Search

Your search keyword '"Fogar, P"' showing total 307 results
Start Over Author "Fogar, P"
307 results on '"Fogar, P"'

1. Flow Cytometry Analysis in Breast Implant-Associated Anaplastic Large Cell Lymphoma: Three Case Reports

Author

Veronica Davanzo, Alessandra Falda, Paola Fogar, Kathrin Ludwig, Jenny Zuin, Maria Cristina Toffanin, Marco Pizzi, Angelo Paolo Dei Tos, and Daniela Basso

Subjects
BIA-ALCL, CD30, flow cytometry, stability, morphology, immunohistochemistry, Biology (General), QH301-705.5, Chemistry, QD1-999
Abstract

Breast Implant-Associated-Anaplastic Large Cell Lymphoma (BIA-ALCL) is a rare T-cell non-Hodgkin lymphoma associated with breast prosthetic implants and represents a diagnostic challenge. The National Comprehensive Cancer Network (NCCN) guidelines, updated in 2024, recommend for diagnosis an integrated work-up that should include cell morphology, CD30 immunohistochemistry (IHC), and flow cytometry (FCM). CD30 IHC, although the test of choice for BIA-ALCL diagnosis, is not pathognomonic, and this supports the recommendation to apply a multidisciplinary approach. A close collaboration between pathologists and laboratory professionals allowed the diagnosis of three BIA-ALCLs, presented as case reports, within a series of 35 patients subjected to periprosthetic effusions aspiration from 2018 to 2023. In one case, rare neoplastic cells were identified by FCM, and this result was essential in leading the anatomopathological picture as indicative of this neoplasm. In fact, the distinction between a lymphomatous infiltrate from reactive cells may be very complex in the cytopathology and IHC setting when neoplastic cells are rare. On the other hand, one limitation of FCM analysis is the need for fresh samples. In this study, we provide evidence that a dedicated fixative allows the maintenance of an unaltered CD30 expression on the cell surface for up to 72 h.

Published
2024
Full Text
View/download PDF

4. Gestión urbana en clave resiliente. Fundamentos teóricos para el Área Metropolitana del Gran Resistencia, Chaco, Argentina

Author

Sandra Raquel Fogar

Subjects
Territorio, Desarrollo, Resiliencia, Territory, Developing, Resilience, Architecture, NA1-9428, Urban groups. The city. Urban sociology, HT101-395
Abstract

La perspectiva crítica posibilita analizar estrategias de intervención en el territorio urbano, desde un enfoque que interpela la noción moderna capitalista de desarrollo. Desde este posicionamiento se revisan concepciones y prácticas impuestas por la cultura dominante. La búsqueda de un paradigma desde el cual proponer otra estrategia de gestión, aplicada al caso de Resistencia, tensiona la lógica urbana fundacional y el manejo mercantilista que se impuso a las condiciones de vulnerabilidad hídrica, y la interpela en clave resiliente, orientada a alcanzar modos de ocupación ambiental y social más equilibrados y equitativos.

Published
2021

6. Complete Systematic Land Registration (PTSL) With Community Participation (PTSL-PM)

Author

Dita Perwitasari, Tamsil, Indri Fogar S., and Mahendra Wardhana

Subjects
land registration, ptsl-pm, technical regulations, Social Sciences
Abstract

The land is a means of life for humans, ranging from a place to live to becoming a development asset of a country. Therefore, it is very necessary to have arrangements or ownership rights over land so that each party who controls the land understands the rights and obligations of land ownership. Therefore, it is necessary to have land registration to obtain the legality of ownership of the land rights. Land registration is a series of activities carried out by the government continuously, continuously, and regularly. The importance of land registration for the first time for unregistered land owners and the Government (BPN) as well as the current problems related to land registration for the first time for unregistered lancd owners.

Published
2022
Full Text
View/download PDF

9. INCLUSION, CHILDHOOD AND TEACHING PRACTICE. ASSUMPTIONS AND TENSIONS IN THE CURRICULUMPROPOSED FOR THE INITIAL EDUCATION OF THE PROVINCE OF CHACO

Author

Mariela del Carmen Fogar and Carlos Alberto Silva

Subjects
políticas inclusivas, educación inicial, currículum, infancias, Education
Abstract

Recentre search developments about theoretical inquiry into the Curriculum of Initial Education of the province of Chaco, through inclusive political categories, initial education and childhood. The theoretical approach is understood as a way of representing reality through concepts that operate as assumptions. The inquiry follows a qualitative logic with documentary analysis. He is part of the ongoing research project "public policies for children: incidence of the obligatory nature of the initial level in the construction of the subjectivity of children from the neighborhood Molina Punta from Resistencia, Chaco", undertaken by Seminary education and society. Curriculum change in NI, was part of inclusive education policies for children implemented by the national Government in the period 2003 / 2015. Education as a practice linked to material, social and symbolic conditions, historical, co-producer of subjectivities (Puiggros, 1995) and social (Frigerio, 2001) is assumed. Frigerio (2005) and McLaren (1998) understand this as a political practice, which includes a cultural and economic policy of distribution of knowledge, desires and identities. This article analyzes the curriculum in association with historical processes on which is inscribed and tensions in the dynamics between the proposed curriculum adjusted to an idea of inclusive education function, and its construction in practice.

