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17 results on '"Bijlsma, M. F."'

1. A pleiotropy scan to discover new susceptibility loci for pancreatic ductal adenocarcinoma

Author

Giaccherini, M, primary, Rende, M, additional, Gentiluomo, M, additional, Corradi, C, additional, Archibugi, L, additional, Ermini, S, additional, Maiello, E, additional, Morelli, L, additional, van Eijck, C H J, additional, Cavestro, G M, additional, Schneider, M, additional, Mickevicius, A, additional, Adamonis, K, additional, Basso, D, additional, Hlavac, V, additional, Gioffreda, D, additional, Talar-Wojnarowska, R, additional, Schöttker, B, additional, Lovecek, M, additional, Vanella, G, additional, Gazouli, M, additional, Uno, M, additional, Malecka-Wojciesko, E, additional, Vodicka, P, additional, Goetz, M, additional, Bijlsma, M F, additional, Petrone, M C, additional, Bazzocchi, F, additional, Kiudelis, M, additional, Szentesi, A, additional, Carrara, S, additional, Nappo, G, additional, Brenner, H, additional, Milanetto, A C, additional, Soucek, P, additional, Katzke, V, additional, Peduzzi, G, additional, Rizzato, C, additional, Pasquali, C, additional, Chen, X, additional, Capurso, G, additional, Hackert, T, additional, Bueno-de-Mesquita, B, additional, Uzunoglu, F G G, additional, Hegyi, P, additional, Greenhalf, W, additional, Theodoropoulos, G E E, additional, Sperti, C, additional, Perri, F, additional, Oliverius, M, additional, Mambrini, A, additional, Tavano, F, additional, Farinella, R, additional, Arcidiacono, P G, additional, Lucchesi, M, additional, Bunduc, S, additional, Kupcinskas, J, additional, Di Franco, G, additional, Stocker, S, additional, Neoptolemos, J P, additional, Bambi, F, additional, Jamroziak, K, additional, Testoni, S G G, additional, Aoki, M N, additional, Mohelnikova-Duchonova, B, additional, Izbicki, J R, additional, Pezzilli, R, additional, Lawlor, R T, additional, Kauffmann, E F, additional, López de Maturana, E, additional, Malats, N, additional, Canzian, F, additional, and Campa, D, additional

Published
2024
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6. Additional file 1 of FOXO transcriptional activity is associated with response to chemoradiation in EAC

Author

Creemers, A., van der Zalm, A. P., van de Stolpe, A., Holtzer, L., Stoffels, M., Hooijer, G. K. J., Ebbing, E. A., van Ooijen, H., van Brussel, A. G. C., Aussems-Custers, E. M. G., van Berge Henegouwen, M. I., Hulshof, M. C. C. M., Bergman, J. J. G. H. M., Meijer, S. L., Bijlsma, M. F., and van Laarhoven, H. W. M.

Abstract

Additional file 1: Figure S1. Poor responder phenotype in patient samples. A Pathway signal transduction activity of six key signal transduction pathways was measured in the resectable disease cohort (i). Pre-treatment biopsy pathway activity scores were subtracted from all matched resections that both passed QC, i.e. delta activity score (N = 69). Two-sided Wilcoxon signed-rank statistical tests were performed between all post-nCRT (N = 56) and surgery only (N = 13) patients. p-values are indicated in the figures. Boxplots represent median with interquartile range. B All post-nCRT resection specimens from the resectable disease cohort were assessed for correlations between FOXO and TGF-β activity. Spearman correlations were performed, N = 138, separated for low (1–2, N = 17, all Mandard 2), middle (3, N = 59) and high (4–5, N = 47) Mandard score. C Pre-treatment biopsies were assessed for correlations between FOXO and TGF-β activity. Spearman correlations were performed, N = 77, separated for low (1–2, N = 22), middle (3, N = 37) and high (4–5, N = 18) Mandard score obtained after nCRT. D Disease free survival of patients with combined low FOXO and TGF-β pathway activity versus combined high pathway activities in post-nCRT resection specimens (N = 83). Cut-off by median pathway activity score.

