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  • 1.
    Bas, A
    et al.
    Umeå University, Faculty of Medicine, Department of Clinical Microbiology, Immunology/Immunchemistry.
    Forsberg, G
    Umeå University, Faculty of Medicine, Department of Clinical Microbiology, Immunology/Immunchemistry. Umeå University, Faculty of Medicine, Department of Clinical Sciences, Paediatrics.
    Sjöberg, Veronika
    Umeå University, Faculty of Medicine, Department of Clinical Microbiology, Immunology/Immunchemistry.
    Hammarström, Sten
    Umeå University, Faculty of Medicine, Department of Clinical Microbiology, Immunology/Immunchemistry.
    Hernell, Olle
    Umeå University, Faculty of Medicine, Department of Clinical Sciences, Paediatrics.
    Hammarström, Marie-Louise
    Umeå University, Faculty of Medicine, Department of Clinical Microbiology, Immunology/Immunchemistry.
    Aberrant extrathymic T cell receptor gene rearrangement in the small intestinal mucosa: a risk factor for coeliac disease?2009In: Gut, ISSN 0017-5749, E-ISSN 1468-3288, Vol. 58, no 2, p. 189-195Article in journal (Refereed)
    Abstract [en]

    BACKGROUND: Coeliac disease is a small intestine enteropathy caused by permanent intolerance to wheat gluten. Gluten intake by patients with coeliac disease provokes a strong reaction by intestinal intraepithelial lymphocytes (IELs), which normalises on a gluten-free diet. AIM: To investigate whether impaired extrathymic T cell maturation and/or secondary T cell receptor (TCR) gene recombination in IELs are features of coeliac disease which could contribute to the failure of establishing tolerance to gluten.

    METHODS: Expression levels of the four splice-forms of recombination activating gene-1 (RAG1) mRNA and preT alpha-chain (preTalpha) mRNA were determined in IEL-subsets of children with coeliac disease and controls. Frequencies of RAG1 expressing IELs were determined by immunomorphometry.

    RESULTS: In controls, the RAG1-1A/2 splice-form selectively expressed outside the thymus, was dominant and expressed in both mature (TCR(+)) and immature (CD2(+)CD7(+)TCR(-)) IELs ( approximately 8 mRNA copies/18S rRNA U). PreTalpha was expressed almost exclusively in CD2(+)CD7(+)TCR(-) IELs ( approximately 40 mRNA copies/18S rRNA U). By contrast, RAG1 and preTalpha mRNA levels were low in patients with coeliac disease compared to controls, both with active disease and with inactive, symptom-free disease on a gluten-free diet (p values <0.01 for mature and <0.05 for immature IELs). Similarly, the frequencies of RAG1+ IELs were significantly lower in patients with coeliac disease compared to controls (p<0.001).

    CONCLUSIONS: Patients with coeliac disease appear to have an impaired capacity for extrathymic TCR gene rearrangement. This is an inherent feature, which probably plays a pivotal role in the failure to efficiently downregulate the T cell response to gluten.

  • 2. Del Chiaro, Marco
    et al.
    Besselink, Marc G.
    Scholten, Lianne
    Bruno, Marco J.
    Cahen, Djuna L.
    Gress, Thomas M.
    van Hooft, Jeanin E.
    Lerch, Markus M.
    Mayerle, Julia
    Hackert, Thilo
    Satoi, Sohei
    Zerbi, Alessandro
    Cunningham, David
    De Angelis, Claudio
    Giovanni, Marc
    de-Madaria, Enrique
    Hegyi, Peter
    Rosendahl, Jonas
    Friess, Helmut
    Manfredi, Riccardo
    Levy, Philippe
    Real, Francisco X.
    Sauvanet, Alain
    Abu Hilal, Mohammed
    Marchegiani, Giovanni
    Esposito, Irene
    Ghaneh, Paula
    Engelbrecht, Marc R. W.
    Fockens, Paul
    van Huijgevoort, Nadine C. M.
    Wolfgang, Christopher
    Bassi, Claudio
    Gubergrits, Natalya B.
    Verbeke, Caroline
    Kloppel, Gunter
    Scarpa, Aldo
    Zamboni, Giuseppe
    Lennon, Anne Marie
    Sund, Malin
    Umeå University, Faculty of Medicine, Department of Surgical and Perioperative Sciences.
    Kartalis, Nikolaos
    Grenacher, Lars
    Falconi, Massimo
    Arnelo, Urban
    Kopchak, Kostantin V.
    Oppong, Kofi
    McKay, Colin
    Hauge, Truls
    Conlon, Kevin
    Adham, Mustapha
    Ceyhan, Guralp O.
    Salvia, Roberto
    Dervenis, Christos
    Allen, Peter
    Paye, Francois
    Bartsch, Detlef K.
    Lohr, Matthias
    Mutignani, Massimiliano
    Laukkarinen, Johanna
    Schulick, Richard
    Valente, Roberto
    Seufferlein, Thomas
    Capurso, Gabriele
    Siriwardena, Ajith
    Neoptolemos, John P.
    Pukitis, Aldis
    Segersvard, Ralf
    Aghdassi, A.
    Andrianello, S.
    Bossuyt, P.
    Bulow, R.
    Cardenas-Jaen, K.
    Cortegoso, P.
    Fontana, M.
    Haeberle, L.
    Heckler, M.
    Litvin, A.
    Mann, K.
    Michalski, C.
    Michl, P.
    Nappo, G.
    Perri, G.
    Persson, S.
    Scheufele, F.
    Sclafani, F.
    Schmidt, M.
    Venezia, L.
    Volker, F.
    Vullierm, M-P
    Wusten, L.
    European evidence-based guidelines on pancreatic cystic neoplasms2018In: Gut, ISSN 0017-5749, E-ISSN 1468-3288, Vol. 67, no 5, p. 789-804Article in journal (Refereed)
    Abstract [en]