Published
2016
Full Text
View/download PDF

11. Resistencia de los botones florales del algodón Gossypium hirsutum L. a Spodoptera frugiperda Smith

Author

M.A. TCACH, M.N. FOGAR, R.D RIOS, and C.A. ACUÑA

Subjects
algodón, mejoramiento de plantas, resistencia a insectos, alelos mutantes, alto gosipol, Agriculture, Agriculture (General), S1-972
Abstract

En el género Gossypium existen alelos mutantes que confieren tolerancia a determinados insectos. Entre los de mayor eficacia se encuentra el rasgo denominado high glanding (presencia de glándulas de gosipol en el tercio superior del cáliz). Es necesario conocer la interacción de esta característica con los insectos plaga. El objetivo del trabajo fue estudiar la relación entre la edad de los botones florales y la resistencia a lepidópteros inducida por las glándulas de gosipol. Se diseñaron bioensayos con larvas de Spodoptera frugiperda Smith y caracterizaciones de la densidad de glándulas en botones florales de diferentes edades. Por un lado, en genotipos high y normal glanding el número de glándulas por unidad de superficie disminuyó en las estructuras reproductivas a medida que estas incrementaron su tamaño. Por otro lado, el peso y el tamaño de larvas de S. frugiperda fueron menores cuando se alimentaron con botones florales high glanding especialmente de menor tamaño. Estas evidencias demuestran que el carácter high glanding se comporta como un factor antibiótico en larvas de S. frugiperda.

Published
2015

13. Population-specific association of genes for telomere-associated proteins with longevity in an Italian population

Author

Crocco, Paolina, Barale, Roberto, Rose, Giuseppina, Rizzato, Cosmeri, Santoro, Aurelia, De Rango, Francesco, Carrai, Maura, Fogar, Paola, Monti, Daniela, Biondi, Fiammetta, Bucci, Laura, Ostan, Rita, Tallaro, Federica, Montesanto, Alberto, Zambon, Carlo-Federico, Franceschi, Claudio, Canzian, Federico, Passarino, Giuseppe, and Campa, Daniele

Published
2015
Full Text
View/download PDF

14. A Randomized Trial of Pharmacogenetic Warfarin Dosing in Naïve Patients with Non-Valvular Atrial Fibrillation.

Author

Vittorio Pengo, Carlo-Federico Zambon, Paola Fogar, Andrea Padoan, Giovanni Nante, Michela Pelloso, Stefania Moz, Anna Chiara Frigo, Francesca Groppa, Dania Bozzato, Enrico Tiso, Elisa Gnatta, Gentian Denas, Seena Padayattil Jose, Roberto Padrini, Daniela Basso, and Mario Plebani

Subjects
Medicine, Science
Abstract

UNLABELLED:Genotype-guided warfarin dosing have been proposed to improve patient’s management. This study is aimed to determine whether a CYP2C9- VKORC1- CYP4F2-based pharmacogenetic algorithm is superior to a standard, clinically adopted, pharmacodynamic method. Two-hundred naïve patients with non-valvular atrial fibrillation were randomized to trial arms and 180 completed the study. No significant differences were found in the number of out-of-range INRs (INR3.0) (p = 0.79) and in the mean percentage of time spent in the therapeutic range (TTR) after 19 days in the pharmacogenetic (51.9%) and in the control arm (53.2%, p = 0.71). The percentage of time spent at INR>4.0 was significantly lower in the pharmacogenetic (0.7%) than in the control arm (1.8%) (p = 0.02). Genotype-guided warfarin dosing is not superior in overall anticoagulation control when compared to accurate clinical standard of care. TRIAL REGISTRATION:ClinicalTrials.gov NCT01178034.

Published
2015
Full Text
View/download PDF

17. Pancreatic tumors and immature immunosuppressive myeloid cells in blood and spleen: role of inhibitory co-stimulatory molecules PDL1 and CTLA4. An in vivo and in vitro study.

Author

Daniela Basso, Paola Fogar, Massimo Falconi, Elisa Fadi, Cosimo Sperti, Chiara Frasson, Eliana Greco, Domenico Tamburrino, Sara Teolato, Stefania Moz, Dania Bozzato, Michela Pelloso, Andrea Padoan, Giuseppe De Franchis, Elisa Gnatta, Monica Facco, Carlo-Federico Zambon, Filippo Navaglia, Claudio Pasquali, Giuseppe Basso, Gianpietro Semenzato, Sergio Pedrazzoli, Paolo Pederzoli, and Mario Plebani

Subjects
Medicine, Science
Abstract

BACKGROUND: Blood and spleen expansion of immature myeloid cells (IMCs) might compromise the immune response to cancer. We studied in vivo circulating and splenic T lymphocyte and IMC subsets in patients with benign and malignant pancreatic diseases. We ascertained in vitro whether pancreatic adenocarcinoma (PDAC)-associated IMC subsets are induced by tumor-derived soluble factors and whether they are immunosuppressive focusing on the inhibitory co-stimulatory molecules PDL1 and CTLA4. METHODOLOGY AND PRINCIPAL FINDINGS: 103 pancreatic and/or splenic surgical patients were enrolled including 52 PDAC, 10 borderline and 10 neuroendocrine tumors (NETs). Lymphocytes and IMCs were analysed by flow cytometry in blood, in spleen and in three PDAC cell conditioned (CM) or non conditioned PBMC. PDL1 and CTLA4 were studied in 30 splenic samples, in control and conditioned PBMC. IMCs were FACS sorted and co-coltured with allogenic T lymphocytes. In PDAC a reduction was found in circulating CD8(+) lymphocytes (p = 0.004) and dendritic cells (p = 0.01), which were reduced in vitro by one PDAC CM (Capan1; p = 0.03). Blood myeloid derived suppressive cells (MDSCs) CD33(+)CD14(-)HLA-DR(-) were increased in PDAC (p = 0.022) and were induced in vitro by BxPC3 CM. Splenic dendritic cells had a higher PDL1 expression (p = 0.007), while CD33(+)CD14(+)HLA-DR(-) IMCs had a lower CTLA4 expression (p = 0.029) in PDAC patients. In vitro S100A8/A9 complex, one of the possible inflammatory mediators of immune suppression in PDAC, induced PDL1 (p = 0.018) and reduced CTLA4 expression (p = 0.028) among IMCs. IMCs not expressing CTLA4 were demonstrated to be immune suppressive. CONCLUSION: In PDAC circulating dendritic and cytotoxic T cells are reduced, while MDSCs are increased and this might favour tumoral growth and progression. The reduced CTLA4 expression found among splenic IMCs of PDAC patients was demonstrated to characterize an immune suppressive phenotype and to be consequent to the direct exposure of myeloid cells to pancreatic cancer derived products, S100A8/A9 complex in particular.

