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Pancreatic Neoplasms: HELP
Articles by Gabriel Capellà
Based on 6 articles published since 2009
(Why 6 articles?)
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Between 2009 and 2019, Gabriel Capella wrote the following 6 articles about Pancreatic Neoplasms.
 
+ Citations + Abstracts
1 Article Cancer risk and survival in 2018

Møller, Pål / Seppälä, Toni T / Bernstein, Inge / Holinski-Feder, Elke / Sala, Paulo / Gareth Evans, D / Lindblom, Annika / Macrae, Finlay / Blanco, Ignacio / Sijmons, Rolf H / Jeffries, Jacqueline / Vasen, Hans F A / Burn, John / Nakken, Sigve / Hovig, Eivind / Rødland, Einar Andreas / Tharmaratnam, Kukatharmini / de Vos Tot Nederveen Cappel, Wouter H / Hill, James / Wijnen, Juul T / Jenkins, Mark A / Green, Kate / Lalloo, Fiona / Sunde, Lone / Mints, Miriam / Bertario, Lucio / Pineda, Marta / Navarro, Matilde / Morak, Monika / Renkonen-Sinisalo, Laura / Valentin, Mev Dominguez / Frayling, Ian M / Plazzer, John-Paul / Pylvanainen, Kirsi / Genuardi, Maurizio / Mecklin, Jukka-Pekka / Moeslein, Gabriela / Sampson, Julian R / Capella, Gabriel / Anonymous1441036. ·Department of Medical Genetics, The Norwegian Radium Hospital, Oslo University Hospital, Oslo, Norway. · Department of Tumor Biology, Institute of Cancer Research, The Norwegian Radium Hospital, part of Oslo University Hospital, Olso, Norway. · Center for Hereditary Tumors, HELIOS-Klinikum Wuppertal, University of Witten-Herdecke, Wuppertal, Germany. · Department of Gastrointestinal Surgery, Helsinki University Central Hospital, University of Helsinki, Helsinki, Finland. · The Danish Hereditary Non-polyposis Colorectal Cancer Register, Clinical Research Centre, Copenhagen University Hospital, Hvidovre, Denmark. · Department of Surgical Gastroenterology, Aalborg University Hospital, Aalborg, Denmark. · Medizinische Klinik und Poliklinik IV, Campus Innenstadt, Klinikum der Universität München, Ziemssenstr, Germany. · MGZ - Medizinisch Genetisches Zentrum, Munich, Germany. · Unit of Hereditary Digestive Tract Tumors IRCCS Istituto Nazionale Tumori Milan, Milano, Italy. · Manchester Centre for Genomic Medicine, Central Manchester University Hospitals NHS Foundation Trust, London, UK. · Manchester Centre for Genomic Medicine, University of Manchester, London, UK. · Department of Molecular Medicine and Surgery, Karolinska Institutet, Stockholm, Sweden. · Colorectal Medicine and Genetics, The Royal Melbourne Hospital, Melborne, Australia. · Department of Medicine, Melbourne University, Melborne, Australia. · Hereditary Cancer Program, Institut Català d'Oncologia-IDIBELL, L'Hospitalet de Llobregat, Barcelona, Spain. · Department of Genetics, University of Groningen, University Medical Center Groningen, Groningen, The Netherlands. · Division of Cancer and Genetics, Institute of Medical Genetics, Cardiff University School of Medicine, Heath Park, UK. · Department of Gastroenterology and Hepatology, Leiden University Medical Centre, Leiden, The Netherlands. · Institute of Genetic Medicine Newcastle University, Newcastle upon Tyne, UK. · Institute of Cancer Genetics and Informatics, The Norwegian Radium Hospital, part of Oslo University Hospital, Olso, Norway. · Department of Informatics, University of Oslo, Olso, Norway. · Department of Mathematics and Statistics, Lancaster University, Lancaster, UK. · Department of Gastroenterology and Hepatology, Isala Clinics, Zwolle, The Netherlands. · Department of Surgery, Central Manchester University Hospitals NHS Foundation Trust and University of Manchester, London, UK. · Department of Clinical Genetics and Department of Human Genetics Leiden, University Medical Centre, Leiden, The Netherlands. · Centre for Epidemiology and Biostatistics, Melbourne School of Population and Global Health, The University of Melbourne, Parkville, Victoria, Australia. · Department of Clinical Genetics, Aarhus University Hospital, Aarhus, Denmark. · Department of Biomedicine, Aarhus University, Aarhus, Denmark. · Department of Women's and Children's health, Division of Obstetrics and Gyneacology, Karolinska Institutet, Karolinska University Hospital, Solna, Stockholm, Sweden. · Genome-Scale Biology Research Program, University of Helsinki, Helsinki, Finland. · Department of Education and Science, Central Finland Health Care District, yväskylä, Finland. · Institute of Genomic Medicine, "A. Gemelli" Faculty of Medicine, Catholic University of the Sacred Heart, Rome, Italy. · University of Eastern Finland, Kuopio, Finland. ·Gut · Pubmed #28754778.

