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Real Arribas, Francisco

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Francisco
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Real Arribas
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CNIO
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Author: Malats, Nuria × Has files: false ×

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    Publication
    Reply to 'Mosaic loss of chromosome Y in leukocytes matters'.
    (Nature Publishing Group, 2019-01) Zhou, Weiyin; Machiela, Mitchell J; Freedman, Neal D; Rothman, Nathaniel; Malats, Nuria; Dagnall, Casey; Caporaso, Neil; Teras, Lauren T; Gaudet, Mia M; Gapstur, Susan M; Stevens, Victoria L; Jacobs, Kevin B; Sampson, Joshua; Albanes, Demetrius; Weinstein, Stephanie; Virtamo, Jarmo; Berndt, Sonja; Hoover, Robert N; Black, Amanda; Silverman, Debra; Figueroa, Jonine; Garcia-Closas, Montserrat; Real Arribas, Francisco; Earl, Julie; Marenne, Gaelle; Rodriguez-Santiago, Benjamin; Karagas, Margaret; Johnson, Alison; Schwenn, Molly; Wu, Xifeng; Gu, Jian; Ye, Yuanqing; Hutchinson, Amy; Tucker, Margaret; Perez-Jurado, Luis A; Dean, Michael; Yeager, Meredith; Chanock, Stephen J; United States Department of Health and Human Services
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    CD8+ Cytotoxic Immune Infiltrate in Non-Muscle Invasive Bladder Cancer: A Standardized Methodology to Study Association with Clinico-Pathological Features and Prognosis.
    (IOS Press, 2019-08-16) Masson-Lecomte, Alexandra; Maillé, Pascale; Pineda, Silvia; Soyeux, Pascale; Sagrera, Ana; Rava, Marta; de Maturana, Evangelina Lopez; Márquez, Mirari; Tardón, Adonina; Carrato, Alfredo; Kogevinas, Manolis; de la Taille, Alexandre; Hartmann, Arndt; Malats, Nuria; Real Arribas, Francisco; Allory, Yves; Instituto de Salud Carlos III; Asociación Española Contra el Cáncer; NIH - National Cancer Institute (NCI) (Estados Unidos); European Association of Urology
    BACKGROUND Major interest lies in the evaluation of immune infiltrate in bladder cancer. CD8+ cytotoxic lymphocytes are key effectors of adaptive immune response. OBJECTIVES The aims of the study were to set up a standardized methodology for CD8+ lymphocytes estimation in NMIBC and investigate how intra-tumoral heterogeneity influences CD8+ immune infiltrate. METHODS We considered 995 NMIBC included in the Spanish Bladder Cancer (SBC)/EPICURO Study. Duplicate 0.6mm TMA spots and paired full sections (FS) for 50 selected cases were double stained with anti-pan cytokeratin antibody and anti-CD8 antibody. Slides were digitalized and CD8+ cells were automatically counted after tissue recognition (tumor vs stroma). Spatial heterogeneity was assessed and a resampling strategy was applied to estimate the proper number of 0.6mm TMA spots providing an adequate CD8+ cell estimate. Association between CD8+ count and expression of urothelial differentiation markers was estimated. Cox regression models were performed to assess association between CD8+ cell count and risk of recurrence and progression. RESULTS Microscopic examination of full sections showed spatial heterogeneity for CD8+ infiltrates. Simulation analyses demonstrated that 5 TMA regions provided a correct sampling of tumor and stromal compartments in Ta while 2 and 6 TMA regions were necessary in T1, respectively. CD8+ cells infiltration was associated with stage, regardless of the histological compartment analyzed (median CD8+ /mm2 were 25/mm2 and 129/mm2 in tumor and stroma respectively in Ta and 111/mm2 and 344/mm2 in T1; p-value = 0.006). CD8+ infiltration in tumor compartment was significantly associated with low FGFR3 expression. CD8+/mm2 count in the tumor compartment was not associated with prognosis. CONCLUSION Differences identified between Ta and T1 tumours supported the hypothesis that rigorous efforts should be placed in proper study design. These results provide a new framework to investigate microenvironment complexity in bladder cancer.
