sonic hedgehog and Gli1 expression predict outcome in resected pancreatic adenocarcinoma. 2015

Maréchal, Raphaël / Bachet, Jean-Baptiste / Calomme, Annabelle / Demetter, Pieter / Delpero, Jean Robert / Svrcek, Magali / Cros, Jérôme / Bardier-Dupas, Armelle / Puleo, Francesco / Monges, Geneviève / Hammel, Pascal / Louvet, Christophe / Paye, François / Bachelier, Philippe / Le Treut, Yves Patrice / Vaillant, Jean-Christophe / Sauvanet, Alain / André, Thierry / Salmon, Isabelle / Devière, Jacques / Emile, Jean-François / Van Laethem, Jean-Luc. ·Saint Antoine Department of Gastroenterology and Gastrointestinal Cancer Unit, Erasme Hospital, Université Libre de Bruxelles, Brussels, Belgium. Laboratory of Experimental Gastroenterology, Erasme Hospital, Université Libre de Bruxelles, Brussels, Belgium. raphael.marechal@erasme.ulb.ac.be. · Medical University Pierre et Marie Curie, UFR Paris VI, Paris, France. EA4340 "Epidémiologie et oncogènes des tumeurs digestives," Versailles Saint-Quentin-en-Yvelines University, Versailles, France. Department of Hepato-Gastroenterology, Pitié Salpêtrière Hospital, APHP, Paris, France. · Saint Antoine Department of Gastroenterology and Gastrointestinal Cancer Unit, Erasme Hospital, Université Libre de Bruxelles, Brussels, Belgium. Laboratory of Experimental Gastroenterology, Erasme Hospital, Université Libre de Bruxelles, Brussels, Belgium. · Department of Pathology, Erasme Hospital, Université Libre de Bruxelles, and DiaPath, Brussels, Belgium. · Department of Surgery, Institute Paoli Calmettes, Marseille, France. Aix Marseille Université, Marseille, France. · Department of Pathology, Saint Antoine Hospital, APHP, Paris, France. · Department of Pathology, Beaujon Hospital, APHP, Clichy, France. · Medical University Pierre et Marie Curie, UFR Paris VI, Paris, France. Department of Pathology, Pitié Salpêtrière Hospital, APHP, Paris, France. · Department of Pathology, Institute Paoli Calmettes, Marseille, France. · Department of Gastroenterology, Beaujon Hospital, APHP, Clichy, France. · Medical University Pierre et Marie Curie, UFR Paris VI, Paris, France. Department of Oncology, Institut Mutualiste Montsouris, Paris, France. · Medical University Pierre et Marie Curie, UFR Paris VI, Paris, France. Department of Surgery, Saint Antoine Hospital, APHP, Paris, France. · Department of Surgery, University Hospital of Hautepierre, Strasbourg, France. · Department of Digestive Surgery, Conception Hospital, Marseille, France. · Medical University Pierre et Marie Curie, UFR Paris VI, Paris, France. Department of Digestive Surgery, Pitié Salpêtrière Hospital, Paris, France. · Department of Digestive Surgery, Beaujon Hospital, APHP, Clichy, France. · Department of Oncology, Saint-Antoine Hospital, APHP, Paris, France. · Department of Pathology, Erasme Hospital, Université Libre de Bruxelles, and DiaPath, Brussels, Belgium. DIAPath - Center for Microscopy and Molecular Imaging (CMMI), Université Libre de Bruxelles, Gosselies, Belgium. · EA4340 "Epidémiologie et oncogènes des tumeurs digestives," Versailles Saint-Quentin-en-Yvelines University, Versailles, France. Department of Pathology, Ambroise Paré Hospital, APHP, Boulogne Billancourt, France. · Saint Antoine Department of Gastroenterology and Gastrointestinal Cancer Unit, Erasme Hospital, Université Libre de Bruxelles, Brussels, Belgium. ·Clin Cancer Res · Pubmed #25552484.