ABSTRACT: BACKGROUND: Most patients with OBJECTIVE AND DESIGN: This observational, international, multicentre study aimed to determine prospectively observed incidences of cancers and survival in RESULTS: 3119 patients were followed for a total of 24 475 years. Cumulative incidences at 75 years (risks) for colorectal cancer were 46%, 43% and 15% in path_ CONCLUSION: Carriers of different

2 Article Helicobacter pylori infection, chronic corpus atrophic gastritis and pancreatic cancer risk in the European Prospective Investigation into Cancer and Nutrition (EPIC) cohort: A nested case-control study. 2017

Huang, Jiaqi / Zagai, Ulrika / Hallmans, Göran / Nyrén, Olof / Engstrand, Lars / Stolzenberg-Solomon, Rachael / Duell, Eric J / Overvad, Kim / Katzke, Verena A / Kaaks, Rudolf / Jenab, Mazda / Park, Jin Young / Murillo, Raul / Trichopoulou, Antonia / Lagiou, Pagona / Bamia, Christina / Bradbury, Kathryn E / Riboli, Elio / Aune, Dagfinn / Tsilidis, Konstantinos K / Capellá, Gabriel / Agudo, Antonio / Krogh, Vittorio / Palli, Domenico / Panico, Salvatore / Weiderpass, Elisabete / Tjønneland, Anne / Olsen, Anja / Martínez, Begoña / Redondo-Sanchez, Daniel / Chirlaque, Maria-Dolores / Hm Peeters, Petra / Regnér, Sara / Lindkvist, Björn / Naccarati, Alessio / Ardanaz, Eva / Larrañaga, Nerea / Boutron-Ruault, Marie-Christine / Rebours, Vinciane / Barré, Amélie / Bueno-de-Mesquita, H B As / Ye, Weimin. ·Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Solna, Sweden. · Department of Public Health and Clinical Nutrition, Umeå University, Umeå, Sweden. · Department of Microbiology, Tumor and Cell Biology, Karolinska Institutet, Stockholm, Sweden. · Metabolic Epidemiology Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Rockville, MD. · Unit of Nutrition and Cancer, Cancer Epidemiology Research Program, Catalan Institute of Oncology (ICO-IDIBELL), Barcelona, Spain. · Department of Public Health, Section for Epidemiology, Aarhus University, Aarhus, Denmark. · Division of Cancer Epidemiology, German Cancer Research Center (DKFZ), Heidelberg, Germany. · Prevention and Implementation Group, Section of Early Detection and Prevention, Section of Nutrition and Metabolism, International Agency for Research on Cancer, Lyon, France. · Hellenic Health Foundation, Athens, Greece. · WHO Collaborating Center for Nutrition and Health, Unit of Nutritional Epidemiology and Nutrition in Public Health, Department of Hygiene, Epidemiology and Medical Statistics, School of Medicine, National and Kapodistrian University of Athens, Athens, Greece. · Department of Epidemiology, Harvard T. H. Chan School of Public Health, Boston, MA. · Cancer Epidemiology Unit, Nuffield Department of Population Health, University of Oxford, Oxford, United Kingdom. · Department of Epidemiology and Biostatistics, School of Public Health, Imperial College London, London, United Kingdom. · Department of Hygiene and Epidemiology, University of Ioannina School of Medicine, Ioannina, Greece. · Translational Research Laboratory, IDIBELL-Catalan Institute of Oncology, Barcelona, Spain. · Unit of Nutrition and Cancer. Cancer Epidemiology Research Program. Catalan Institute of Oncology-IDIBELL. L'Hospitalet de Llobregat, Barcelona, Spain. · Epidemiology and Prevention Unit, Fondazione IRCCS Istituto Nazionale dei Tumori, Milano, Italy. · Cancer Risk Factors and Life-Style Epidemiology Unit, Cancer Research and Prevention Institute - ISPO, Florence, Italy. · Dipartimento di medicina clinica e chirurgia Federico II, Naples, Italy. · Department of Community Medicine, University of Tromsø, The Arctic University of Norway, Tromsø, Norway. · Department of Research, Cancer Registry of Norway, Institute of Population-Based Cancer Research, Oslo, Norway. · Genetic Epidemiology Group, Folkhälsan Research Center, Helsinki, Finland. · Danish Cancer Society Research Center, Copenhagen, Denmark. · Andalusian School of Public Health, Instituto De Investigación Biosanitaria Ibs, Granada, Spain. · CIBER of Epidemiology and Public Health (CIBERESP), Madrid, Spain. · Escuela Andaluza de Salud Pública, Instituto de Investigación Biosanitaria ibs, Granada, Hospitales Universitarios de Granada/Universidad de Granada, Granada, Spain. · Department of Epidemiology, Regional Health Council, IMIB-Arrixaca, Murcia, Spain. · Department of Health and Social Sciences, Universidad de Murcia, Murcia, Spain. · Department of Epidemiology, Julius Center for Health Sciences and Primary Care, University Medical Center Utrecht, Utrecht, The Netherlands. · Department of Surgery, Institution of Clinical Sciences Malmö, Lund University, Malmö, Sweden. · Department of Medicine, Sahlgrenska University Hospital, Gothenburg, Sweden. · Molecular and Genetic Epidemiology Unit, Human Genetics Foundation, Turin, Italy. · Navarra Public Health Institute, Pamplona, Spain; IdiSNA, Navarra Institute for Health Research, Pamplona, Spain. · Public Health Division of Gipuzkoa, Regional Government of the Basque Country, Spain. · Hormones and Women's Health Team, INSERM, Centre for Research in Epidemiology and Population Health (CESP), U1018, Nutrition, Villejuif, F-94805, France. · Université Paris Sud, UMRS 1018, Villejuif, F-94805, France. · Institut Gustave Roussy, Villejuif, F-94805, France. · Department of Gastroenterology and Pancreatology, Beaujon Hospital, University Paris 7, Clichy, France. · Université Paris Sud and Gastroenterology Unit, Hôpitaux Universitaires Paris Sud, CHU de Bicêtre, AP-HP, Le Kremlin Bicêtre, France. · Department for Determinants of Chronic Diseases (DCD), National Institute for Public Health and the Environment (RIVM), Bilthoven, The Netherlands. · Department of Gastroenterology and Hepatology, University Medical Centre, Utrecht, The Netherlands. · Department of Epidemiology and Biostatistics, The School of Public Health, Imperial College London, London, United Kingdom. · Department of Social & Preventive Medicine, Faculty of Medicine, University of Malaya, Kuala Lumpur, Malaysia. · The Medical Biobank at Umeå University, Umeå, Sweden. ·Int J Cancer · Pubmed #28032715.