    Evidence-based guidelines on the management of pancreatic cystic neoplasms (PCN) are lacking. This guideline is a joint initiative of the European Study Group on Cystic Tumours of the Pancreas, United European Gastroenterology, European Pancreatic Club, European-African Hepato-Pancreato-Biliary Association, European Digestive Surgery, and the European Society of Gastrointestinal Endoscopy. It replaces the 2013 European consensus statement guidelines on PCN. European and non-European experts performed systematic reviews and used GRADE methodology to answer relevant clinical questions on nine topics (biomarkers, radiology, endoscopy, intraductal papillary mucinous neoplasm (IPMN), mucinous cystic neoplasm (MCN), serous cystic neoplasm, rare cysts, (neo)adjuvant treatment, and pathology). Recommendations include conservative management, relative and absolute indications for surgery. A conservative approach is recommended for asymptomatic MCN and IPMN measuring < 40 mm without an enhancing nodule. Relative indications for surgery in IPMN include a main pancreatic duct (MPD) diameter between 5 and 9.9 mm or a cyst diameter >= 40 mm. Absolute indications for surgery in IPMN, due to the high-risk of malignant transformation, include jaundice, an enhancing mural nodule > 5 mm, and MPD diameter > 10 mm. Lifelong follow-up of IPMN is recommended in patients who are fit for surgery. The European evidence-based guidelines on PCN aim to improve the diagnosis and management of PCN.

  • 3. Ek, Weronica E.
    et al.
    Reznichenko, Anna
    Ripke, Stephan
    Niesler, Beate
    Zucchelli, Marco
    Rivera, Natalia V.
    Schmidt, Peter T.
    Pedersen, Nancy L.
    Magnusson, Patrik
    Talley, Nicholas J.
    Holliday, Elizabeth G.
    Houghton, Lesley
    Gazouli, Maria
    Karamanolis, George
    Rappold, Gudrun
    Burwinkel, Barbara
    Surowy, Harald
    Rafter, Joseph
    Assadi, Ghazaleh
    Li, Ling
    Papadaki, Evangelia
    Gambaccini, Dario
    Marchi, Santino
    Colucci, Rocchina
    Blandizzi, Corrado
    Barbaro, Raffaella
    Karling, Pontus
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Medicine.
    Walter, Susanna
    Ohlsson, Bodil
    Tornblom, Hans
    Bresso, Francesca
    Andreasson, Anna
    Dlugosz, Aldona
    Simren, Magnus
    Agreus, Lars
    Lindberg, Greger
    Boeckxstaens, Guy
    Bellini, Massimo
    Stanghellini, Vincenzo
    Barbara, Giovanni
    Daly, Mark J.
    Camilleri, Michael
    Wouters, Mira M.
    D'Amato, Mauro
    Exploring the genetics of irritable bowel syndrome: a GWA study in the general population and replication in multinational case-control cohorts2015In: Gut, ISSN 0017-5749, E-ISSN 1468-3288, Vol. 64, no 11, p. 1774-1782Article in journal (Refereed)
    Abstract [en]

    Objective IBS shows genetic predisposition, but adequately powered gene-hunting efforts have been scarce so far. We sought to identify true IBS genetic risk factors by means of genome-wide association (GWA) and independent replication studies. Design We conducted a GWA study (GWAS) of IBS in a general population sample of 11 326 Swedish twins. IBS cases (N=534) and asymptomatic controls (N=4932) were identified based on questionnaire data. Suggestive association signals were followed-up in 3511 individuals from six case-control cohorts. We sought genotype-gene expression correlations through single nucleotide polymorphism (SNP)-expression quantitative trait loci interactions testing, and performed in silico prediction of gene function. We compared candidate gene expression by real-time qPCR in rectal mucosal biopsies of patients with IBS and controls. Results One locus at 7p22.1, which includes the genes KDELR2 (KDEL endoplasmic reticulum protein retention receptor 2) and GRID2IP (glutamate receptor, ionotropic, delta 2 (Grid2) interacting protein), showed consistent IBS risk effects in the index GWAS and all replication cohorts and reached p=9.31 x 10(-6) in a meta-analysis of all datasets. Several SNPs in this region are associated with cis effects on KDELR2 expression, and a trend for increased mucosal KDLER2 mRNA expression was observed in IBS cases compared with controls. Conclusions Our results demonstrate that general population-based studies combined with analyses of patient cohorts provide good opportunities for gene discovery in IBS. The 7p22.1 and other risk signals detected in this study constitute a good starting platform for hypothesis testing in future functional investigations.

  • 4. Henström, Maria
    et al.
    Diekmann, Lena
    Bonfiglio, Ferdinando
    Hadizadeh, Fatemeh
    Kuech, Eva-Maria
    von Köckritz-Blickwede, Maren
    Thingholm, Louise B.
    Zheng, Tenghao
    Assadi, Ghazaleh
    Dierks, Claudia
    Heine, Martin
    Philipp, Ute
    Distl, Ottmar
    Money, Mary E.
    Belheouane, Meriem
    Heinsen, Femke-Anouska
    Rafter, Joseph
    Nardone, Gerardo
    Cuomo, Rosario
    Usai-Satta, Paolo
    Galeazzi, Francesca
    Neri, Matteo
    Walter, Susanna
    Simrén, Magnus
    Karling, Pontus
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Medicine.
    Ohlsson, Bodil
    Schmidt, Peter T.
    Lindberg, Greger
    Dlugosz, Aldona
    Agreus, Lars
    Andreasson, Anna
    Mayer, Emeran
    Baines, John F.
    Engstrand, Lars
    Portincasa, Piero
    Bellini, Massimo
    Stanghellini, Vincenzo
    Barbara, Giovanni
    Chang, Lin
    Camilleri, Michael
    Franke, Andre
    Naim, Hassan Y.
    D'Amato, Mauro
    Functional variants in the sucrase-isomaltase gene associate with increased risk of irritable bowel syndrome2018In: Gut, ISSN 0017-5749, E-ISSN 1468-3288, Vol. 67, no 2, p. 263-270Article in journal (Refereed)
    Abstract [en]

    OBJECTIVE: IBS is a common gut disorder of uncertain pathogenesis. Among other factors, genetics and certain foods are proposed to contribute. Congenital sucrase-isomaltase deficiency (CSID) is a rare genetic form of disaccharide malabsorption characterised by diarrhoea, abdominal pain and bloating, which are features common to IBS. We tested sucrase-isomaltase (SI) gene variants for their potential relevance in IBS.