ABSTRACT: PURPOSE: Aberrant activation of the hedgehog (Hh) pathway is implicated in pancreatic ductal adenocarcinoma (PDAC) tumorigenesis. We investigated the prognostic and predictive value of four Hh signaling proteins and of the tumor stromal density. EXPERIMENTAL DESIGN: Using tissue microarray and immunohistochemistry, the expression of Shh, Gli1, SMO, and PTCH1 was assessed in 567 patients from three independent cohorts who underwent surgical resection for PDAC. In 82 patients, the tumor stromal index (SI) was calculated, and its association with overall survival (OS) and disease-free survival (DFS) was investigated. RESULTS: Shh and Gli1 protein abundance were independent prognostic factors in resected PDACs; low expressors for those proteins experiencing a better OS and DFS. The combination of Shh and Gli1 levels was the most significant predictor for OS and defined 3 clinically relevant subgroups of patients with different prognosis (Gli1 and Shh low; HR set at 1 vs. 3.08 for Shh or Gli1 high vs. 5.69 for Shh and Gli1 high; P < 0.001). The two validating cohorts recapitulated the findings of the training cohort. After further stratification by lymph node status, the prognostic significance of combined Shh and Gli1 was maintained. The tumor SI was correlated with Shh levels and was significantly associated with OS (P = 0.023). CONCLUSIONS: Shh and Gli1 are prognostic biomarkers for patients with resected PDAC.

4 Article S100A2 is a predictive biomarker of adjuvant therapy benefit in pancreatic adenocarcinoma. 2013

Bachet, Jean-Baptiste / Maréchal, Raphael / Demetter, Pieter / Bonnetain, Franck / Cros, Jérôme / Svrcek, Magali / Bardier-Dupas, Armelle / Hammel, Pascal / Sauvanet, Alain / Louvet, Christophe / Paye, François / Vaillant, Jean-Christophe / André, Thierry / Closset, Jean / Salmon, Isabelle / Emile, Jean-François / Van Laethem, Jean-Luc. ·Medical University Pierre et Marie Curie, UFR Paris VI, 91-105 Boulevard de l'Hôpital, Paris, France. jean-baptiste.bachet@psl.aphp.fr ·Eur J Cancer · Pubmed #23726265.

ABSTRACT: BACKGROUND: Prognosis of patients with pancreatic adenocarcinoma (PAC) remains poor. S100A2 has been recently suggested as a negative prognostic biomarker in PAC. We aimed to investigate its prognostic and/or predictive value in a large independent multicentric cohort of patients with resected PAC. METHODS: Sequential samples of 471 patients were retrospectively collected; 142 patients did not receive adjuvant treatment (30%) and 329 (70%) received an adjuvant treatment. We measured protein levels of S100A2 by semiquantitative immunohistochemistry with tissue microarrays and correlated with patients' overall survival (OS) and disease-free survival (DFS). RESULTS: S100A2 protein status was obtained in 462 (98%) patients. Its expression was low, moderate or high in 59%, 12% and 2% of cases, respectively. It was not correlated with DFS or OS in the whole population, neither in the subgroup of patients who did not receive adjuvant treatment. However among patients who received an adjuvant therapy, moderate/high levels of S100A2 were significantly associated with longer OS and DFS in multivariate analysis (hazard ratios of 0.63, p=0.022 and 0.67, p=0.017, respectively), whereas low S100A2 was not. Interaction tests for adjuvant therapy were statistically significant both for the OS and the DFS (p=0.001 and p=0.023, respectively). On multivariate analysis, S100A2 retained independent predictive values (OS: p<0.001, DFS: p=0.003) with a significant benefit of adjuvant therapy for those patients with moderate/high S100A2. CONCLUSIONS: S100A2 expression predicts longer DFS and OS in patients treated with adjuvant therapy and should be evaluated as a predictive biomarker.