Published
2013
Full Text
View/download PDF

19. Altered Glucose Metabolism and Proteopysis in Pancreatic Cancer Cell Conditioned Myoblasts: Searching for a Gene Expression Pattern with a Microarray Analysis of 5000 Skeletal Muscle Genes

Author

Basso, D., Millino, C., Greco, E., Romualdi, C., Fogar, P., Valerio, A., Bellin, M., Zamabon, C., Navaglia, F., Dussini, N., Avogaro, A., Pedrazzoli, S., Lanfranchi, G., and Plebani, M.

Subjects
Proteolysis -- Analysis, Pancreatic cancer -- Causes of, Lactates -- Analysis, Glucose metabolism -- Analysis, Cachexia -- Causes of, Health
Published
2004

23. Germline BRCA2 K3326X and CHEK2 I157T mutations increase risk for sporadic pancreatic ductal adenocarcinoma

Author

Obazee, O., Archibugi, L., Andriulli, A., Soucek, P., Malecka-Panas, E., Ivanauskas, A., Johnson, T., Gazouli, M., Pausch, T., Lawlor, R. T., Cavestro, G. M., Milanetto, A. C., Di Leo, M., Pasquali, C., Hegyi, P., Szentesi, A., Radu, C. E., Gheorghe, C., Theodoropoulos, G. E., Bergmann, F., Brenner, H., Vodickova, L., Katzke, V., Campa, D., Strobel, O., Kaiser, J., Pezzilli, R., Federici, F., Mohelnikova-Duchonova, B., Boggi, U., Lemstrova, R., Johansen, J. S., Bojesen, S. E., Chen, I., Jensen, B. V., Capurso, G., Pazienza, V., Dervenis, C., Sperti, C., Mambrini, A., Hackert, T., Kaaks, R., Basso, D., Talar-Wojnarowska, R., Maiello, E., Izbicki, J. R., Cuk, K., Saum, K. U., Cantore, M., Kupcinskas, J., Palmieri, O., Delle Fave, G., Landi, S., Salvia, R., Fogar, P., Vashist, Y. K., Scarpa, A., Vodicka, P., Tjaden, C., Iskierka-Jazdzewska, E., Canzian, F., Obazee, O., Archibugi, L., Andriulli, A., Soucek, P., Malecka-Panas, E., Ivanauskas, A., Johnson, T., Gazouli, M., Pausch, T., Lawlor, R. T., Cavestro, G. M., Milanetto, A. C., Di Leo, M., Pasquali, C., Hegyi, P., Szentesi, A., Radu, C. E., Gheorghe, C., Theodoropoulos, G. E., Bergmann, F., Brenner, H., Vodickova, L., Katzke, V., Campa, D., Strobel, O., Kaiser, J., Pezzilli, R., Federici, F., Mohelnikova-Duchonova, B., Boggi, U., Lemstrova, R., Johansen, J. S., Bojesen, S. E., Chen, I., Jensen, B. V., Capurso, G., Pazienza, V., Dervenis, C., Sperti, C., Mambrini, A., Hackert, T., Kaaks, R., Basso, D., Talar-Wojnarowska, R., Maiello, E., Izbicki, J. R., Cuk, K., Saum, K. U., Cantore, M., Kupcinskas, J., Palmieri, O., Delle Fave, G., Landi, S., Salvia, R., Fogar, P., Vashist, Y. K., Scarpa, A., Vodicka, P., Tjaden, C., Iskierka-Jazdzewska, E., and Canzian, F.

Subjects
Male, Cancer Research, pancreatic cancer, Genes, BRCA2, I157T, Polymorphism, Single Nucleotide, Humans, Genetic Predisposition to Disease, Germ-Line Mutation, Aged, BRCA2 Protein, K3326X, PANDoRA consortium, rs11571833, rs17879961, Oncology, Pancreatic cancer, Middle Aged, Pancreatic Neoplasms, Checkpoint Kinase 2, Case-Control Studies, Female, Carcinoma, Pancreatic Ductal
Abstract

Rare truncating BRCA2 K3326X (rs11571833) and pathogenic CHEK2 I157T (rs17879961) variants have previously been implicated in familial pancreatic ductal adenocarcinoma (PDAC), but not in sporadic cases. The effect of both mutations in important DNA repair genes on sporadic PDAC risk may shed light on the genetic architecture of this disease. Both mutations were genotyped in germline DNA from 2,935 sporadic PDAC cases and 5,626 control subjects within the PANcreatic Disease ReseArch (PANDoRA) consortium. Risk estimates were evaluated using multivariate unconditional logistic regression with adjustment for possible confounders such as sex, age and country of origin. Statistical analyses were two-sided with p values