Published
2022
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7. Additional file 3 of FOXO transcriptional activity is associated with response to chemoradiation in EAC

Author

Creemers, A., van der Zalm, A. P., van de Stolpe, A., Holtzer, L., Stoffels, M., Hooijer, G. K. J., Ebbing, E. A., van Ooijen, H., van Brussel, A. G. C., Aussems-Custers, E. M. G., van Berge Henegouwen, M. I., Hulshof, M. C. C. M., Bergman, J. J. G. H. M., Meijer, S. L., Bijlsma, M. F., and van Laarhoven, H. W. M.

Subjects
genetic structures
Abstract

Additional file 3: Figure S3. PI3K inhibitors can revert CRT-induced EMT. A Correlation of gene expression of Broad Hallmark Pi3K_AKT_mTor_signalling gene set with the Broad Hallmark Epithelial_Mesenchymal_transition gene set in two publicly available datasets, GSE96669 and Esophageal Carcinoma Tumor Cancer Genome Atlas (TCGA-ESCA), respectively. B FACS analyses of mesenchymal marker CXCR4 after 7 days of treatment with CRT with or without 500 nM LY3023414. 031 M poor CRT responder, 289B good CRT responder. gMFI = geometric mean fluorescent intensity.

Published
2022
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8. Additional file 5 of FOXO transcriptional activity is associated with response to chemoradiation in EAC

Author

Creemers, A., van der Zalm, A. P., van de Stolpe, A., Holtzer, L., Stoffels, M., Hooijer, G. K. J., Ebbing, E. A., van Ooijen, H., van Brussel, A. G. C., Aussems-Custers, E. M. G., van Berge Henegouwen, M. I., Hulshof, M. C. C. M., Bergman, J. J. G. H. M., Meijer, S. L., Bijlsma, M. F., and van Laarhoven, H. W. M.

Abstract

Additional file 5: Table S1. Characteristics of the five established patient derived cell lines. Table S2. FDA approved PI3K inhibitors tested in this study. Table S3 Western blot antibodies used in this study.

Published
2022
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9. Additional file 4 of FOXO transcriptional activity is associated with response to chemoradiation in EAC

Author

Creemers, A., van der Zalm, A. P., van de Stolpe, A., Holtzer, L., Stoffels, M., Hooijer, G. K. J., Ebbing, E. A., van Ooijen, H., van Brussel, A. G. C., Aussems-Custers, E. M. G., van Berge Henegouwen, M. I., Hulshof, M. C. C. M., Bergman, J. J. G. H. M., Meijer, S. L., Bijlsma, M. F., and van Laarhoven, H. W. M.

Abstract

Additional file 4: Figure S4. Apoptosis induced by PI3K pathway inhibitors in poor responder CRT cell lines. Poor CRT responder cell lines 007B, 058 M and 081R and good responder cell lines Flo1, OE19 and OE33 were treated for 7 days with the CRT regimen in addition to 500 nM of PI3K pathway inhibitors (based on average IC50 of four compounds). Apoptosis measured by percentage of green fluorescent Annexin V-FITC. Data points represent biological replicates, mean with SD.

Published
2022
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11. Novel pancreatic cancer susceptibility loci discovered through genome-wild association studies

Author

Canzian, F., Campa, D., Rizzato, C., Bijlsma, M. F., Brenner, H., Bueno de Mesquita, H. B., Capurso, G., Cavestro, G. M., Funel, N., Gazouli, M., Hackert, T., Key, T. J., Kupcinskas, J., Landi, S., Małecka Panas, E., Mambrini, A., Mohelnikova Duchonova, B., Neoptolemos, J. P., Pasquali, Claudio, Pezzilli, R., Scarpa, A., Strobel, O., Tavano, F., Vahist, Y. K., Vodicka, P., Stolzenberg Solomon, R., Wolpin, B., Klein, A., and Amundadottir, L. T.