ABSTRACT: The association between H. pylori infection and pancreatic cancer risk remains controversial. We conducted a nested case-control study with 448 pancreatic cancer cases and their individually matched control subjects, based on the European Prospective Investigation into Cancer and Nutrition (EPIC) cohort, to determine whether there was an altered pancreatic cancer risk associated with H. pylori infection and chronic corpus atrophic gastritis. Conditional logistic regression models were applied to calculate odds ratios (ORs) and corresponding 95% confidence intervals (CIs), adjusted for matching factors and other potential confounders. Our results showed that pancreatic cancer risk was neither associated with H. pylori seropositivity (OR = 0.96; 95% CI: 0.70, 1.31) nor CagA seropositivity (OR = 1.07; 95% CI: 0.77, 1.48). We also did not find any excess risk among individuals seropositive for H. pylori but seronegative for CagA, compared with the group seronegative for both antibodies (OR = 0.94; 95% CI: 0.63, 1.38). However, we found that chronic corpus atrophic gastritis was non-significantly associated with an increased pancreatic cancer risk (OR = 1.35; 95% CI: 0.77, 2.37), and although based on small numbers, the excess risk was particularly marked among individuals seronegative for both H. pylori and CagA (OR = 5.66; 95% CI: 1.59, 20.19, p value for interaction < 0.01). Our findings provided evidence supporting the null association between H. pylori infection and pancreatic cancer risk in western European populations. However, the suggested association between chronic corpus atrophic gastritis and pancreatic cancer risk warrants independent verification in future studies, and, if confirmed, further studies on the underlying mechanisms.