    DESIGN: We sequenced SI exons in seven familial cases, and screened four CSID mutations (p.Val557Gly, p.Gly1073Asp, p.Arg1124Ter and p.Phe1745Cys) and a common SI coding polymorphism (p.Val15Phe) in a multicentre cohort of 1887 cases and controls. We studied the effect of the 15Val to 15Phe substitution on SI function in vitro. We analysed p.Val15Phe genotype in relation to IBS status, stool frequency and faecal microbiota composition in 250 individuals from the general population.

    RESULTS: CSID mutations were more common in patients than asymptomatic controls (p=0.074; OR=1.84) and Exome Aggregation Consortium reference sequenced individuals (p=0.020; OR=1.57). 15Phe was detected in 6/7 sequenced familial cases, and increased IBS risk in case-control and population-based cohorts, with best evidence for diarrhoea phenotypes (combined p=0.00012; OR=1.36). In the population-based sample, 15Phe allele dosage correlated with stool frequency (p=0.026) and Parabacteroides faecal microbiota abundance (p=0.0024). The SI protein with 15Phe exhibited 35% reduced enzymatic activity in vitro compared with 15Val (p<0.05).

    CONCLUSIONS: SI gene variants coding for disaccharidases with defective or reduced enzymatic activity predispose to IBS. This may help the identification of individuals at risk, and contribute to personalising treatment options in a subset of patients.

  • 5. Henström, Maria
    et al.
    Hadizadeh, Fatemeh
    Beyder, Arthur
    Bonfiglio, Ferdinando
    Zheng, Tenghao
    Assadi, Ghazaleh
    Rafter, Joseph
    Bujanda, Luis
    Agreus, Lars
    Andreasson, Anna
    Dlugosz, Aldona
    Lindberg, Greger
    Schmidt, Peter T.
    Karling, Pontus
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Medicine.
    Ohlsson, Bodil
    Talley, Nicholas J.
    Simren, Magnus
    Walter, Susanna
    Wouters, Mira
    Farrugia, Gianrico
    D'Amato, Mauro
    TRPM8 polymorphisms associated with increased risk of IBS-C and IBS-M2017In: Gut, ISSN 0017-5749, E-ISSN 1468-3288, Vol. 66, no 9, p. 1725-1727Article in journal (Refereed)
  • 6. Humes, D. J.
    et al.
    Järvholm, Bengt
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Occupational and Environmental Medicine.
    Ludvigsson, J. F.
    Body mass index and the risk of symptomatic diverticular disease: A Swedish population based cohort study2015In: Gut, ISSN 0017-5749, E-ISSN 1468-3288, Vol. 64, p. A164-A164Article in journal (Other academic)
  • 7. Humes, D. J.
    et al.
    Järvholm, Bengt
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Occupational and Environmental Medicine.
    Ludvigsson, J. F.
    PTU-230 Smoking and the risk of symptomatic diverticular disease: a swedish population based cohort study2015In: Gut, ISSN 0017-5749, E-ISSN 1468-3288, Vol. 64, p. A164-A164Article in journal (Other academic)
  • 8. Michaud, Dominique S
    et al.
    Izard, Jacques
    Wilhelm-Benartzi, Charlotte S
    You, Doo-Ho
    Grote, Verena A
    Tjønneland, Anne
    Dahm, Christina C
    Overvad, Kim
    Jenab, Mazda
    Fedirko, Veronika
    Boutron-Ruault, Marie Christine
    Clavel-Chapelon, Françoise
    Racine, Antoine
    Kaaks, Rudolf
    Boeing, Heiner
    Foerster, Jana
    Trichopoulou, Antonia
    Lagiou, Pagona
    Trichopoulos, Dimitrios
    Sacerdote, Carlotta
    Sieri, Sabina
    Palli, Domenico
    Tumino, Rosario
    Panico, Salvatore
    Siersema, Peter D
    Peeters, Petra Hm
    Lund, Eiliv
    Barricarte, Aurelio
    Huerta, José-María
    Molina-Montes, Esther
    Dorronsoro, Miren
    Quirós, J Ramón
    Duell, Eric J
    Ye, Weimin
    Umeå University, Faculty of Medicine, Department of Biobank Research.
    Sund, Malin
    Umeå University, Faculty of Medicine, Department of Surgical and Perioperative Sciences, Surgery. Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Nutritional Research.
    Lindkvist, Björn
    Johansen, Dorthe
    Khaw, Kay-Tee
    Wareham, Nick
    Travis, Ruth C
    Vineis, Paolo
    Bueno-de-Mesquita, H Bas
    Riboli, Elio
    Plasma antibodies to oral bacteria and risk of pancreatic cancer in a large European prospective cohort study2013In: Gut, ISSN 0017-5749, E-ISSN 1468-3288, Vol. 62, no 12, p. 1764-1770Article in journal (Refereed)
    Abstract [en]

    OBJECTIVE: Examine the relationship between antibodies to 25 oral bacteria and pancreatic cancer risk in a prospective cohort study. DESIGN: We measured antibodies to oral bacteria in prediagnosis blood samples from 405 pancreatic cancer cases and 416 matched controls, nested within the European Prospective Investigation into Cancer and Nutrition study. Analyses were conducted using conditional logistic regression and additionally adjusted for smoking status and body mass index. RESULTS: Individuals with high levels of antibodies against Porphyromonas gingivalis ATTC 53978, a pathogenic periodontal bacteria, had a twofold higher risk of pancreatic cancer than individuals with lower levels of these antibodies (OR 2.14; 95% CI 1.05 to 4.36; >200 ng/ml vs ≤200 ng/ml). To explore the association with commensal (non-pathogenic) oral bacteria, we performed a cluster analysis and identified two groups of individuals, based on their antibody profiles. A cluster with overall higher levels of antibodies had a 45% lower risk of pancreatic cancer than a cluster with overall lower levels of antibodies (OR 0.55; 95% CI 0.36 to 0.83). CONCLUSIONS: Periodontal disease might increase the risk for pancreatic cancer. Moreover, increased levels of antibodies against specific commensal oral bacteria, which can inhibit growth of pathogenic bacteria, might reduce the risk of pancreatic cancer. Studies are needed to determine whether oral bacteria have direct effects on pancreatic cancer pathogenesis or serve as markers of the immune response.

