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Journal Cover Gut
  [SJR: 6.474]   [H-I: 222]   [181 followers]  Follow
   Full-text available via subscription Subscription journal
   ISSN (Print) 0017-5749 - ISSN (Online) 1468-3288
   Published by BMJ Publishing Group Homepage  [58 journals]
  • Global elimination of viral hepatitis and hepatocellular carcinoma:
           opportunities and challenges
    • Authors: Chen; C.-J.
      Pages: 595 - 598
      Abstract: Global disease burden of viral hepatitis and hepatocellular carcinoma The most common causes of hepatitis worldwide is a group of viruses known as hepatitis A, B, C, D and E virus. Most deaths from viral hepatitis are due to hepatitis B and hepatitis C. Globally, an estimated 257 million people were living with HBV and 71 million people were living with HCV, which caused 1.34 million deaths in 2015 comparable with deaths from tuberculosis and exceeding deaths from HIV.1 Both liver cancer, mostly hepatocellular carcinoma (HCC), and cirrhosis are end-stage clinical outcomes of chronic hepatitis B (CHB) and chronic hepatitis C (CHC).2 HBV and HCV are the main causes of liver cancer worldwide, and liver cancer was the seventh commonly diagnosed cancer and the second common cause of cancer death as reported in GLOBOCAN 2012.3 There was a significant increase in global deaths from liver...
      Keywords: Gut
      PubDate: 2018-03-08T07:15:46-08:00
      DOI: 10.1136/gutjnl-2017-315407
      Issue No: Vol. 67, No. 4 (2018)
  • Minimal access necrosectomy: the newest advance of many in the treatment
           of necrotising pancreatitis
    • Authors: Sarr M. G.
      Pages: 599 - 600
      Abstract: This study by van Brunschott and international colleagues1 has shown that when possible in high-risk patients with severe acute necrotising pancreatitis, a minimal access approach for drainage combined with a necrosectomy, either via an operative (ie, laparoscopic like) or an endoscopic transgastric or transduodenal approach, decreases mortality of this horrible disease when compared with the classic open operation (laparotomy). These data are convincing and support the use of such minimal access approaches whenever feasible. This study reviews the data on another huge advance in our treatment and understanding of this horrific disease. In this commentary, I want to use this study as an example of the marked changes in our thinking of pancreatitis over the last 40 years. Our current approach to the treatment of necrotising pancreatitis really had its origin in the 1970s with the introduction of the new concept of an operative ‘necrosectomy’ rather than...
      Keywords: Gut
      PubDate: 2018-03-08T07:15:46-08:00
      DOI: 10.1136/gutjnl-2017-314660
      Issue No: Vol. 67, No. 4 (2018)
  • Morphine worsens the severity and prevents pancreatic regeneration in
           mouse models of acute pancreatitis
    • Authors: Barlass, U; Dutta, R, Cheema, H, George, J, Sareen, A, Dixit, A, Yuan, Z, Giri, B, Meng, J, Banerjee, S, Banerjee, S, Dudeja, V, Dawra, R. K, Roy, S, Saluja, A. K.
      Pages: 600 - 602
      Abstract: BackgroundOpioids such as morphine are widely used for the management of pain associated with acute pancreatitis. Interestingly, opioids are also known to affect the immune system and modulate inflammatory pathways in non-pancreatic diseases. However, the impact of morphine on the progression of acute pancreatitis has never been evaluated. In the current study, we evaluated the impact of morphine on the progression and severity of acute pancreatitis.MethodsEffect of morphine treatment on acute pancreatitis in caerulein, L-arginine and ethanol–palmitoleic acid models was evaluated after induction of the disease. Inflammatory response, gut permeability and bacterial translocation were compared. Experiments were repeated in mu (µ) opioid receptor knockout mice (MORKO) and in wild-type mice in the presence of opioid receptor antagonist naltrexone to evaluate the role of µ-opioid receptors in morphine’s effect on acute pancreatitis. Effect of morphine treatment on pathways activated during pancreatic regeneration like sonic Hedgehog and activation of embryonic transcription factors like pdx-1 and ptf-1 were measured by immunofluorescence and quantitative PCR.ResultsHistological data show that treatment with morphine after induction of acute pancreatitis exacerbates the disease with increased pancreatic neutrophilic infiltration and necrosis in all three models of acute pancreatitis. Morphine also exacerbated acute pancreatitis-induced gut permeabilisation and bacteraemia. These effects were antagonised in the MORKO mice or in the presence of naltrexone suggesting that morphine’s effect on severity of acute pancreatitis are mediated through the µ-opioid receptors. Morphine treatment delayed macrophage infiltration, sonic Hedgehog pathway activation and expression of pdx-1 and ptf-1.ConclusionMorphine treatment worsens the severity of acute pancreatitis and delays resolution and regeneration. Considering our results, the safety of morphine for analgesia during acute pancreatitis should be re-evaluated in future human studies.