3 Article Ribonucleoprotein HNRNPA2B1 interacts with and regulates oncogenic KRAS in pancreatic ductal adenocarcinoma cells. 2014

Barceló, Carles / Etchin, Julia / Mansour, Marc R / Sanda, Takaomi / Ginesta, Mireia M / Sanchez-Arévalo Lobo, Victor J / Real, Francisco X / Capellà, Gabriel / Estanyol, Josep M / Jaumot, Montserrat / Look, A Thomas / Agell, Neus. ·Departament de Biologia Cellular, Immunologia i Neurociències, Facultat de Medicina, IDIBAPS, Universitat de Barcelona, Barcelona, Spain. · Department of Pediatric Oncology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, Massachusetts. · Department of Pediatric Oncology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, Massachusetts; Cancer Science Institute of Singapore, National University of Singapore, Singapore. · Hereditary Cancer Program, Translational Research Laboratory, Catalan Institute of Oncology, ICO-IDIBELL, Hospitalet de Llobregat, Barcelona, Spain. · Grupo de Carcinogénesis Epitelial, Programa de Patología Molecular, CNIO-Spanish National Cancer Research Center, Madrid, Spain. · Centres Científics i Tecnològics-UB (CCiTUB), Universitat de Barcelona, Barcelona, Spain. · Departament de Biologia Cellular, Immunologia i Neurociències, Facultat de Medicina, IDIBAPS, Universitat de Barcelona, Barcelona, Spain. Electronic address: neusagell@ub.edu. ·Gastroenterology · Pubmed #24998203.

ABSTRACT: BACKGROUND & AIMS: Development of pancreatic ductal adenocarcinoma (PDAC) involves activation of c-Ki-ras2 Kirsten rat sarcoma oncogene homolog (KRAS) signaling, but little is known about the roles of proteins that regulate the activity of oncogenic KRAS. We investigated the activities of proteins that interact with KRAS in PDAC cells. METHODS: We used mass spectrometry to demonstrate that heterogeneous nuclear ribonucleoproteins (HNRNP) A2 and B1 (encoded by the gene HNRNPA2B1) interact with KRAS G12V. We used co-immunoprecipitation analyses to study interactions between HNRNPA2B1 and KRAS in KRAS-dependent and KRAS-independent PDAC cell lines. We knocked down HNRNPA2B1 using small hairpin RNAs and measured viability, anchorage-independent proliferation, and growth of xenograft tumors in mice. We studied KRAS phosphorylation using the Phos-tag system. RESULTS: We found that interactions between HRNPA2B1 and KRAS correlated with KRAS-dependency of some human PDAC cell lines. Knock down of HNRNPA2B1 significantly reduced viability, anchorage-independent proliferation, and formation of xenograft tumors by KRAS-dependent PDAC cells. HNRNPA2B1 knock down also increased apoptosis of KRAS-dependent PDAC cells, inactivated c-akt murine thymoma oncogene homolog 1 signaling via mammalian target of rapamycin, and reduced interaction between KRAS and phosphatidylinositide 3-kinase. Interaction between HNRNPA2B1 and KRAS required KRAS phosphorylation at serine 181. CONCLUSIONS: In KRAS-dependent PDAC cell lines, HNRNPA2B1 interacts with and regulates the activity of KRAS G12V and G12D. HNRNPA2B1 is required for KRAS activation of c-akt murine thymoma oncogene homolog 1-mammalian target of rapamycin signaling, interaction with phosphatidylinositide 3-kinase, and PDAC cell survival and tumor formation in mice. HNRNPA2B1 might be a target for treatment of pancreatic cancer.

4 Article Phosphorylation at Ser-181 of oncogenic KRAS is required for tumor growth. 2014

Barceló, Carles / Paco, Noelia / Morell, Mireia / Alvarez-Moya, Blanca / Bota-Rabassedas, Neus / Jaumot, Montserrat / Vilardell, Felip / Capella, Gabriel / Agell, Neus. ·Authors' Affiliations: Departament de Biologia Cel·lular, Immunologia i Neurociències, Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), Facultat de Medicina, Universitat de Barcelona; Hereditary Cancer Program, Translational Research Laboratory, Catalan Institute of Oncology, ICO-IDIBELL, Hospitalet de Llobregat, Barcelona, Spain; Gran Via 199-203, 08907- L'Hospitalet de Llobregat, Llobregat; Servei d'Anatomia Patològica i Institut de Recerca Biomèdica de Lleida, Lleida, Spain. ·Cancer Res · Pubmed #24371225.