  • 9. Romanos, Jihane
    et al.
    Rosén, Anna
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Epidemiology and Global Health. Umeå University, Faculty of Medicine, Department of Medical Biosciences.
    Kumar, Vinod
    Trynka, Gosia
    Franke, Lude
    Szperl, Agata
    Gutierrez-Achury, Javier
    van Diemen, Cleo C
    Kanninga, Roan
    Jankipersadsing, Soesma A
    Steck, Andrea
    Eisenbarth, Georges
    van Heel, David A
    Cukrowska, Bozena
    Bruno, Valentina
    Mazzilli, Maria Cristina
    Núñez, Concepcion
    Bilbao, Jose Ramon
    Mearin, M Luisa
    Barisani, Donatella
    Rewers, Marian
    Norris, Jill M
    Ivarsson, Anneli
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Epidemiology and Global Health.
    Boezen, H Marieke
    Liu, Edwin
    Wijmenga, Cisca
    Improving coeliac disease risk prediction by testing non-HLA variants additional to HLA variants2014In: Gut, ISSN 0017-5749, E-ISSN 1468-3288, Vol. 63, no 3, p. 415-422Article in journal (Refereed)
    Abstract [en]

    BACKGROUND: The majority of coeliac disease (CD) patients are not being properly diagnosed and therefore remain untreated, leading to a greater risk of developing CD-associated complications. The major genetic risk heterodimer, HLA-DQ2 and DQ8, is already used clinically to help exclude disease. However, approximately 40% of the population carry these alleles and the majority never develop CD. OBJECTIVE: We explored whether CD risk prediction can be improved by adding non-HLA-susceptible variants to common HLA testing. DESIGN: We developed an average weighted genetic risk score with 10, 26 and 57 single nucleotide polymorphisms (SNP) in 2675 cases and 2815 controls and assessed the improvement in risk prediction provided by the non-HLA SNP. Moreover, we assessed the transferability of the genetic risk model with 26 non-HLA variants to a nested case-control population (n=1709) and a prospective cohort (n=1245) and then tested how well this model predicted CD outcome for 985 independent individuals. RESULTS: Adding 57 non-HLA variants to HLA testing showed a statistically significant improvement compared to scores from models based on HLA only, HLA plus 10 SNP and HLA plus 26 SNP. With 57 non-HLA variants, the area under the receiver operator characteristic curve reached 0.854 compared to 0.823 for HLA only, and 11.1% of individuals were reclassified to a more accurate risk group. We show that the risk model with HLA plus 26 SNP is useful in independent populations. CONCLUSIONS: Predicting risk with 57 additional non-HLA variants improved the identification of potential CD patients. This demonstrates a possible role for combined HLA and non-HLA genetic testing in diagnostic work for CD.

  • 10. Smith, Todd
    et al.
    Muller, David C
    Moons, Karel G M
    Cross, Amanda J
    Johansson, Mattias
    Ferrari, Pietro
    Fagherazzi, Guy
    Peeters, Petra H M
    Severi, Gianluca
    Hüsing, Anika
    Kaaks, Rudolf
    Tjonneland, Anne
    Olsen, Anja
    Overvad, Kim
    Bonet, Catalina
    Rodriguez-Barranco, Miguel
    Huerta, Jose Maria
    Barricarte Gurrea, Aurelio
    Bradbury, Kathryn E
    Trichopoulou, Antonia
    Bamia, Christina
    Orfanos, Philippos
    Palli, Domenico
    Pala, Valeria
    Vineis, Paolo
    Bueno-de-Mesquita, Bas
    Ohlsson, Bodil
    Harlid, Sophia
    Umeå University, Faculty of Medicine, Department of Radiation Sciences, Oncology.
    Van Guelpen, Bethany
    Skeie, Guri
    Weiderpass, Elisabete
    Jenab, Mazda
    Murphy, Neil
    Riboli, Elio
    Gunter, Marc J
    Aleksandrova, Krasimira Jekova
    Tzoulaki, Ioanna
    Comparison of prognostic models to predict the occurrence of colorectal cancer in asymptomatic individuals: a systematic literature review and external validation in the EPIC and UK Biobank prospective cohort studies.2018In: Gut, ISSN 0017-5749, E-ISSN 1468-3288, article id gutjnl-2017-315730Article in journal (Refereed)
    Abstract [en]

    OBJECTIVE: To systematically identify and validate published colorectal cancer risk prediction models that do not require invasive testing in two large population-based prospective cohorts.

    DESIGN: Models were identified through an update of a published systematic review and validated in the European Prospective Investigation into Cancer and Nutrition (EPIC) and the UK Biobank. The performance of the models to predict the occurrence of colorectal cancer within 5 or 10 years after study enrolment was assessed by discrimination (C-statistic) and calibration (plots of observed vs predicted probability).

    RESULTS: The systematic review and its update identified 16 models from 8 publications (8 colorectal, 5 colon and 3 rectal). The number of participants included in each model validation ranged from 41 587 to 396 515, and the number of cases ranged from 115 to 1781. Eligible and ineligible participants across the models were largely comparable. Calibration of the models, where assessable, was very good and further improved by recalibration. The C-statistics of the models were largely similar between validation cohorts with the highest values achieved being 0.70 (95% CI 0.68 to 0.72) in the UK Biobank and 0.71 (95% CI 0.67 to 0.74) in EPIC.

    CONCLUSION: Several of these non-invasive models exhibited good calibration and discrimination within both external validation populations and are therefore potentially suitable candidates for the facilitation of risk stratification in population-based colorectal screening programmes. Future work should both evaluate this potential, through modelling and impact studies, and ascertain if further enhancement in their performance can be obtained.