Published
2015

12. Stimulation of the vagus nerve attenuates macrophage activation by activating the Jak2-STAT3 signaling pathway (vol 6, pg 844, 2005)

Author

de Jonge, W. J., van der Zanden, E. P., O The, F., Bijlsma, M. F., van Westerloo, D. J., Bennink, R. J., Berthoud, H. R., Uematsu, S., Akira, S., van den Wijngaard, R. M., Boeckxstaens, G. E., Amsterdam Gastroenterology Endocrinology Metabolism, Gastroenterology and Hepatology, Center of Experimental and Molecular Medicine, Intensive Care Medicine, Amsterdam institute for Infection and Immunity, Cancer Center Amsterdam, and Nuclear Medicine

Published
2005

13. Genetic Polymorphisms Involved in Mitochondrial Metabolism and Pancreatic Cancer Risk

Author

Raffaele Pezzilli, Pavel Vodicka, Andrea Párniczky, George Theodoropoulos, Renata Talar-Wojnarowska, Paolo Giorgio Arcidiacono, Ugo Boggi, Bálint Erőss, Ewa Małecka-Panas, Martin Oliverius, Daniele Campa, Rita T. Lawlor, Faik G. Uzunoglu, Maria Chiara Petrone, Livia Archibugi, Stefania Bunduc, Edita Kreivenaite, Beatrice Mohelnikova-Duchonova, Manuel Gentiluomo, Maria Liliana Piredda, Giulia Peduzzi, Thilo Hackert, Francesco Perri, Giuseppe Vanella, Olivier R. Busch, Hermann Brenner, Pavel Soucek, John P. Neoptolemos, Martin Schneider, Sabrina Gloria Giulia Testoni, Luca Morelli, Krzysztof Jamroziak, Federico Canzian, Daniela Basso, Silvia Carrara, Maria Gazouli, Juozas Kupcinskas, Konstantinos Georgiou, Xīn Gào, Claudio Pasquali, Cosimo Sperti, Evaristo Maiello, Vytautas Kiudelis, Mara Götz, Martin Loos, Gabriele Capurso, Francesca Bazzocchi, Martin Lovecek, Bas Bueno-de-Mesquita, Viktor Hlavac, Niccola Funel, Roel Vermeulen, Maarten F. Bijlsma, Anna Caterina Milanetto, Ye Lu, Giulia Martina Cavestro, Stefano Ermini, Andrea Szentesi, Jakob R. Izbicki, William Greenhalf, Francesca Tavano, Feng Guo, Marta Puzzono, Domenica Gioffreda, Péter Hegyi, Eithne Costello, Casper H.J. van Eijck, Stefano Landi, Peduzzi, G., Gentiluomo, M., Tavano, F., Arcidiacono, P. G., Ermini, S., Vodicka, P., Boggi, U., Cavestro, G. M., Capurso, G., Morelli, L., Milanetto, A. C., Pezzilli, R., Lawlor, R. T., Carrara, S., Lovecek, M., Soucek, P., Guo, F., Hackert, T., Uzunoglu, F. G., Gazouli, M., Parniczky, A., Kupcinskas, J., Bijlsma, M. F., Bueno-De-Mesquita, B., Vermeulen, R., van Eijck, C. H. J., Jamroziak, K., Talar-Wojnarowska, R., Greenhalf, W., Gioffreda, D., Petrone, M. C., Landi, S., Archibugi, L., Puzzono, M., Funel, N., Sperti, C., Piredda, M. L., Mohelnikova-Duchonova, B., Lu, Y., Hlavac, V., Gao, X., Schneider, M., Izbicki, J. R., Theodoropoulos, G., Bunduc, S., Kreivenaite, E., Busch, O. R., Malecka-Panas, E., Costello, E., Perri, F., Giulia Testoni, S. G., Vanella, G., Pasquali, C., Oliverius, M., Brenner, H., Loos, M., Gotz, M., Georgiou, K., Eross, B., Maiello, E., Szentesi, A., Bazzocchi, F., Basso, D., Neoptolemos, J. P., Hegyi, P., Kiudelis, V., Canzian, F., Campa, D., Surgery, CCA - Cancer biology and immunology, CCA - Imaging and biomarkers, Center of Experimental and Molecular Medicine, and AGEM - Amsterdam Gastroenterology Endocrinology Metabolism