      Keywords: Gut
      PubDate: 2018-03-08T07:15:46-08:00
      DOI: 10.1136/gutjnl-2017-313717
      Issue No: Vol. 67, No. 4 (2018)
  • High on drugs: lessons from opiates in pancreatitis
    • Authors: Singh V. P.
      Pages: 600 - 602
      Abstract: The current opiate epidemic, the widespread clinical utilisation of opiates, along with the controversies that revolve around their use, mandate that we take a fresh look at the risks and benefits of this invaluable yet potentially hazardous class of drugs. Pancreatitis is a common illness in which opiates are used extensively for pain control. With the well-known overlap between the complications of acute pancreatitis and opiate use, that is, ileus and bacterial translocation, and the difficulty in identifying the underlying causality in a clinical scenario, it is appropriate that this dilemma be approached using animal models. Additionally, the recent paradigm1 that chronic pancreatitis (for which opioids may be used for long periods) evolves from recurrent acute attacks reinforces the need to weigh the risks this usage may create apart from opiate abuse. In the study entitled ‘Morphine worsens the severity and prevents pancreatic regeneration in mouse models...
      Keywords: Gut
      PubDate: 2018-03-08T07:15:46-08:00
      DOI: 10.1136/gutjnl-2017-314506
      Issue No: Vol. 67, No. 4 (2018)
  • Deciphering the biology of IgG4-related disease: specific antigens and
    • Authors: Haldar, D; Hirschfield, G. M.
      Pages: 602 - 605
      Abstract: Immunoglobulin G4-related disease (IgG4-RD) is the name applied to a corticosteroid and/or B-cell depletion responsive illness, in which patients present with the consequences of usually multiorgan, relapsing and remitting, fibroinflammation.1 The disease is histologically characterised by obliterative phlebitis, storiform fibrosis and a dense lymphoplasmacytic infiltrate.2 IgG4-RD is not a new disease, but is benefiting from the application of new technologies in the pursuit of better biological understanding. The histologic enrichment of IgG4-expressing plasma cells is a diagnostic hallmark of disease that additionally serves as a biological phenomenon driving scientific evaluation.3 Key disease themes have evolved to include a large clonal expansion of activated plasmablasts and CD4+ cytotoxic, inflammatory and profibrotic lymphocytes. Therapeutically, a reduced frequency of CD4+ cytotoxic lymphocytes are seen after B-cell depletion; such therapy may consequently impact on antigen presentation.4–6 To date, the activity of IgG4-RD is not readily tracked...
      Keywords: Open access, Gut
      PubDate: 2018-03-08T07:15:46-08:00
      DOI: 10.1136/gutjnl-2017-314861
      Issue No: Vol. 67, No. 4 (2018)
  • Aspirin prevents NF-{kappa}B activation and CDX2 expression stimulated by
           acid and bile salts in oesophageal squamous cells of patients with
           Barrett's oesophagus
    • Authors: Huo, X; Zhang, X, Yu, C, Cheng, E, Zhang, Q, Dunbar, K. B, Pham, T. H, Lynch, J. P, Wang, D. H, Bresalier, R. S, Spechler, S. J, Souza, R. F.