  • 11. Stange, D E
    et al.
    Engel, F
    Longerich, T
    Koo, B K
    Koch, M
    Delhomme, N
    Aigner, M
    Toedt, G
    Schirmacher, P
    Lichter, P
    Weitz, J
    Radlwimmer, B
    Expression of an ASCL2 related stem cell signature and IGF2 in colorectal cancer liver metastases with 11p15.5 gain.2010In: Gut, ISSN 0017-5749, E-ISSN 1468-3288, Vol. 59, no 9Article in journal (Refereed)
    Abstract [en]

    BACKGROUND AND AIMS: Liver metastases are the leading cause of death in colorectal cancer. To gain better insight into the biology of metastasis and possibly identify new therapeutic targets we systematically investigated liver-metastasis-specific molecular aberrations.

    METHODS: Primary colorectal cancer (pCRC) and matched liver metastases (LMs) from the same patients were analysed by microarray-based comparative genomic hybridisation in 21 pairs and gene expression profiling in 18 pairs. Publicly available databases were used to confirm findings in independent datasets.

    RESULTS: Chromosome aberration patterns and expression profiles of pCRC and matched LMs were strikingly similar. Unsupervised cluster analysis of genomic data showed that 20/21 pairs were more similar to each other than to any other analysed tumour. A median of only 11 aberrations per patient was found to be different between pCRC and LM, and expression of only 16 genes was overall changed upon metastasis. One region on chromosome band 11p15.5 showed a characteristic gain in LMs in 6/21 patients. This gain could be confirmed in an independent dataset of LMs (n=50). Localised within this region, the growth factor IGF2 (p=0.003) and the intestinal stem cell specific transcription factor ASCL2 (p=0.029) were found to be over-expressed in affected LM. Several ASCL2 target genes were upregulated in this subgroup of LM, including the intestinal stem cell marker OLFM4 (p=0.013). The correlation between ASCL2 expression and four known direct transcriptional targets (LGR5, EPHB3, ETS2 and SOX9) could be confirmed in an independent expression dataset (n=50).

    CONCLUSIONS: With unprecedented resolution a striking conservation of genomic alterations was demonstrated in liver metastases, suggesting that metastasis typically occurs after the pCRC has fully matured. In addition, we characterised a subset of liver metastases with an ASCL2-related stem-cell signature likely to affect metastatic behaviour of tumour cells.

  • 12. Sundkvist, Anneli
    et al.
    Myte, Robin
    Palmqvist, Richard
    Harlid, Sophia
    Umeå University, Faculty of Medicine, Department of Radiation Sciences, Oncology.
    Van Guelpen, Bethany
    Plasma ghrelin is probably not a useful biomarker for risk prediction or early detection of colorectal cancer.2018In: Gut, ISSN 0017-5749, E-ISSN 1468-3288, article id gutjnl-2018-316110Article in journal (Refereed)
  • 13. Tjonneland, A
    et al.
    Overvad, K
    Bergmann, M M
    Nagel, G
    Linseisen, J
    Hallmans, Göran
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Nutritional Research.
    Palmqvist, Richard
    Umeå University, Faculty of Medicine, Department of Medical Biosciences, Pathology.
    Sjödin, Hubert
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Nutritional Research.
    Hägglund, G
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Nutritional Research.
    Berglund, G
    Lindgren, S
    Grip, O
    Palli, D
    Day, N E
    Khaw, K-T
    Bingham, S
    Riboli, E
    Kennedy, H
    Hart, A
    Danielsson, A
    Linoleic acid, a dietary n-6 polyunsaturated fatty acid, and the aetiology of ulcerative colitis: a nested case-control study within a European prospective cohort study2009In: Gut, ISSN 0017-5749, E-ISSN 1468-3288, Vol. 58, no 12, p. 1606-1611Article in journal (Refereed)
    Abstract [en]

    OBJECTIVE: Dietary linoleic acid, an n-6 polyunsaturated fatty acid, is metabolised to arachidonic acid, a component of colonocyte membranes. Metabolites of arachidonic acid have pro-inflammatory properties and are increased in the mucosa of patients with ulcerative colitis. The aim of this investigation was to conduct the first prospective cohort study investigating if a high dietary intake of linoleic acid increases the risk of developing incident ulcerative colitis. DESIGN AND SETTING: Dietary data from food frequency questionnaires were available for 203 193 men and women aged 30-74 years, resident in the UK, Sweden, Denmark, Germany or Italy and participating in a prospective cohort study, the European Prospective Investigation into Cancer and Nutrition (EPIC). These participants were followed up for the diagnosis of ulcerative colitis. Each case was matched with four controls and the risk of disease calculated by quartile of intake of linoleic acid adjusted for gender, age, smoking, total energy intake and centre. RESULTS: A total of 126 participants developed ulcerative colitis (47% women) after a median follow-up of 4.0 years (range, 1.7-11.3 years). The highest quartile of intake of linoleic acid was associated with an increased risk of ulcerative colitis (odds ratio (OR) = 2.49, 95% confidence interval (CI) = 1.23 to 5.07, p = 0.01) with a significant trend across quartiles (OR = 1.32 per quartile increase, 95% CI = 1.04 to 1.66, p = 0.02 for trend). CONCLUSIONS: The data support a role for dietary linoleic acid in the aetiology of ulcerative colitis. An estimated 30% of cases could be attributed to having dietary intakes higher than the lowest quartile of linoleic acid intake.