Subjects
Mitochondrial DNA, Pancreatic ductal adenocarcinoma, Nuclear gene, endocrine system diseases, Epidemiology, Biology, SUSCEPTIBILITY, Polymorphism, Single Nucleotide, SDG 3 - Good Health and Well-being, Pancreatic cancer, medicine, Humans, 03.02. Klinikai orvostan, Genetic variability, Carcinoma, Pancreatic Ductal, Case-Control Studies, Genetic Variation, Genome, Mitochondrial, Mitochondria, Pancreatic Neoplasms, Polymorphism, GENOME-WIDE ASSOCIATION, Gene, Genetics, Genome, GENOME-WIDE ASSOCIATION, SUSCEPTIBILITY, Carcinoma, Single Nucleotide, Metabolism, medicine.disease, digestive system diseases, Mitochondrial, Oncology, Pancreatic Ductal
Abstract

Background: The mitochondrial metabolism has been associated with pancreatic ductal adenocarcinoma (PDAC) risk. Recent evidence also suggests the involvement of the genetic variability of the mitochondrial function in several traits involved in PDAC etiology. However, a systematic investigation of the genetic variability of mitochondrial genome (mtSNP) and of all the nuclear genes involved in its functioning (n-mtSNPs) has never been reported. Methods: We conducted a two-phase association study of mtSNPs and n-mtSNPs to assess their effect on PDAC risk. We analyzed 35,297 n-mtSNPs and 101 mtSNPs in up to 55,870 individuals (12,884 PDAC cases and 42,986 controls). In addition, we also conducted a gene-based analysis on 1,588 genes involved in mitochondrial metabolism using Multi-marker Analysis of GenoMic Annotation (MAGMA) software. Results: In the discovery phase, we identified 49 n-mtSNPs and no mtSNPs associated with PDAC risk (P < 0.05). In the second phase, none of the findings were replicated. In the gene-level analysis, we observed that three genes (TERT, SUGCT, and SURF1) involved in the mitochondrial metabolism showed an association below the Bonferroni-corrected threshold of statistical significance (P = 0.05/1588 = 3.1 × 10−5). Conclusions: Even though the mitochondrial metabolism might be involved in PDAC etiology, our results, obtained in a study with one of the largest sample sizes to date, show that neither n-mtSNPs nor mtSNPs are associated with PDAC risk. Impact: This large case–control study does not support a role of the genetic variability of the mitochondrial function in PDAC risk.

Published
2021

14. Polygenic and multifactorial scores for pancreatic ductal adenocarcinoma risk prediction

Author

John P. Neoptolemos, Markus W. Büchler, Jakob R. Izbicki, Ben Schöttker, Cosmeri Rizzato, Cornelia Schroeder, Salvatore Paiella, Hanneke W. M. van Laarhoven, William Greenhalf, Simona Bursi, Renata Talar-Wojnarowska, Christos Dervenis, Ludmila Vodickova, Francesca Tavano, Giulia Martina Cavestro, Thilo Hackert, Claudio Pasquali, Ewa Małecka-Panas, Gabriele Capurso, Andrea Mambrini, Daniele Campa, Andrea Padoan, Ioannis S. Papanikolaou, Raffaele Pezzilli, Péter Hegyi, Beatrice Mohelnikova-Duchonova, Federica Gemignani, Michael F. Nentwich, Pavel Vodicka, Stefano Landi, Richárd Szmola, Anna Caterina Milanetto, Eithne Costello, Rudolf Kaaks, Laura Ginocchi, Bernd Holleczek, Erika Darvasi, Verena Katzke, Evaristo Maiello, Manuel Gentiluomo, Ondrej Strouhal, Orazio Palmieri, Juozas Kupcinskas, Alice Alessandra Galeotti, Viktor Hlavac, George Theodoropoulos, Audrius Ivanauskas, Maria Gazouli, Ferenc Izbéki, Federico Canzian, Oliver Strobel, Ofure Obazee, Martin Lovecek, Timothy J. Key, Domenica Gioffreda, Pavel Soucek, Ugo Boggi, Krzysztof Jamroziak, Cosimo Sperti, Maarten F. Bijlsma, Yogesh K. Vashist, Andrea Szentesi, Hermann Brenner, Livia Archibugi, Giuseppe Vanella, Daniela Basso, Radiotherapy, Center of Experimental and Molecular Medicine, CCA - Cancer Treatment and Quality of Life, Oncology, AGEM - Amsterdam Gastroenterology Endocrinology Metabolism, Galeotti, A. A., Gentiluomo, M., Rizzato, C., Obazee, O., Neoptolemos, J. P., Pasquali, C., Nentwich, M., Cavestro, G. M., Pezzilli, R., Greenhalf, W., Holleczek, B., Schroeder, C., Schottker, B., Ivanauskas, A., Ginocchi, L., Key, T. J., Hegyi, P., Archibugi, L., Darvasi, E., Basso, D., Sperti, C., Bijlsma, M. F., Palmieri, O., Hlavac, V., Talar-Wojnarowska, R., Mohelnikova-Duchonova, B., Hackert, T., Vashist, Y., Strouhal, O., Van Laarhoven, H., Tavano, F., Lovecek, M., Dervenis, C., Izbeki, F., Padoan, A., Malecka-Panas, E., Maiello, E., Vanella, G., Capurso, G., Izbicki, J. R., Theodoropoulos, G. E., Jamroziak, K., Katzke, V., Kaaks, R., Mambrini, A., Papanikolaou, I. S., Szmola, R., Szentesi, A., Kupcinskas, J., Bursi, S., Costello, E., Boggi, U., Milanetto, A. C., Landi, S., Gazouli, M., Vodickova, L., Soucek, P., Gioffreda, D., Gemignani, F., Brenner, H., Strobel, O., Buchler, M., Vodicka, P., Paiella, S., Canzian, F., and Campa, D.

