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Pancreatic Neoplasms: HELP
Articles by Pascale Cervera
Based on 2 articles published since 2010
(Why 2 articles?)
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Between 2010 and 2020, Pascale Cervera wrote the following 2 articles about Pancreatic Neoplasms.
 
+ Citations + Abstracts
1 Review Changing pathology with changing drugs: tumors of the gastrointestinal tract. 2011

Cervera, Pascale / Fléjou, Jean-François. ·Service d'Anatomie et Cytologie Pathologiques, Hôpital Saint-Antoine, Paris, France. pascale.cervera@sat.aphp.fr ·Pathobiology · Pubmed #21677471.

ABSTRACT: Gastrointestinal cancer treatment is being based more and more on pathology that yields integrated information leading to targeted therapy, i.e. morphological identification of the histological type of the tumor and its context, staging of the tumor, and identification of various targets. This provides a realistic appraisal of the tumor and allows surgeons and oncologists to choose the best treatment from an increased range of drug options. An accurate diagnosis remains the major determinant of treatment, but new drugs and new insights into molecular pathways acting in carcinogenesis enhance molecular diagnosis in cancer. In most adenocarcinomas, therapy is only organ orientated and staging dependent, and not patient targeted. Currently, the identification and validation of new targets as well as molecular classification of the tumors are inducing the incorporation of new tests into the daily practice of surgical pathology. These new tests require appropriate tissue preservation and selection of the tissue to be analyzed and harmonized to morphological criteria. In colorectal adenocarcinoma, which is the second most common malignant tumor in both genders, the biomarkers that are relevant at the present time are the genetic instability status of the tumor, the KRAS mutation status as a negative predictive marker for the overall rate of response to anti-EGFR treatment in patients with metastatic cancer, and BRAF mutation as an unfavorable prognostic marker. In gastric adenocarcinoma, HER2 overexpression is correlated with poor outcomes and more aggressive disease in a subset of cases with clinical response to trastuzumab. Met mutations have also been evidenced. Hepatocellular carcinoma is a highly chemoresistant tumor with several genetic alterations. Pancreatic adenocarcinoma is a leading cause of cancer death with frequent KRAS mutations. No biomarker has been clearly identified in either of these tumors. Gastrointestinal stromal tumors that constitute less than 3% of all gastrointestinal malignancies have been individualized since 1988. They express the KIT protein, a membrane receptor, and respond to imatinib which is a tyrosine kinase receptor inhibitor, depending on the mutational status of the tumor.

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.