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    Publication
    Genome-Wide Association Study Data Reveal Genetic Susceptibility to Chronic Inflammatory Intestinal Diseases and Pancreatic Ductal Adenocarcinoma Risk.
    (American Association for Cancer Research (AACR), 2020-09-15) Yuan, Fangcheng; Hung, Rayjean J; Walsh, Naomi; Zhang, Han; Platz, Elizabeth A; Wheeler, William; Song, Lei; Arslan, Alan A; Beane Freeman, Laura E; Bracci, Paige; Canzian, Federico; Du, Mengmeng; Gallinger, Steven; Giles, Graham G; Goodman, Phyllis J; Kooperberg, Charles; Le Marchand, Loic; Neale, Rachel E; Rosendahl, Jonas; Scelo, Ghislaine; Shu, Xiao-Ou; Visvanathan, Kala; White, Emily; Zheng, Wei; Albanes, Demetrius; Amiano, Pilar; Andreotti, Gabriella; Babic, Ana; Bamlet, William R; Berndt, Sonja I; Brennan, Paul; Bueno-de-Mesquita, Bas; Buring, Julie E; Campbell, Peter T; Chanock, Stephen J; Fuchs, Charles S; Gaziano, J Michael; Goggins, Michael G; Hackert, Thilo; Hartge, Patricia; Hassan, Manal M; Holly, Elizabeth A; Hoover, Robert N; Katzke, Verena; Kirsten, Holger; Kurtz, Robert C; Lee, I-Min; Malats, Nuria; Milne, Roger L; Murphy, Neil; Ng, Kimmie; Oberg, Ann L; Porta, Miquel; Rabe, Kari G; Real Arribas, Francisco; Rothman, Nathaniel; Sesso, Howard D; Silverman, Debra T; Thompson, Ian M; Wactawski-Wende, Jean; Wang, Xiaoliang; Wentzensen, Nicolas; Wilkens, Lynne R; Yu, Herbert; Zeleniuch-Jacquotte, Anne; Shi, Jianxin; Duell, Eric J; Amundadottir, Laufey T; Li, Donghui; Petersen, Gloria M; Wolpin, Brian M; Risch, Harvey A; Yu, Kai; Klein, Alison P; Stolzenberg-Solomon, Rachael; NIH - National Cancer Institute (NCI) (Estados Unidos)
    Registry-based epidemiologic studies suggest associations between chronic inflammatory intestinal diseases and pancreatic ductal adenocarcinoma (PDAC). As genetic susceptibility contributes to a large proportion of chronic inflammatory intestinal diseases, we hypothesize that the genomic regions surrounding established genome-wide associated variants for these chronic inflammatory diseases are associated with PDAC. We examined the association between PDAC and genomic regions (±500 kb) surrounding established common susceptibility variants for ulcerative colitis, Crohn's disease, inflammatory bowel disease, celiac disease, chronic pancreatitis, and primary sclerosing cholangitis. We analyzed summary statistics from genome-wide association studies data for 8,384 cases and 11,955 controls of European descent from two large consortium studies using the summary data-based adaptive rank truncated product method to examine the overall association of combined genomic regions for each inflammatory disease group. Combined genomic susceptibility regions for ulcerative colitis, Crohn disease, inflammatory bowel disease, and chronic pancreatitis were associated with PDAC at P values < 0.05 (0.0040, 0.0057, 0.011, and 3.4 × 10-6, respectively). After excluding the 20 PDAC susceptibility regions (±500 kb) previously identified by GWAS, the genomic regions for ulcerative colitis, Crohn disease, and inflammatory bowel disease remained associated with PDAC (P = 0.0029, 0.0057, and 0.0098, respectively). Genomic regions for celiac disease (P = 0.22) and primary sclerosing cholangitis (P = 0.078) were not associated with PDAC. Our results support the hypothesis that genomic regions surrounding variants associated with inflammatory intestinal diseases, particularly, ulcerative colitis, Crohn disease, inflammatory bowel disease, and chronic pancreatitis are associated with PDAC. SIGNIFICANCE: The joint effects of common variants in genomic regions containing susceptibility loci for inflammatory bowel disease and chronic pancreatitis are associated with PDAC and may provide insights to understanding pancreatic cancer etiology.