Published
2018

24. Germline BRCA2 K3326X and CHEK2 I157T mutations increase risk for sporadic pancreatic ductal adenocarcinoma

Author

Obazee, O. Archibugi, L. Andriulli, A. Soucek, P. Małecka-Panas, E. Ivanauskas, A. Johnson, T. Gazouli, M. Pausch, T. Lawlor, R.T. Cavestro, G.M. Milanetto, A.C. Di Leo, M. Pasquali, C. Hegyi, P. Szentesi, A. Radu, C.E. Gheorghe, C. Theodoropoulos, G.E. Bergmann, F. Brenner, H. Vodickova, L. Katzke, V. Campa, D. Strobel, O. Kaiser, J. Pezzilli, R. Federici, F. Mohelnikova-Duchonova, B. Boggi, U. Lemstrova, R. Johansen, J.S. Bojesen, S.E. Chen, I. Jensen, B.V. Capurso, G. Pazienza, V. Dervenis, C. Sperti, C. Mambrini, A. Hackert, T. Kaaks, R. Basso, D. Talar-Wojnarowska, R. Maiello, E. Izbicki, J.R. Cuk, K. Saum, K.U. Cantore, M. Kupcinskas, J. Palmieri, O. Delle Fave, G. Landi, S. Salvia, R. Fogar, P. Vashist, Y.K. Scarpa, A. Vodicka, P. Tjaden, C. Iskierka-Jazdzewska, E. Canzian, F.

Abstract

Rare truncating BRCA2 K3326X (rs11571833) and pathogenic CHEK2 I157T (rs17879961) variants have previously been implicated in familial pancreatic ductal adenocarcinoma (PDAC), but not in sporadic cases. The effect of both mutations in important DNA repair genes on sporadic PDAC risk may shed light on the genetic architecture of this disease. Both mutations were genotyped in germline DNA from 2,935 sporadic PDAC cases and 5,626 control subjects within the PANcreatic Disease ReseArch (PANDoRA) consortium. Risk estimates were evaluated using multivariate unconditional logistic regression with adjustment for possible confounders such as sex, age and country of origin. Statistical analyses were two-sided with p values

Published
2019

26. Abstract of the Symposium

Author

Vecchia, Carlo La, Negri, Eva, Franceschi, Silvia, D’Avanzo, Barbara, Boyle, Peter, Larsson, J., Permert, J., Del Favero, G., Basso, D., Fogar, P., Panozzo, M. P., Meggiato, T., Ferrara, C, D’Angeli, F., Brigato, L., Plebani, M., Ishikawa, Osamu, Nakamori, Shoji, Ohigashi, Hiroaki, Imaoka, Singi, AndrénSandberg, Åke, Ariyama, Joe, Permert, Johan, Larsson, Jörgen, Pour, Parviz M., Permert, Johan, Mogaki, Masashito, Kazakoff, Katherine, Gullo, Lucio, Pezzilli, Raffaele, Adrian, Thomas E., Permert, Johan, Larsson, Jörgen, Westermark, Gunilla T., and Antonio Maria Morselli-Labate

Published
1994
Full Text
View/download PDF

29. Germline BRCA2 K3326X and CHEK2 I157T mutations increase risk for sporadic pancreatic ductal adenocarcinoma

Author

Obazee, O, Archibugi, L, Andriulli, A, Soucek, P, Małecka-Panas, E, Ivanauskas, A, Johnson, T, Gazouli, M, Pausch, T, Lawlor, R T, Cavestro, G M, Milanetto, A C, Di Leo, M, Pasquali, C, Hegyi, P, Szentesi, A, Radu, C E, Gheorghe, C, Theodoropoulos, G E, Bergmann, F, Brenner, H, Vodickova, L, Katzke, V, Campa, D, Strobel, O, Kaiser, J, Pezzilli, R, Federici, F, Mohelnikova-Duchonova, B, Boggi, U, Lemstrova, R, Johansen, J S, Bojesen, S E, Chen, I, Jensen, B V, Capurso, G, Pazienza, V, Dervenis, C, Sperti, C, Mambrini, A, Hackert, T, Kaaks, R, Basso, D, Talar-Wojnarowska, R, Maiello, E, Izbicki, J R, Cuk, K, Saum, K U, Cantore, M, Kupcinskas, J, Palmieri, O, Delle Fave, G, Landi, S, Salvia, R, Fogar, P, Vashist, Y K, Scarpa, A, Vodicka, P, Tjaden, C, Iskierka-Jazdzewska, E, Canzian, F, Obazee, O, Archibugi, L, Andriulli, A, Soucek, P, Małecka-Panas, E, Ivanauskas, A, Johnson, T, Gazouli, M, Pausch, T, Lawlor, R T, Cavestro, G M, Milanetto, A C, Di Leo, M, Pasquali, C, Hegyi, P, Szentesi, A, Radu, C E, Gheorghe, C, Theodoropoulos, G E, Bergmann, F, Brenner, H, Vodickova, L, Katzke, V, Campa, D, Strobel, O, Kaiser, J, Pezzilli, R, Federici, F, Mohelnikova-Duchonova, B, Boggi, U, Lemstrova, R, Johansen, J S, Bojesen, S E, Chen, I, Jensen, B V, Capurso, G, Pazienza, V, Dervenis, C, Sperti, C, Mambrini, A, Hackert, T, Kaaks, R, Basso, D, Talar-Wojnarowska, R, Maiello, E, Izbicki, J R, Cuk, K, Saum, K U, Cantore, M, Kupcinskas, J, Palmieri, O, Delle Fave, G, Landi, S, Salvia, R, Fogar, P, Vashist, Y K, Scarpa, A, Vodicka, P, Tjaden, C, Iskierka-Jazdzewska, E, and Canzian, F