Subjects
0301 basic medicine, Oncology, Male, medicine.medical_specialty, Multifactorial Inheritance, Pancreatic disease, genetic epidemiology, Population, Single-nucleotide polymorphism, Disease, pancreas and biliary tract, Polymorphism, Single Nucleotide, Risk Assessment, ABO Blood-Group System, 03 medical and health sciences, 0302 clinical medicine, Gene Frequency, Pancreatic cancer, Internal medicine, Genetics, medicine, oncology, Humans, education, Genetics (clinical), Alleles, Early Detection of Cancer, Genetic association, education.field_of_study, business.industry, medicine.disease, Pancreatic Neoplasms, 030104 developmental biology, Genetic epidemiology, 030220 oncology & carcinogenesis, Cohort, Female, business, Carcinoma, Pancreatic Ductal
Abstract

BackgroundMost cases of pancreatic ductal adenocarcinoma (PDAC) are asymptomatic in early stages, and the disease is typically diagnosed in advanced phases, resulting in very high mortality. Tools to identify individuals at high risk of developing PDAC would be useful to improve chances of early detection.ObjectiveWe generated a polygenic risk score (PRS) for PDAC risk prediction, combining the effect of known risk SNPs, and carried out an exploratory analysis of a multifactorial score.MethodsWe tested the associations of the individual known risk SNPs on up to 2851 PDAC cases and 4810 controls of European origin from the PANcreatic Disease ReseArch (PANDoRA) consortium. Thirty risk SNPs were included in a PRS, which was computed on the subset of subjects that had 100% call rate, consisting of 839 cases and 2040 controls in PANDoRA and 6420 cases and 4889 controls from the previously published Pancreatic Cancer Cohort Consortium I–III and Pancreatic Cancer Case-Control Consortium genome-wide association studies. Additional exploratory multifactorial scores were constructed by complementing the genetic score with smoking and diabetes.ResultsThe scores were associated with increased PDAC risk and reached high statistical significance (OR=2.70, 95% CI 1.99 to 3.68, p=2.54×10−10 highest vs lowest quintile of the weighted PRS, and OR=14.37, 95% CI 5.57 to 37.09, p=3.64×10−8, highest vs lowest quintile of the weighted multifactorial score).ConclusionWe found a highly significant association between a PRS and PDAC risk, which explains more than individual SNPs and is a step forward in the direction of the construction of a tool for risk stratification in the population.