5 Article Levels of gemcitabine transport and metabolism proteins predict survival times of patients treated with gemcitabine for pancreatic adenocarcinoma. 2012

Maréchal, Raphaël / Bachet, Jean-Baptiste / Mackey, John R / Dalban, Cécile / Demetter, Pieter / Graham, Kathryn / Couvelard, Anne / Svrcek, Magali / Bardier-Dupas, Armelle / Hammel, Pascal / Sauvanet, Alain / Louvet, Christophe / Paye, François / Rougier, Philippe / Penna, Christophe / André, Thierry / Dumontet, Charles / Cass, Carol E / Jordheim, Lars Petter / Matera, Eva-Laure / Closset, Jean / Salmon, Isabelle / Devière, Jacques / Emile, Jean-François / Van Laethem, Jean-Luc. ·Department of Gastroenterology and Gastrointestinal Cancer Unit, Erasme Hospital, Université Libre de Bruxelles, Brussels, Belgium. Electronic address: raphael.marechal@erasme.ulb.ac.be. · Medical University Pierre et Marie Curie, UFR Paris VI, Paris, France; EA4340 "Epidémiologie et oncogènes des tumeurs digestives," Versailles Saint-Quentin-en-Yvelines University, Saint-Quentin-en-Yvelines, France; Department of Hepato-Gastroenterology, Pitié Salpêtrière Hospital, APHP, Paris, France. · Department of Oncology, University of Alberta, Cross Cancer Institute, Edmonton, Alberta, Canada. · Department of Biostatistics and Epidemiology (EA4184), Georges François Leclerc Center, Dijon, France. · Department of Pathology, Erasme Hospital, Université Libre de Bruxelles, and DIAPATH, Brussels, Belgium. · Department of Pathology, Beaujon Hospital, APHP, Clichy, France. · Department of Pathology, Saint Antoine Hospital, APHP, Paris, France. · Medical University Pierre et Marie Curie, UFR Paris VI, Paris, France; Department of Pathology, Pitié Salpêtrière Hospital, APHP, Paris, France. · Department of Gastroenterology, Beaujon Hospital, APHP, Clichy, France. · Department of Surgery, Beaujon Hospital, APHP, Clichy, France. · Medical University Pierre et Marie Curie, UFR Paris VI, Paris, France; Department of Oncology, Saint Antoine Hospital, APHP, Paris, France. · Medical University Pierre et Marie Curie, UFR Paris VI, Paris, France; Department of Surgery, Saint Antoine Hospital, APHP, Paris, France. · EA4340 "Epidémiologie et oncogènes des tumeurs digestives," Versailles Saint-Quentin-en-Yvelines University, Saint-Quentin-en-Yvelines, France; Department of Digestive Oncology, Hôpital Européen Georges Pompidou, APHP, Paris, France. · EA4340 "Epidémiologie et oncogènes des tumeurs digestives," Versailles Saint-Quentin-en-Yvelines University, Saint-Quentin-en-Yvelines, France; Department of Surgery, Ambroise Paré Hospital, APHP, Boulogne Billancourt, France. · Medical University Pierre et Marie Curie, UFR Paris VI, Paris, France; Department of Hepato-Gastroenterology, Pitié Salpêtrière Hospital, APHP, Paris, France. · Centre de Cancer de Lyon, Lyon, France; Hospices Civils de Lyon, Lyon, France. · Centre de Cancer de Lyon, Lyon, France. · Department of Surgery, Erasme Hospital, Université Libre de Bruxelles, Brussels, Belgium. · Department of Gastroenterology and Gastrointestinal Cancer Unit, Erasme Hospital, Université Libre de Bruxelles, Brussels, Belgium. · EA4340 "Epidémiologie et oncogènes des tumeurs digestives," Versailles Saint-Quentin-en-Yvelines University, Saint-Quentin-en-Yvelines, France; Department of Pathology, Ambroise Paré Hospital, APHP, Boulogne Billancourt, France. ·Gastroenterology · Pubmed #22705007.