      Pages: 606 - 615
      Abstract: ObjectiveIn previous studies using oesophageal squamous cells from patients with Barrett's oesophagus (normal oesophageal squamous (NES)-B cells) and from patients without Barrett's oesophagus (NES-G cells), we showed that acid and bile salts induced caudal-related homeobox transcription factor 2 (CDX2) expression only in NES-B cells. CDX2, a transcription factor required to form intestinal epithelium, is a target of nuclear factor kappa-light-chain-enhancer of activated B cells (NF-B) signalling, which can be inhibited by aspirin. We explored mechanisms underlying differences between NES-B and NES-G cells in CDX2 expression and effects of aspirin on that CDX2 expression.DesignWe exposed NES-B and NES-G cells to acid and bile salts, with and without aspirin, and evaluated effects on IB-NF-B-PKAc complex activation, p65 NF-B subunit function, and CDX2 expression.ResultsIn both NES-B and NES-G cells, acid and bile salts activated nicotinamide adenine dinucleotide phosphate oxidase to generate H2O2, which activated the IB-NF-B-PKAc complex. NES-B cells exhibited higher levels of phosphorylated IB and p65 and greater NF-B transcriptional activity than NES-G cells, indicating greater IB-NF-B-PKAc complex activation by acid and bile salts in NES-B cells, and p65 siRNA prevented their increased expression of CDX2. Aspirin blocked IB phosphorylation, p65 nuclear translocation, CDX2 promoter activation and CDX2 expression induced by acid and bile salts in NES-B cells.ConclusionsDifferences between NES-B and NES-G cells in NF-B activation by acid and bile salts can account for their differences in CDX2 expression, and their CDX2 expression can be blocked by aspirin. These findings might explain why some patients with GORD develop Barrett's oesophagus while others do not, and why aspirin might protect against development of Barrett's oesophagus.
      PubDate: 2018-03-08T07:15:46-08:00
      DOI: 10.1136/gutjnl-2016-313584
      Issue No: Vol. 67, No. 4 (2018)
  • Are random biopsies still useful for the detection of neoplasia in
           patients with IBD undergoing surveillance colonoscopy with
    • Authors: Moussata; D., Allez, M., Cazals-Hatem, D., Treton, X., Laharie, D., Reimund, J.-M., Bertheau, P., Bourreille, A., Lavergne-Slove, A., Brixi, H., Branche, J., Gornet, J.-M., Stefanescu, C., Moreau, J., Marteau, P., Pelletier, A.-L., Carbonnel, F., Seksik, P., Simon, M., Flejou, J.-F., Colombel, J.-F., Charlois, A.-L., Roblin, X., Nancey, S., Bouhnik, Y., Berger, F., Flourie, B., the GETAID
      Pages: 616 - 624
      Abstract: BackgroundColonoscopy with pan-chromoendoscopy (CE) is superior to standard colonoscopy in detecting neoplasia in patients with IBD. Performing random biopsies in unsuspicious mucosa after CE remains controversial.MethodsConsecutive patients with IBD who underwent surveillance colonoscopy using CE were prospectively included. The standardised procedure used CE, performed targeted biopsies or endoscopic resection on suspicious lesions and then quadrant random biopsies every 10 cm. A panel of five expert pathologists reviewed histological slides with dysplasia. Logistic regression model was used to evidence the factors associated with neoplasia in any or in random biopsies.Results1000 colonoscopes were performed in 1000 patients (495 UC, 505 Crohn's colitis). In 82 patients, neoplasia was detected from targeted biopsies or removed lesions, and among them dysplasia was detected also by random biopsies in 7 patients. Importantly, in 12 additional patients dysplasia was only detected by random biopsies. Overall, 140 neoplastic sites were found in 94 patients, 112 (80%) from targeted biopsies or removed lesions and 28 (20%) by random biopsies. The yield of neoplasia by random biopsies only was 0.2% per-biopsy (68/31 865), 1.2% per-colonoscopy (12/1000) but 12.8% per-patient with neoplasia (12/94). Dysplasia detected by random biopsies was associated with a personal history of neoplasia, a tubular appearing colon and the presence of primary sclerosing cholangitis (PSC).ConclusionsDespite their low yield, random biopsies should be performed in association with CE in patients with IBD with a personal history of neoplasia, concomitant PSC or a tubular colon during colonoscopy.Trial registration numberIRB 001508, Paris 7 University.
      PubDate: 2018-03-08T07:15:46-08:00
      DOI: 10.1136/gutjnl-2016-311892
      Issue No: Vol. 67, No. 4 (2018)
  • The microbiome of professional athletes differs from that of more
           sedentary subjects in composition and particularly at the functional
           metabolic level
    • Authors: Barton, W; Penney, N. C, Cronin, O, Garcia-Perez, I, Molloy, M. G, Holmes, E, Shanahan, F, Cotter, P. D, O'Sullivan, O.