Published
2020

16. Clinical value of ctDNA in upper-GI cancers: A systematic review and meta-analysis.

Author

Creemers A, Krausz S, Strijker M, van der Wel MJ, Soer EC, Reinten RJ, Besselink MG, Wilmink JW, van de Vijver MJ, van Noesel CJM, Verheij J, Meijer SL, Dijk F, Bijlsma MF, van Oijen MGH, and van Laarhoven HWM

Subjects
Esophageal Neoplasms genetics, Esophageal Neoplasms mortality, Humans, Pancreatic Neoplasms genetics, Pancreatic Neoplasms mortality, Prognosis, Proto-Oncogene Proteins p21(ras) genetics, Receptor, ErbB-2 genetics, Stomach Neoplasms genetics, Stomach Neoplasms mortality, Biomarkers, Tumor analysis, Circulating Tumor DNA analysis, Esophageal Neoplasms diagnosis, Pancreatic Neoplasms diagnosis, Stomach Neoplasms diagnosis
Abstract

Background: The recent expanding technical possibilities to detect tumor derived mutations in blood, so-called circulating tumor DNA (ctDNA), has rapidly increased the interest in liquid biopsies. This review and meta-analysis explores the clinical value of ctDNA in malignancies of the upper gastro-intestinal tract., Methods: PubMed, Cochrane and Embase databases were searched to identify studies reporting the diagnostic, prognostic or predictive value of ctDNA in patients with esophageal, gastric and pancreatic cancer, until January 2017. The diagnostic accuracy and, using random-effect pair-wise meta-analyses, the prognostic value of ctDNA was assessed., Results: A total of 34 studies met the inclusion criteria. For esophageal and gastric cancer, amplification of oncogenes in blood, such as HER2 and MYC, can be relevant for diagnostic purposes, and to predict treatment response in certain patient subpopulations. Given the limited number of studies assessing the role of ctDNA in esophageal and gastric cancer, the meta-analysis estimated the diagnostic accuracy and predictive value of ctDNA in pancreatic cancer only (n=10). The pooled sensitivity and specificity of ctDNA as a diagnostic tool in pancreatic cancer were 28% and 95%, respectively. Patients with pancreatic cancer and detectable ctDNA demonstrated a worse overall survival compared to patients with undetectable ctDNA (HR 1.92, 95% confidence interval (CI) 1.15-3.22, p=0.01)., Conclusion: The presence of ctDNA is significantly associated with a poor prognosis in patients with pancreatic cancer. The use of ctDNA in clinical practice is promising, although standardization of sequencing techniques and further development of high-sensitive detection methods is needed., (Copyright © 2017 Elsevier B.V. All rights reserved.)

Published
2017
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17. Key biological processes driving metastatic spread of pancreatic cancer as identified by multi-omics studies.

Author

Le Large TYS, Bijlsma MF, Kazemier G, van Laarhoven HWM, Giovannetti E, and Jimenez CR

Subjects
Adenocarcinoma pathology, Carcinoma, Pancreatic Ductal pathology, Gene Expression Regulation, Neoplastic genetics, Humans, Mutation, Neoplasm Metastasis pathology, Prognosis, Proteomics, Adenocarcinoma genetics, Carcinoma, Pancreatic Ductal genetics, Neoplasm Metastasis genetics, Neoplasm Proteins genetics
Abstract

Pancreatic ductal adenocarcinoma (PDAC) is an extremely aggressive malignancy, characterized by a high metastatic burden, already at the time of diagnosis. The metastatic potential of PDAC is one of the main reasons for the poor outcome next to lack of significant improvement in effective treatments in the last decade. Key mutated driver genes, such as activating KRAS mutations, are concordantly expressed in primary and metastatic tumors. However, the biology behind the metastatic potential of PDAC is not fully understood. Recently, large-scale omic approaches have revealed new mechanisms by which PDAC cells gain their metastatic potency. In particular, genomic studies have shown that multiple heterogeneous subclones reside in the primary tumor with different metastatic potential. The development of metastases may be correlated to a more mesenchymal transcriptomic subtype. However, for cancer cells to survive in a distant organ, metastatic sites need to be modulated into pre-metastatic niches. Proteomic studies identified the influence of exosomes on the Kuppfer cells in the liver, which could function to prepare this tissue for metastatic colonization. Phosphoproteomics adds an extra layer to the established omic techniques by unravelling key functional signaling. Future studies integrating results from these large-scale omic approaches will hopefully improve PDAC prognosis through identification of new therapeutic targets and patient selection tools. In this article, we will review the current knowledge on the biology of PDAC metastasis unravelled by large scale multi-omic approaches., (Copyright © 2017 The Author(s). Published by Elsevier Ltd.. All rights reserved.)

Published
2017
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