Abstract

Rare truncating BRCA2 K3326X (rs11571833) and pathogenic CHEK2 I157T (rs17879961) variants have previously been implicated in familial pancreatic ductal adenocarcinoma (PDAC), but not in sporadic cases. The effect of both mutations in important DNA repair genes on sporadic PDAC risk may shed light on the genetic architecture of this disease. Both mutations were genotyped in germline DNA from 2,935 sporadic PDAC cases and 5,626 control subjects within the PANcreatic Disease ReseArch (PANDoRA) consortium. Risk estimates were evaluated using multivariate unconditional logistic regression with adjustment for possible confounders such as sex, age and country of origin. Statistical analyses were two-sided with p values <0.05 considered significant. K3326X and I157T were associated with increased risk of developing sporadic PDAC (odds ratio (ORdom ) = 1.78, 95% confidence interval (CI) = 1.26-2.52, p = 1.19 × 10-3 and ORdom = 1.74, 95% CI = 1.15-2.63, p = 8.57 × 10-3 , respectively). Neither mutation was significantly associated with risk of developing early-onset PDAC. This retrospective study demonstrates novel risk estimates of K3326X and I157T in sporadic PDAC which suggest that upon validation and in combination with other established genetic and non-genetic risk factors, these mutations may be used to improve pancreatic cancer risk assessment in European populations. Identification of carriers of these risk alleles as high-risk groups may also facilitate screening or prevention strategies for such individuals, regardless of family history.

Published
2019

35. Corrigendum: Common genetic variants associated with pancreatic adenocarcinoma may also modify risk of pancreatic neuroendocrine neoplasms [Carcinogenesis, 39, 3, (2018), (360-367)] DOI: 10.1093/carcin/bgx150

Author

Obazee, O. Capurso, G. Tavano, F. Archibugi, L. De Bonis, A. Greenhalf, W. Key, T. Pasquali, C. Milanetto, A.C. Hackert, T. Fogar, P. Lico, V. Dervenis, C. Lawlor, R.T. Landoni, L. Gazouli, M. Zambon, C.F. Funel, N. Strobel, O. Jamroziak, K. Cantu, C. Malecka-Panas, E. Landi, S. Neoptolemos, J.P. Basso, D. Talar-Wojnarowska, R. Rinzivillo, M. Andriulli, A. Canzian, F. Campa, D.

Subjects
GeneralLiterature_REFERENCE(e.g.,dictionaries,encyclopedias,glossaries), GeneralLiterature_MISCELLANEOUS
Abstract

In the originally published version of this article, the institutional affiliations of some authors were listed incorrectly. The correct affiliations are as listed above. This has been corrected online. The authors wish to apologize for this error. © The Author(s) 2018. Published by Oxford University Press. All rights reserved.

Published
2018

36. SLC22A3 polymorphisms may influence overall patient survival-PANDORA study

Author

Mohelnikova-Duchonova, B, Strouhal, O, Hughes, Dj, Lovecek, M, Holcatova, I, Oliverius, M, Kala, Z, Campa, D, Rizzato, C, Canzian, F, Pezzilli, R, Talar-Wojnarowska, R, Malecka-Panas, E, Sperti, C, Zambon, Cf, Pedrazzoli, S, Fogar, P, Milanetto, A. C., Capurso, G, Delle Fave, G, Valente, R, Gazouli, M, Malleo, G, Lawlor, Rt, Strobel, O, Hackert, T, Giese, N, Vodicka, P, Vodickova, L, Landi, S, Tavano, F, Gioffreda, D, Piepoli, A, Pazienza, V, Mambrini, A, Bursi, S, Pacetti, P, Bambi, F, Ermini, S, Funel, N, and Soucek, P

Published
2018

37. Common genetic variants associated with pancreatic adenocarcinoma may also modify risk of pancreatic neuroendocrine neoplasms

Author

Obazee, O. Capurso, G. Tavano, F. Archibugi, L. Bonis, A.D. Greenhalf, W. Key, T. Pasquali, C. Milanetto, A.C. Hackert, T. Fogar, P. Liço, V. Dervenis, C. Lawlor, R.T. Landoni, L. Gazouli, M. Zambon, C.F. Funel, N. Strobel, O. Jamroziak, K. Cantù, C. Malecka-Panas, E. Landi, S. Neoptolemos, J.P. Basso, D. Talar-Wojnarowska, R. Rinzivillo, M. Andriulli, A. Canzian, F. Campa, D.

Abstract

Pancreatic neuroendocrine neoplasms (pNEN) account for less than 5% of all pancreatic neoplasms and genetic association studies on susceptibility to the disease are limited. We sought to identify possible overlap of genetic susceptibility loci between pancreatic ductal adenocarcinoma (PDAC) and pNEN; therefore, PDAC susceptibility variants (n = 23) from Caucasian genome-wide association studies (GWAS) were genotyped in 369 pNEN cases and 3277 controls from the PANcreatic Disease ReseArch (PANDoRA) consortium to evaluate the odds associated with pNEN risk, disease onset and tumor characteristics. Main effect analyses showed four PDAC susceptibility variants-rs9854771, rs1561927, rs9543325 and rs10919791 to be associated with pNEN risk. Subsequently, only associations with rs9543325, rs10919791 and rs1561927 were noteworthy with false positive report probability (FPRP) tests. Stratified analyses considering age at onset (50-year threshold), showed rs2736098, rs16986825 and rs9854771 to be associated with risk of developing pNEN at a younger age. Stratified analyses also showed some single nucleotide polymorphisms to be associated with different degrees of tumor grade, metastatic potential and functionality. Our results identify known GWAS PDAC susceptibility loci, which may also be involved in sporadic pNEN etiology and suggest that some genetic mechanisms governing pathogenesis of these two entities may be similar, with few of these loci being more influential in younger cases or tumor subtypes. © The Author(s) 2018. Published by Oxford University Press. All rights reserved.