ABSTRACT: KRAS phosphorylation has been reported recently to modulate the activity of mutant KRAS protein in vitro. In this study, we defined S181 as a specific phosphorylation site required to license the oncogenic function of mutant KRAS in vivo. The phosphomutant S181A failed to induce tumors in mice, whereas the phosphomimetic mutant S181D exhibited an enhanced tumor formation capacity, compared with the wild-type KRAS protein. Reduced growth of tumors composed of cells expressing the nonphosphorylatable KRAS S181A mutant was correlated with increased apoptosis. Conversely, increased growth of tumors composed of cells expressing the phosphomimetic KRAS S181D mutant was correlated with increased activation of AKT and ERK, two major downstream effectors of KRAS. Pharmacologic treatment with PKC inhibitors impaired tumor growth associated with reduced levels of phosphorylated KRAS and reduced effector activation. In a panel of human tumor cell lines expressing various KRAS isoforms, we showed that KRAS phosphorylation was essential for survival and tumorigenic activity. Furthermore, we identified phosphorylated KRAS in a panel of primary human pancreatic tumors. Taken together, our findings establish that KRAS requires S181 phosphorylation to manifest its oncogenic properties, implying that its inhibition represents a relevant target to attack KRAS-driven tumors.

5 Article Metronomic chemotherapy following the maximum tolerated dose is an effective anti-tumour therapy affecting angiogenesis, tumour dissemination and cancer stem cells. 2013

Vives, Marta / Ginestà, Mireia M / Gracova, Kristina / Graupera, Mariona / Casanovas, Oriol / Capellà, Gabriel / Serrano, Teresa / Laquente, Berta / Viñals, Francesc. ·Translational Research Laboratory, Catalan Institute of Oncology, IDIBELL, Hospital Duran i Reynals, L'Hospitalet de Llobregat, Barcelona, Spain. ·Int J Cancer · Pubmed #23649709.

ABSTRACT: In this article, the effectiveness of a multi-targeted chemo-switch (C-S) schedule that combines metronomic chemotherapy (MET) after treatment with the maximum tolerated dose (MTD) is reported. This schedule was tested with gemcitabine in two distinct human pancreatic adenocarcinoma orthotopic models and with cyclophosphamide in an orthotopic ovarian cancer model. In both models, the C-S schedule had the most favourable effect, achieving at least 80% tumour growth inhibition without increased toxicity. Moreover, in the pancreatic cancer model, although peritoneal metastases were observed in control and MTD groups, no dissemination was observed in the MET and C-S groups. C-S treatment caused a decrease in angiogenesis, and its effect on tumour growth was similar to that produced by the MTD followed by anti-angiogenic DC101 treatment. C-S treatment combined an increase in thrombospondin-1 expression with a decrease in the number of CD133+ cancer cells and triple-positive CD133+/CD44+/CD24+ cancer stem cells (CSCs). These findings confirm that the C-S schedule is a challenging clinical strategy with demonstrable inhibitory effects on tumour dissemination, angiogenesis and CSCs.

6 Article Genetic and epigenetic markers in the evaluation of pancreatic masses. 2013

Ginestà, Mireia M / Mora, Josefina / Mayor, Regina / Farré, Antoni / Peinado, Miquel Angel / Busquets, Juli / Serrano, Teresa / Capellá, Gabriel / Fabregat, Joan. ·Translational Research Laboratory, Hereditary Cancer Program, Institut Català d´Oncologia-IDIBELL, Barcelona, Spain. ·J Clin Pathol · Pubmed #23135349.

ABSTRACT: BACKGROUND: Methylation markers have shown promise in the early diagnosis of pancreatic carcinoma. The aim of this study was to assess the diagnostic utility of hypermethylation status of candidate genes in combination with KRAS mutation detection in the evaluation of pancreatic masses. EXPERIMENTAL DESIGN: Sixty-one fine needle aspirates of pancreatic masses (43 pancreatic adenocarcinomas and 18 chronic pancreatitis) were studied. Methylation status of HRH2, EN1, SPARC, CDH13 and APC were analysed using melting curve analysis after DNA bisulfite treatment. KRAS mutations were also analysed. RESULTS: The methylation panel had a sensitivity of 73% (27 of 37, CI 95% 56 to 86%) and a specificity of 100% whenever two or more promoters were found hypermethylated. KRAS mutations showed a sensitivity of 77% (33 of 43, CI 95% 62 to 88%) and a specificity of 100%. Both molecular analyses added useful information to cytology by increasing the number of informative cases. When genetic and epigenetic analyses were combined sensitivity was 84% (36 of 43 CI 95% 69 to 93%) maintaining a 100% specificity. CONCLUSIONS: Analysis of hypermethylation status of a panel of genes and KRAS mutation detection offer a similar diagnostic yield in the evaluation of pancreatic masses. The combined molecular analysis increases the number of informative cases without diminishing specificity.