      Pages: 625 - 633
      Abstract: ObjectiveIt is evident that the gut microbiota and factors that influence its composition and activity effect human metabolic, immunological and developmental processes. We previously reported that extreme physical activity with associated dietary adaptations, such as that pursued by professional athletes, is associated with changes in faecal microbial diversity and composition relative to that of individuals with a more sedentary lifestyle. Here we address the impact of these factors on the functionality/metabolic activity of the microbiota which reveals even greater separation between exercise and a more sedentary state.DesignMetabolic phenotyping and functional metagenomic analysis of the gut microbiome of professional international rugby union players (n=40) and controls (n=46) was carried out and results were correlated with lifestyle parameters and clinical measurements (eg, dietary habit and serum creatine kinase, respectively).ResultsAthletes had relative increases in pathways (eg, amino acid and antibiotic biosynthesis and carbohydrate metabolism) and faecal metabolites (eg, microbial produced short-chain fatty acids (SCFAs) acetate, propionate and butyrate) associated with enhanced muscle turnover (fitness) and overall health when compared with control groups.ConclusionsDifferences in faecal microbiota between athletes and sedentary controls show even greater separation at the metagenomic and metabolomic than at compositional levels and provide added insight into the diet–exercise–gut microbiota paradigm.
      PubDate: 2018-03-08T07:15:46-08:00
      DOI: 10.1136/gutjnl-2016-313627
      Issue No: Vol. 67, No. 4 (2018)
  • Bacteriophage transfer during faecal microbiota transplantation in
           Clostridium difficile infection is associated with treatment outcome
    • Authors: Zuo, T; Wong, S. H, Lam, K, Lui, R, Cheung, K, Tang, W, Ching, J. Y. L, Chan, P. K. S, Chan, M. C. W, Wu, J. C. Y, Chan, F. K. L, Yu, J, Sung, J. J. Y, Ng, S. C.
      Pages: 634 - 643
      Abstract: ObjectiveFaecal microbiota transplantation (FMT) is effective for the treatment of recurrent Clostridium difficile infection (CDI). Studies have shown bacterial colonisation after FMT, but data on viral alterations in CDI are scarce. We investigated enteric virome alterations in CDI and the association between viral transfer and clinical outcome in patients with CDI.DesignUltra-deep metagenomic sequencing of virus-like particle preparations and bacterial 16S rRNA sequencing were performed on stool samples from 24 subjects with CDI and 20 healthy controls. We longitudinally assessed the virome and bacterial microbiome changes in nine CDI subjects treated with FMT and five treated with vancomycin. Enteric virome alterations were assessed in association with treatment response.ResultsSubjects with CDI demonstrated a significantly higher abundance of bacteriophage Caudovirales and a lower Caudovirales diversity, richness and evenness compared with healthy household controls. Significant correlations were observed between bacterial families Proteobacteria, Actinobacteria and Caudovirales taxa in CDI. FMT treatment resulted in a significant decrease in the abundance of Caudovirales in CDI. Cure after FMT was observed when donor-derived Caudovirales contigs occupied a larger fraction of the enteric virome in the recipients (p=0.024). In treatment responders, FMT was associated with alterations in the virome and the bacterial microbiome, while vancomycin treatment led to alterations in the bacterial community alone.ConclusionsIn a preliminary study, CDI is characterised by enteric virome dysbiosis. Treatment response in FMT was associated with a high colonisation level of donor-derived Caudovirales taxa in the recipient. Caudovirales bacteriophages may play a role in the efficacy of FMT in CDI.Trial registration numberNCT02570477
      Keywords: Open access, Editor's choice
      PubDate: 2018-03-08T07:15:46-08:00
      DOI: 10.1136/gutjnl-2017-313952
      Issue No: Vol. 67, No. 4 (2018)
  • T-cell repertoires in refractory coeliac disease
    • Authors: Ritter, J; Zimmermann, K, Jöhrens, K, Mende, S, Seegebarth, A, Siegmund, B, Hennig, S, Todorova, K, Rosenwald, A, Daum, S, Hummel, M, Schumann, M.