Published
2018

38. Do pancreatic cancer and chronic pancreatitis share the same genetic risk factors? A PANcreatic Disease ReseArch (PANDoRA) consortium investigation

Author

Campa, D. Pastore, M. Capurso, G. Hackert, T. Di Leo, M. Izbicki, J.R. Khaw, K.-T. Gioffreda, D. Kupcinskas, J. Pasquali, C. Macinga, P. Kaaks, R. Stigliano, S. Peeters, P.H. Key, T.J. Talar-Wojnarowska, R. Vodicka, P. Valente, R. Vashist, Y.K. Salvia, R. Papaconstantinou, I. Shimizu, Y. Valsuani, C. Zambon, C.F. Gazouli, M. Valantiene, I. Niesen, W. Mohelnikova-Duchonova, B. Hara, K. Soucek, P. Malecka-Panas, E. Bueno-de-Mesquita, H.B. Johnson, T. Brenner, H. Tavano, F. Fogar, P. Ito, H. Sperti, C. Butterbach, K. Latiano, A. Andriulli, A. Cavestro, G.M. Busch, O.R.C. Dijk, F. Greenhalf, W. Matsuo, K. Lombardo, C. Strobel, O. König, A.-K. Cuk, K. Strothmann, H. Katzke, V. Cantore, M. Mambrini, A. Oliverius, M. Pezzilli, R. Landi, S. Canzian, F.

Subjects
endocrine system diseases, digestive system diseases
Abstract

Pancreatic ductal adenocarcinoma (PDAC) is a very aggressive tumor with a five-year survival of less than 6%. Chronic pancreatitis (CP), an inflammatory process in of the pancreas, is a strong risk factor for PDAC. Several genetic polymorphisms have been discovered as susceptibility loci for both CP and PDAC. Since CP and PDAC share a consistent number of epidemiologic risk factors, the aim of this study was to investigate whether specific CP risk loci also contribute to PDAC susceptibility. We selected five common SNPs (rs11988997, rs379742, rs10273639, rs2995271 and rs12688220) that were identified as susceptibility markers for CP and analyzed them in 2,914 PDAC cases, 356 CP cases and 5,596 controls retrospectively collected in the context of the international PANDoRA consortium. We found a weak association between the minor allele of the PRSS1-PRSS2-rs10273639 and an increased risk of developing PDAC (ORhomozygous = 1.19, 95% CI 1.02–1.38, p = 0.023). Additionally all the SNPs confirmed statistically significant associations with risk of developing CP, the strongest being PRSS1-PRSS2-rs10273639 (ORheterozygous = 0.51, 95% CI 0.39–0.67, p = 1.10 × 10−6) and MORC4-rs 12837024 (ORhomozygous = 2.07 (1.55–2.77, ptrend = 0.7 × 10−11). Taken together, the results from our study do not support variants rs11988997, rs379742, rs10273639, rs2995271 and rs12688220 as strong predictors of PDAC risk, but further support the role of these SNPs in CP susceptibility. Our study suggests that CP and PDAC probably do not share genetic susceptibility, at least in terms of high frequency variants. © 2017 UICC

Published
2018

40. Germline BRCA2 K3326X and CHEK2 I157T mutations increase risk for sporadic pancreatic ductal adenocarcinoma

Author

Obazee, O., primary, Archibugi, L., additional, Andriulli, A., additional, Soucek, P., additional, Małecka-Panas, E., additional, Ivanauskas, A., additional, Johnson, T., additional, Gazouli, M., additional, Pausch, T., additional, Lawlor, R. T., additional, Cavestro, G. M., additional, Milanetto, A. C., additional, Di Leo, M., additional, Pasquali, C., additional, Hegyi, P., additional, Szentesi, A., additional, Radu, C. E., additional, Gheorghe, C., additional, Theodoropoulos, G. E., additional, Bergmann, F., additional, Brenner, H., additional, Vodickova, L., additional, Katzke, V., additional, Campa, D., additional, Strobel, O., additional, Kaiser, J., additional, Pezzilli, R., additional, Federici, F., additional, Mohelnikova-Duchonova, B., additional, Boggi, U., additional, Lemstrova, R., additional, Johansen, J. S., additional, Bojesen, S. E., additional, Chen, I., additional, Jensen, B. V., additional, Capurso, G., additional, Pazienza, V., additional, Dervenis, C., additional, Sperti, C., additional, Mambrini, A., additional, Hackert, T., additional, Kaaks, R., additional, Basso, D., additional, Talar-Wojnarowska, R., additional, Maiello, E., additional, Izbicki, J. R., additional, Cuk, K., additional, Saum, K. U., additional, Cantore, M., additional, Kupcinskas, J., additional, Palmieri, O., additional, Delle Fave, G., additional, Landi, S., additional, Salvia, R., additional, Fogar, P., additional, Vashist, Y. K., additional, Scarpa, A., additional, Vodicka, P., additional, Tjaden, C., additional, Iskierka-Jazdzewska, E., additional, and Canzian, F., additional

Published
2019
Full Text
View/download PDF

42. Do pancreatic cancer and chronic pancreatitis share the same genetic risk factors? A PANcreatic Disease ReseArch (PANDoRA) consortium investigation