  • 14. van Duijnhoven, Fränzel J B
    et al.
    Bueno-De-Mesquita, H Bas
    Calligaro, Miriam
    Jenab, Mazda
    Pischon, Tobias
    Jansen, Eugène H J M
    Frohlich, Jiri
    Ayyobi, Amir
    Overvad, Kim
    Toft-Petersen, Anne Pernille
    Tjønneland, Anne
    Hansen, Louise
    Boutron-Ruault, Marie-Christine
    Clavel-Chapelon, Françoise
    Cottet, Vanessa
    Palli, Domenico
    Tagliabue, Giovanna
    Panico, Salvatore
    Tumino, Rosario
    Vineis, Paolo
    Kaaks, Rudolf
    Teucher, Birgit
    Boeing, Heiner
    Drogan, Dagmar
    Trichopoulou, Antonia
    Lagiou, Pagona
    Dilis, Vardis
    Peeters, Petra H M
    Siersema, Peter D
    Rodríguez, Laudina
    González, Carlos A
    Molina-Montes, Esther
    Dorronsoro, Miren
    Tormo, Maria-Jose
    Barricarte, Aurelio
    Palmqvist, Richard
    Umeå University, Faculty of Medicine, Department of Medical Biosciences, Pathology.
    Hallmans, Göran
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Nutritional Research.
    Khaw, Kay-Tee
    Tsilidis, Kostas K
    Crowe, Francesca L
    Chajes, Veronique
    Fedirko, Veronika
    Rinaldi, Sabina
    Norat, Teresa
    Riboli, Elio
    Blood lipid and lipoprotein concentrations and colorectal cancer risk in the European Prospective Investigation into Cancer and Nutrition2011In: Gut, ISSN 0017-5749, E-ISSN 1468-3288, Vol. 60, no 8, p. 1094-1102Article in journal (Refereed)
    Abstract [en]

    OBJECTIVE: To examine the association between serum concentrations of total cholesterol, high density lipoprotein cholesterol (HDL), low density lipoprotein cholesterol, triglycerides, apolipoprotein A-I (apoA), apolipoprotein B and the incidence of colorectal cancer (CRC).

    DESIGN: Nested case-control study.

    SETTING: The study was conducted within the European Prospective Investigation into Cancer and Nutrition (EPIC), a cohort of more than 520,000 participants from 10 western European countries.

    PARTICIPANTS: 1238 cases of incident CRC, which developed after enrolment into the cohort, were matched with 1238 controls for age, sex, centre, follow-up time, time of blood collection and fasting status.

    MAIN OUTCOME MEASURES: Serum concentrations were quantitatively determined by colorimetric and turbidimetric methods. Dietary and lifestyle data were obtained from questionnaires. Conditional logistic regression models were used to estimate incidence rate ratios (RRs) and 95% CIs which were adjusted for height, weight, smoking habits, physical activity, education, consumption of fruit, vegetables, meat, fish, alcohol, fibre and energy.

    RESULTS: After adjustments, the concentrations of HDL and apoA were inversely associated with the risk of colon cancer (RR for 1 SD increase of 16.6 mg/dl in HDL and 32.0 mg/dl in apoA of 0.78 (95% CI 0.68 to 0.89) and 0.82 (95% CI 0.72 to 0.94), respectively). No association was observed with the risk of rectal cancer. Additional adjustment for biomarkers of systemic inflammation, insulin resistance and oxidative stress or exclusion of the first 2 years of follow-up did not influence the association between HDL and risk of colon cancer.

    CONCLUSIONS: These findings show that high concentrations of serum HDL are associated with a decreased risk of colon cancer. The mechanism behind this association needs further elucidation.

  • 15.
    Van Guelpen, Bethany
    et al.
    Umeå University, Faculty of Medicine, Department of Medical Biosciences, Pathology.
    Hultdin, Johan
    Umeå University, Faculty of Medicine, Department of Medical Biosciences, Clinical chemistry.
    Johansson, Ingegerd
    Umeå University, Faculty of Medicine, Department of Odontology, Cariology.
    Hallmans, Göran
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Nutritional Research.
    Stenling, Roger
    Umeå University, Faculty of Medicine, Department of Medical Biosciences, Pathology.
    Riboli, E
    Winkvist, A
    Palmqvist, Richard
    Umeå University, Faculty of Medicine, Department of Medical Biosciences, Pathology.
    Low folate levels may protect against colorectal cancer2006In: Gut, ISSN 0017-5749, E-ISSN 1468-3288, Vol. 55, no 10, p. 1461-1466Article in journal (Other academic)
    Abstract [en]

    BACKGROUND AND AIMS: Dietary folate is believed to protect against colorectal cancer (CRC). However, few studies have addressed the role of circulating levels of folate. The aim of this study was to relate prediagnostic plasma folate and homocysteine concentrations and the methylenetetrahydrofolate reductase (MTHFR) 677C>T and 1298A>C polymorphisms to the risk of developing CRC.

    SUBJECTS: Subjects were 226 cases and 437 matched referents from the population based Northern Sweden Health and Disease Cohort.

    RESULTS: We observed a bell-shaped association between plasma folate concentrations and CRC risk; multivariate odds ratio for middle versus lowest quintile 2.00 (95% confidence interval (CI) 1.13-3.56). In subjects with follow up times greater than the median of 4.2 years however, plasma folate concentrations were strongly positively related to CRC risk; multivariate odds ratio for highest versus lowest quintile 3.87 (95% CI 1.52-9.87; p trend = 0.007). Homocysteine was not associated with CRC risk. Multivariate odds ratios for the MTHFR polymorphisms were, for 677 TT versus CC, 0.41 (95% CI 0.19-0.85; p trend = 0.062), and for 1298 CC versus AA, 1.62 (95% CI 0.94-2.81; p trend = 0.028). Interaction analysis suggested that the result for 1298A>C may have been largely due to linkage disequilibrium with 677C>T. The reduced CRC risk in 677 TT homozygotes was independent of plasma folate status.

    CONCLUSIONS: Our findings suggest a decreased CRC risk in subjects with low folate status. This possibility of a detrimental component to the role of folate in carcinogenesis could have implications in the ongoing debate in Europe concerning mandatory folate fortification of foods.