ABSTRACT: BACKGROUND & AIMS: Patients who undergo surgery for pancreatic ductal adenocarcinoma (PDAC) frequently receive adjuvant gemcitabine chemotherapy. Key determinants of gemcitabine cytotoxicity include the activities of the human equilibrative nucleoside transporter 1 (hENT1), deoxycytidine kinase (dCK), and ribonucleotide reductase subunit 1 (RRM1). We investigated whether tumor levels of these proteins were associated with efficacy of gemcitabine therapy following surgery. METHODS: Sequential samples of resected PDACs were retrospectively collected from 434 patients at 5 centers; 142 patients did not receive adjuvant treatment (33%), 243 received adjuvant gemcitabine-based regimens (56%), and 49 received nongemcitabine regimens (11%). We measured protein levels of hENT1, dCK, and RRM1 by semiquantitative immunohistochemistry with tissue microarrays and investigated their relationship with patients' overall survival time. RESULTS: The median overall survival time of patients was 32.0 months. Among patients who did not receive adjuvant treatment, levels of hENT1, RRM1, and dCK were not associated with survival time. Among patients who received gemcitabine, high levels of hENT1 and dCK were significantly associated with longer survival time (hazard ratios of 0.34 [P < .0001] and 0.57 [P = .012], respectively). Interaction tests for gemcitabine administration and hENT1 and dCK status were statistically significant (P = .0007 and P = .016, respectively). On multivariate analysis of this population, hENT1 and dCK retained independent predictive values, and those patients with high levels of each protein had the longest survival times following adjuvant therapy with gemcitabine. CONCLUSIONS: High levels of hENT1 and dCK in PDAC predict longer survival times in patients treated with adjuvant gemcitabine.

6 Article Contribution of CXCR4 and SMAD4 in predicting disease progression pattern and benefit from adjuvant chemotherapy in resected pancreatic adenocarcinoma. 2012

Bachet, J B / Maréchal, R / Demetter, P / Bonnetain, F / Couvelard, A / Svrcek, M / Bardier-Dupas, A / Hammel, P / Sauvanet, A / Louvet, C / Paye, F / Rougier, P / Penna, C / Vaillant, J C / André, T / Closset, J / Salmon, I / Emile, J F / Van Laethem, J L. ·Medical University Pierre et Marie Curie, UFR Paris VI, Paris. jean-baptiste.bachet@psl.aphp.fr ·Ann Oncol · Pubmed #22377565.

ABSTRACT: BACKGROUND: Prognosis of patients with pancreatic adenocarcinoma is poor. Many prognostic biomarkers have been tested, but most studies included heterogeneous patients. We aimed to investigate the prognostic and/or predictive values of four relevant biomarkers in a multicentric cohort of patients. PATIENTS AND METHODS: A total of 471 patients who had resected pancreatic adenocarcinoma were included. Using tissue microarray, we assessed the relationship of biomarker expressions with the overall survival: Smad4, type II TGF-β receptor, CXCR4, and LKB1. RESULTS: High CXCR4 expression was found to be the only independent negative prognostic biomarker [hazard ratio (HR) = 1.74; P < 0.0001]. In addition, it was significantly associated with a distant relapse pattern (HR = 2.19; P < 0.0001) and was the strongest prognostic factor compared with clinicopathological factors. In patients who did not received adjuvant treatment, there was a trend toward decrease in the overall survival for negative Smad4 expression. Loss of Smad4 expression was not correlated with recurrence pattern but was shown to be predictive for adjuvant chemotherapy (CT) benefit (HR = 0.59; P = 0.002). CONCLUSIONS: CXCR4 is a strong independent prognostic biomarker associated with distant metastatic recurrence and appears as an attractive target to be evaluated in pancreatic adenocarcinoma. Negative SMAD4 expression should be considered as a potential predictor of adjuvant CT benefit.