Author

Campa, D, Pastore, M, Capurso, G, Hackert, T, Di Leo, M, Izbicki, JR, Khaw, K-T, Gioffreda, D, Kupcinskas, J, Pasquali, C, Macinga, P, Kaaks, R, Stigliano, S, Peeters, PH, Key, TJ, Talar-Wojnarowska, R, Vodicka, P, Valente, R, Vashist, YK, Salvia, R, Papaconstantinou, I, Shimizu, Y, Valsuani, C, Zambon, CF, Gazouli, M, Valantiene, I, Niesen, W, Mohelnikova-Duchonova, B, Hara, K, Soucek, P, Malecka-Panas, E, Bueno-de-Mesquita, HBA, Johnson, T, Brenner, H, Tavano, F, Fogar, P, Ito, H, Sperti, C, Butterbach, K, Latiano, A, Andriulli, A, Cavestro, GM, Busch, ORC, Dijk, F, Greenhalf, W, Matsuo, K, Lombardo, C, Strobel, O, König, A-K, Cuk, K, Strothmann, H, Katzke, V, Cantore, M, Mambrini, A, Oliverius, M, Pezzilli, R, Landi, S, Canzian, F, Other departments, CCA - Imaging and biomarkers, AGEM - Amsterdam Gastroenterology Endocrinology Metabolism, Campa, Daniele, Pastore, Manuela, Capurso, Gabriele, Hackert, Thilo, Di Leo, Milena, Izbicki, Jakob R, Khaw, Kay tee, Gioffreda, Domenica, Kupcinskas, Juoza, Pasquali, Claudio, Macinga, Peter, Kaaks, Rudolf, Stigliano, Serena, Peeters, Petra H, Key, Timothy J, Talar wojnarowska, Renata, Vodicka, Pavel, Valente, Roberto, Vashist, Yogesh K, Salvia, Roberto, Papaconstantinou, Ioanni, Shimizu, Yasuhiro, Valsuani, Chiara, Zambon, Carlo Federico, Gazouli, Maria, Valantiene, Irena, Niesen, Willem, Mohelnikova duchonova, Beatrice, Hara, Kazuo, Soucek, Pavel, Malecka panas, Ewa, Bueno de mesquita, H. Ba, Johnson, Theron, Brenner, Herman, Tavano, Francesca, Fogar, Paola, Ito, Hidemi, Sperti, Cosimo, Butterbach, Katja, Latiano, Anna, Andriulli, Angelo, Cavestro, GIULIA MARTINA, Busch, Olivier R. C, Dijk, Frederike, Greenhalf, William, Matsuo, Keitaro, Lombardo, Carlo, Strobel, Oliver, König, Anna katharina, Cuk, Katarina, Strothmann, Hendrik, Katzke, Verena, Cantore, Maurizio, Mambrini, Andrea, Oliverius, Martin, Pezzilli, Raffaele, Landi, Stefano, and Canzian, Federico

Subjects
Adult, Male, Cancer Research, endocrine system diseases, Chronic pancreatiti, pancreatic ductal adenocarcinoma, Adenocarcinoma, Polymorphism, Single Nucleotide, genetic polymorphisms, Risk Factors, Pancreatitis, Chronic, Biomarkers, Tumor, genetic polymorphism, Humans, Trypsin, Chronic, Polymorphism, Aged, Retrospective Studies, Tumor, Carcinoma, association, Nuclear Proteins, Single Nucleotide, Middle Aged, ACUTE PANCREATITIS, Prognosis, digestive system diseases, PANCREATIC CANCER, Pancreatic Neoplasms, Pancreatitis, Oncology, Pancreatic Ductal, Case-Control Studies, Chronic pancreatitis, Carcinoma, Pancreatic Ductal, Female, Follow-Up Studies, Trypsinogen, Biomarkers
Abstract

Pancreatic ductal adenocarcinoma (PDAC) is a very aggressive tumor with a five-year survival of less than 6%. Chronic pancreatitis (CP), an inflammatory process in of the pancreas, is a strong risk factor for PDAC. Several genetic polymorphisms have been discovered as susceptibility loci for both CP and PDAC. Since CP and PDAC share consistent number of epidemiologic risk factors, the aim of this study was to investigate whether specific CP risk loci also contribute to PDAC susceptibility. We selected five common SNPs (rs11988997, rs379742, rs10273639 rs2995271 and rs12688220) that were identified as susceptibility markers for CP and analyzed them in 2,914 PDAC cases, 356 CP cases and 5,596 controls retrospectively collected in the context of the international PANDoRA consortium. We found a weak association between the minor allele of the PRSS1-PRSS2-rs10273639 and an increased risk of developing PDAC (ORhomozygous =1.19, 95% CI 1.02-1.38, p=0.023). Additionally all the SNPs confirmed statistically significant associations with risk of developing CP, the strongest being PRSS1-PRSS2-rs10273639 (ORheterozygous =0.51, 95% CI 0.39-0.67, p=1.10x10(-6) ) and MORC4-rs 12837024 (ORhomozygous =2.07 (1.55-2.77, ptrend =0.7x10(-11) ). Taken together, the results from our study do not support variants rs11988997, rs379742, rs10273639 rs2995271 and rs12688220 as strong predictors of PDAC risk, but further support the role of these SNPs in CP susceptibility. Our study suggests that CP and PDAC probably do not share genetic susceptibility, at least in terms of high frequency variants. This article is protected by copyright. All rights reserved.