  • 16. Wouters, Mira M.
    et al.
    Lambrechts, Diether
    Knapp, Michael
    Cleynen, Isabelle
    Whorwell, Peter
    Agreus, Lars
    Dlugosz, Aldona
    Schmidt, Peter Thelin
    Halfvarson, Jonas
    Simren, Magnus
    Ohlsson, Bodil
    Karling, Pontus
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Medicine.
    Van Wanrooy, Sander
    Mondelaers, Stephanie
    Vermeire, Severine
    Lindberg, Greger
    Spiller, Robin
    Dukes, George
    D'Amato, Mauro
    Boeckxstaens, Guy
    Genetic variants in CDC42 and NXPH1 as susceptibility factors for constipation and diarrhoea predominant irritable bowel syndrome2014In: Gut, ISSN 0017-5749, E-ISSN 1468-3288, Vol. 63, no 7, p. 1103-1111Article in journal (Refereed)
    Abstract [en]

    Objective The complex genetic aetiology underlying irritable bowel syndrome (IBS) needs to be assessed in large-scale genetic studies. Two independent IBS cohorts were genotyped to assess whether genetic variability in immune, neuronal and barrier integrity genes is associated with IBS. Design 384 single nucleotide polymorphisms (SNPs) covering 270 genes were genotyped in an exploratory cohort (935 IBS patients, 639 controls). 33 SNPs with P-uncorrected<0.05 were validated in an independent set of 497 patients and 887 controls. Genotype distributions of single SNPs were assessed using an additive genetic model in IBS and clinical subtypes, IBS-C and IBS-D, both in individual and combined cohorts. Trait anxiety (N=614 patients, 533 controls), lifetime depression (N=654 patients, 533 controls) and mRNA expression in rectal biopsies (N=22 patients, 29 controls) were correlated with SNP genotypes. Results Two SNPs associated independently in the exploratory and validation cohort: rs17837965-CDC42 with IBS-C (ORexploratory=1.59 (1.05 to 1.76); ORvalidation=1.76 (1.03 to 3.01)) and rs2349775-NXPH1 with IBS-D (ORexploratory=1.28 (1.06 to 1.56); ORvalidation=1.42 (1.08 to 1.88)). When combining both cohorts, the association of rs2349775 withstood post hoc correction for multiple testing in the IBS-D subgroup. Additionally, three SNPs in immune-related genes (rs1464510-LPP, rs1881457-IL13, rs2104286-IL2RA), one SNP in a neuronal gene (rs2349775-NXPH1) and two SNPs in epithelial genes (rs245051-SLC26A2, rs17837965-CDC42) were weakly associated with total-IBS (P-uncorrected<0.05). At the functional level, rs1881457 increased IL13 mRNA levels, whereas anxiety and depression scores did not correlate with rs2349775-NXPH1. Conclusions Rs2349775 (NXPH1) and rs17837965 (CDC42) were associated with IBS-D and IBS-C, respectively, in two independent cohorts. Further studies are warranted to validate our findings and to determine the mechanisms underlying IBS pathophysiology.

  • 17. Wu, Chen
    et al.
    Kraft, Peter
    Stolzenberg-Solomon, Rachael
    Steplowski, Emily
    Brotzman, Michelle
    Xu, Mousheng
    Mudgal, Poorva
    Amundadottir, Laufey
    Arslan, Alan A
    Bueno-de-Mesquita, H Bas
    Gross, Myron
    Helzlsouer, Kathy
    Jacobs, Eric J
    Kooperberg, Charles
    Petersen, Gloria M
    Zheng, Wei
    Albanes, Demetrius
    Boutron-Ruault, Marie-Christine
    Buring, Julie E
    Canzian, Federico
    Cao, Guangwen
    Duell, Eric J
    Elena, Joanne W
    Gaziano, J Michael
    Giovannucci, Edward L
    Hallmans, Göran
    Umeå University, Faculty of Medicine, Department of Biobank Research. Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Nutritional Research.
    Hutchinson, Amy
    Hunter, David J
    Jenab, Mazda
    Jiang, Guoliang
    Khaw, Kay-Tee
    Lacroix, Andrea
    Li, Zhaoshen
    Mendelsohn, Julie B
    Panico, Salvatore
    Patel, Alpa V
    Qian, Zhi Rong
    Riboli, Elio
    Sesso, Howard
    Shen, Hongbing
    Shu, Xiao-Ou
    Tjonneland, Anne
    Tobias, Geoffrey S
    Trichopoulos, Dimitrios
    Virtamo, Jarmo
    Visvanathan, Kala
    Wactawski-Wende, Jean
    Wang, Chengfeng
    Yu, Kai
    Zeleniuch-Jacquotte, Anne
    Chanock, Stephen
    Hoover, Robert
    Hartge, Patricia
    Fuchs, Charles S
    Lin, Dongxin
    Wolpin, Brian M
    Genome-wide association study of survival in patients with pancreatic adenocarcinoma2014In: Gut, ISSN 0017-5749, E-ISSN 1468-3288, Vol. 63, no 1, p. 152-160Article in journal (Refereed)
    Abstract [en]

    BACKGROUND AND OBJECTIVE: Survival of patients with pancreatic adenocarcinoma is limited and few prognostic factors are known. We conducted a two-stage genome-wide association study (GWAS) to identify germline variants associated with survival in patients with pancreatic adenocarcinoma. METHODS: We analysed overall survival in relation to single nucleotide polymorphisms (SNPs) among 1005 patients from two large GWAS datasets, PanScan I and ChinaPC. Cox proportional hazards regression was used in an additive genetic model with adjustment for age, sex, clinical stage and the top four principal components of population stratification. The first stage included 642 cases of European ancestry (PanScan), from which the top SNPs (p≤10(-5)) were advanced to a joint analysis with 363 additional patients from China (ChinaPC). RESULTS: In the first stage of cases of European descent, the top-ranked loci were at chromosomes 11p15.4, 18p11.21 and 1p36.13, tagged by rs12362504 (p=1.63×10(-7)), rs981621 (p=1.65×10(-7)) and rs16861827 (p=3.75×10(-7)), respectively. 131 SNPs with p≤10(-5) were advanced to a joint analysis with cases from the ChinaPC study. In the joint analysis, the top-ranked SNP was rs10500715 (minor allele frequency, 0.37; p=1.72×10(-7)) on chromosome 11p15.4, which is intronic to the SET binding factor 2 (SBF2) gene. The HR (95% CI) for death was 0.74 (0.66 to 0.84) in PanScan I, 0.79 (0.65 to 0.97) in ChinaPC and 0.76 (0.68 to 0.84) in the joint analysis. CONCLUSIONS: Germline genetic variation in the SBF2 locus was associated with overall survival in patients with pancreatic adenocarcinoma of European and Asian ancestry. This association should be investigated in additional large patient cohorts.