Published
2017

43. SLC22A3 polymorphisms do not modify pancreatic cancer risk, but may influence overall patient survival

Author

Mohelnikova-Duchonova, B. Strouhal, O. Hughes, D.J. Holcatova, I. Oliverius, M. Kala, Z. Campa, D. Rizzato, C. Canzian, F. Pezzilli, R. Talar-Wojnarowska, R. Malecka-Panas, E. Sperti, C. Federico Zambon, C. Pedrazzoli, S. Fogar, P. Milanetto, A.C. Capurso, G. Delle Fave, G. Valente, R. Gazouli, M. Malleo, G. Teresa Lawlor, R. Strobel, O. Hackert, T. Giese, N. Vodicka, P. Vodickova, L. Landi, S. Tavano, F. Gioffreda, D. Piepoli, A. Pazienza, V. Mambrini, A. Pedata, M. Cantore, M. Bambi, F. Ermini, S. Funel, N. Lemstrova, R. Soucek, P.

Abstract

Expression of the solute carrier (SLC) transporter SLC22A3 gene is associated with overall survival of pancreatic cancer patients. This study tested whether genetic variability in SLC22A3 associates with pancreatic cancer risk and prognosis. Twenty four single nucleotide polymorphisms (SNPs) tagging the SLC22A3 gene sequence and regulatory elements were selected for analysis. Of these, 22 were successfully evaluated in the discovery phase while six significant or suggestive variants entered the validation phase, comprising a total study number of 1,518 cases and 3,908 controls. In the discovery phase, rs2504938, rs9364554, and rs2457571 SNPs were significantly associated with pancreatic cancer risk. Moreover, rs7758229 associated with the presence of distant metastases, while rs512077 and rs2504956 correlated with overall survival of patients. Although replicated, the association for rs9364554 did not pass multiple testing corrections in the validation phase. Contrary to the discovery stage, rs2504938 associated with survival in the validation cohort, which was more pronounced in stage IV patients. In conclusion, common variation in the SLC22A3 gene is unlikely to significantly contribute to pancreatic cancer risk. The rs2504938 SNP in SLC22A3 significantly associates with an unfavorable prognosis of pancreatic cancer patients. Further investigation of this SNP effect on the molecular and clinical phenotype is warranted. © 2017 The Author(s).

Published
2017

45. TERT gene harbors multiple variants associated with pancreatic cancer susceptibility

Author

Campa, D. Rizzato, C. Stolzenberg-Solomon, R. Pacetti, P. Vodicka, P. Cleary, S.P. Capurso, G. Bueno-De-Mesquita, H.B. Werner, J. Gazouli, M. Butterbach, K. Ivanauskas, A. Giese, N. Petersen, G.M. Fogar, P. Wang, Z. Bassi, C. Ryska, M. Theodoropoulos, G.E. Kooperberg, C. Li, D. Greenhalf, W. Pasquali, C. Hackert, T. Fuchs, C.S. Mohelnikova-Duchonova, B. Sperti, C. Funel, N. Dieffenbach, A.K. Wareham, N.J. Buring, J. Holcátová, I. Costello, E. Zambon, C.-F. Kupcinskas, J. Risch, H.A. Kraft, P. Bracci, P.M. Pezzilli, R. Olson, S.H. Sesso, H.D. Hartge, P. Strobel, O. Małecka-Panas, E. Visvanathan, K. Arslan, A.A. Pedrazzoli, S. Souček, P. Gioffreda, D. Key, T.J. Talar-Wojnarowska, R. Scarpa, A. Mambrini, A. Jacobs, E.J. Jamroziak, K. Klein, A. Tavano, F. Bambi, F. Landi, S. Austin, M.A. Vodickova, L. Brenner, H. Chanock, S.J. Delle Fave, G. Piepoli, A. Cantore, M. Zheng, W. Wolpin, B.M. Amundadottir, L.T. Canzian, F.

Abstract

A small number of common susceptibility loci have been identified for pancreatic cancer, one of which is marked by rs401681 in the TERT-CLPTM1L gene region on chromosome 5p15.33. Because this region is characterized by low linkage disequilibrium, we sought to identify whether additional single nucleotide polymorphisms (SNPs) could be related to pancreatic cancer risk, independently of rs401681. We performed an in-depth analysis of genetic variability of the telomerase reverse transcriptase (TERT) and the telomerase RNA component (TERC) genes, in 5,550 subjects with pancreatic cancer and 7,585 controls from the PANcreatic Disease ReseArch (PANDoRA) and the PanScan consortia. We identified a significant association between a variant in TERT and pancreatic cancer risk (rs2853677, odds ratio=0.85; 95% confidence interval=0.80-0.90, p=8.3 × 10-8). Additional analysis adjusting rs2853677 for rs401681 indicated that the two SNPs are independently associated with pancreatic cancer risk, as suggested by the low linkage disequilibrium between them (r2=0.07, D′=0.28). Three additional SNPs in TERT reached statistical significance after correction for multiple testing: rs2736100 (p=3.0 × 10-5), rs4583925 (p=4.0 × 10-5) and rs2735948 (p=5.0 × 10-5). In conclusion, we confirmed that the TERT locus is associated with pancreatic cancer risk, possibly through several independent variants. What's new? Most pancreatic cancer patients do not survive long after diagnosis, and, so far, there are not many genetic markers to help screen for the disease. In search of genetic predictors of pancreatic cancer, the authors zoomed in on a region linked to susceptibility to the disease. They measured the frequency of different variants of two genes, telomerase reverse transcriptase and telomerase RNA component, among thousands of pancreatic cancer patients and controls. They identified several variants of the TERT gene that indicate a boosted pancreatic cancer risk, and which may develop into useful prognostic tools. © 2015 UICC.

Published
2015

Catalog

Books, media, physical & digital resources
See catalog results