  • 18. Yeung, M M
    et al.
    Melgar, S
    Baranov, Vladimir
    Umeå University, Faculty of Medicine, Department of Clinical Microbiology, Clinical Immunology.
    Oberg, A
    Danielsson, A
    Hammarström, Sten
    Umeå University, Faculty of Medicine, Department of Clinical Microbiology, Immunology/Immunchemistry.
    Hammarström, Marie-Louise
    Umeå University, Faculty of Medicine, Department of Clinical Microbiology, Immunology/Immunchemistry.
    Characterisation of mucosal lymphoid aggregates in ulcerative colitis: immune cell phenotype and TcR-gammadelta expression.2000In: Gut, ISSN 0017-5749, E-ISSN 1468-3288, Vol. 47, no 2, p. 215-27Article in journal (Refereed)
    Abstract [en]

    BACKGROUND AND AIMS: A histopathological feature considered indicative of ulcerative colitis (UC) is the so-called basal lymphoid aggregates. Their relevance in the pathogenesis of UC is, however, unknown. We have performed a comprehensive analysis of the immune cells in these aggregates most likely corresponding to the lymphoid follicular hyperplasia also described in other colitides.

    METHODS: Resection specimens of UC and normal colon were analysed by immunomorphometry, immunoflow cytometry, and immunoelectron microscopy, using a large panel of monoclonal antibodies.

    RESULTS: (1) In all cases of UC, colonic lamina propria contained numerous basal aggregates composed of lymphocytes, follicular dendritic cells, and CD80/B7.1 positive dendritic cells. (2) CD4(+)CD28(-) alphabeta T cells and B cells were the dominant cell types in the aggregates. (3) The aggregates contained a large fraction of cells that are normally associated with the epithelium: that is, gammadelta T cells (11 (7)%) and alpha(E)beta(7)(+) cells (26 (13)%). The gammadelta T cells used Vdelta1 and were CD4(-)CD8(-). Immunoelectron microscopy analysis demonstrated TcR-gammadelta internalisation and surface downregulation, indicating that the gammadelta T cells were activated and engaged in the disease process. (4) One third of cells in the aggregates expressed the antiapoptotic protein bcl-2.

    CONCLUSIONS: Basal lymphoid aggregates in UC colon are a consequence of anomalous lymphoid follicular hyperplasia, characterised by abnormal follicular architecture and unusual cell immunophenotypes. The aggregates increase in size with severity of disease, and contain large numbers of apoptosis resistant cells and activated mucosal gammadelta T cells. The latter probably colonise the aggregates as an immunoregulatory response to stressed lymphocytes or as a substitute for defective T helper cells in B cell activation. gammadelta T cells in the aggregates may be characteristic of UC.

  • 19. Yeung, M-W
    et al.
    Melgar, S
    Baranov, Vladimir
    Umeå University, Faculty of Medicine, Department of Clinical Microbiology, Immunology/Immunchemistry.
    Öberg, Å
    Danielsson, Å
    Hammarström, Sten
    Umeå University, Faculty of Medicine, Department of Clinical Microbiology, Immunology/Immunchemistry.
    Hammarström, Marie-Louise
    Umeå University, Faculty of Medicine, Department of Clinical Microbiology, Immunology/Immunchemistry.
    Characterization of mucosal lymphoid aggregates in ulcerative colitis colon: Immune cell phenotypes and TcR-gammadelta expression.2000In: Gut, ISSN 0017-5749, E-ISSN 1468-3288, Vol. 47, p. 215-227Article in journal (Refereed)
  • 20. Zucchelli, Marco
    et al.
    Camilleri, Michael
    Nixon Andreasson, Anna
    Bresso, Francesca
    Dlugosz, Aldona
    Halfvarson, Jonas
    Törkvist, Leif
    Schmidt, Peter T
    Karling, Pontus
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Medicine.
    Ohlsson, Bodil
    Duerr, Richard H
    Simren, Magnus
    Lindberg, Greger
    Agreus, Lars
    Carlson, Paula
    Zinsmeister, Alan R
    D'Amato, Mauro
    Association of TNFSF15 polymorphism with irritable bowel syndrome2011In: Gut, ISSN 0017-5749, E-ISSN 1468-3288, Vol. 60, no 12, p. 1671-1677Article in journal (Refereed)
    Abstract [en]

    Background: Irritable bowel syndrome (IBS) is the most common gastrointestinal disorder, affecting more than 10% of the general population worldwide. Although a genetic component is suspected, unambiguous susceptibility genes have so far not been identified. This study tested the hypothesis that genes contributing to epithelial barrier integrity, control of mucosal immune responses and interactions with bacteria in the gut are associated with IBS.

    Methods: Single nucleotide polymorphisms (SNPs) corresponding to top signals of association with Crohn's disease at 30 known susceptibility loci were tested for their effect on IBS risk in 1992 individuals from two independent case–control cohorts from Sweden and the USA. Association tests included a conservative Bonferroni correction for multiple comparisons, and were also performed on specific subgroups of patients characterised by constipation (IBS-C), diarrhoea (IBS-D) or alternating constipation and diarrhoea (IBS-A).

    Results: The Crohn's disease risk allele rs4263839 G in the TNFSF15 gene was significantly associated with an increased risk of both IBS (p=2.2×10−5; OR 1.37) and more pronouncedly, IBS-C (p=8.7×10−7; OR 1.79) in the entire sample. Similar associations and risk effects of the same magnitude were observed in the two cohorts analysed separately. A correlation between rs4263839 genotype and TNFSF15 mRNA expression was detected both in peripheral blood and in rectal mucosal biopsies from healthy individuals (combined p=0.0033).

    Conclusions: TNFSF15 is a susceptibility gene for IBS and IBS constipation. As TL1A, the protein encoded by TNFSF15, contributes to the modulation of inflammatory responses, the results support a role of immune activation in IBS.

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