      Pages: 644 - 653
      Abstract: ObjectiveRefractory coeliac disease (RCD) is a potentially hazardous complication of coeliac disease (CD). In contrast to RCD type I, RCD type II is a precursor entity of enteropathy-associated T-cell lymphoma (EATL), which is associated with clonally expanding T-cells that are also found in the sequentially developing EATL. Using high-throughput sequencing (HTS), we aimed to establish the small-intestinal T-cell repertoire (TCR) in CD and RCD to unravel the role of distinct T-cell clonotypes in RCD pathogenesis.DesignDNA extracted from duodenal mucosa specimens of controls (n=9), active coeliacs (n=10), coeliacs on a gluten-free diet (n=9), RCD type I (n=8), RCD type II (n=8) and unclassified Marsh I cases (n=3) collected from 2002 to 2013 was examined by TCRβ-complementarity-determining regions 3 (CDR3) multiplex PCR followed by HTS of the amplicons.ResultsOn average, 106 sequence reads per sample were generated consisting of up to 900 individual TCRβ rearrangements. In RCD type II, the most frequent clonotypes (ie, sequence reads with identical CDR3) represent in average 42.6% of all TCRβ rearrangements, which was significantly higher than in controls (6.8%; p
      Keywords: Open access
      PubDate: 2018-03-08T07:15:46-08:00
      DOI: 10.1136/gutjnl-2016-311816
      Issue No: Vol. 67, No. 4 (2018)
  • Acute lower GI bleeding in the UK: patient characteristics, interventions
           and outcomes in the first nationwide audit
    • Authors: Oakland, K; Guy, R, Uberoi, R, Hogg, R, Mortensen, N, Murphy, M. F, Jairath, V, on behalf of the UK Lower GI Bleeding Collaborative
      Pages: 654 - 662
      Abstract: ObjectiveLower GI bleeding (LGIB) is a common reason for emergency hospital admission, although there is paucity of data on presentations, interventions and outcomes. In this nationwide UK audit, we describe patient characteristics, interventions including endoscopy, radiology and surgery as well as clinical outcomes.DesignMulticentre audit of adults presenting with LGIB to UK hospitals over 2 months in 2015. Consecutive cases were prospectively enrolled by clinical teams and followed for 28 days.ResultsData on 2528 cases of LGIB were provided by 143 hospitals. Most were elderly (median age 74 years) with major comorbidities, 29.4% taking antiplatelets and 15.9% anticoagulants. Shock was uncommon (58/2528, 2.3%), but 666 (26.3%) received a red cell transfusion. Flexible sigmoidoscopy was the most common investigation (21.5%) but only 2.1% received endoscopic haemostasis. Use of embolisation or surgery was rare, used in 19 (0.8%) and 6 (0.2%) cases, respectively. 48% patients underwent no inpatient investigations. The most common diagnoses were diverticular bleeding (26.4%) and benign anorectal conditions (16.7%). Median length of stay was 3 days, 13.6% patients rebled during admission and 4.4% were readmitted with bleeding within 28 days. In-hospital mortality was 85/2528 (3.4%) and was highest in established inpatients (17.8%, p
      PubDate: 2018-03-08T07:15:46-08:00
      DOI: 10.1136/gutjnl-2016-313428
      Issue No: Vol. 67, No. 4 (2018)
  • MED12 is recurrently mutated in Middle Eastern colorectal cancer
    • Authors: Siraj, A. K; Masoodi, T, Bu, R, Pratheeshkumar, P, Al-Sanea, N, Ashari, L. H, Abduljabbar, A, Alhomoud, S, Al-Dayel, F, Alkuraya, F. S, Al-Kuraya, K. S.
      Pages: 663 - 671
      Abstract: ObjectiveColorectal cancer (CRC) is a common cancer and a leading cause of cancer deaths. Previous studies have identified a number of key steps in the evolution of CRC but our knowledge of driver mutations in CRC remains incomplete. Recognising the potential of studying different human populations to reveal novel insights in disease pathogenesis, we conducted genomic analysis of CRC in Saudi patients.DesignIn the discovery phase of the study, we conducted whole genome sequencing of tumour and corresponding germline DNA in 27 patients with CRC. In addition to known driver mutations, we identified three MED12 somatic mutations. In the replication phase, we employed a next-generation sequencing approach to capture and sequence MED12 and other candidate genes in a larger sample of 400 patients with CRC and confirmed the enrichment for recurrent MED12 mutations.ResultsIn order to gain insight into a plausible biological mechanism for the potential role of MED12 mutations in CRC, we studied CRC cell lines that differ substantially in the expression level of MED12, and found the latter to be correlated inversely with transforming growth factor (TGF)-β signalling and directly with apoptosis in response to chemotherapeutic agents. Importantly, these correlations were replicated when MED12 expression was experimentally manipulated.ConclusionsOur data expand the recently described role of MED12 as a tumour suppressor in other cancers to include CRC, and suggest TGF-β signalling as a potential mediator of this effect.
      Keywords: Open access
      PubDate: 2018-03-08T07:15:46-08:00
      DOI: 10.1136/gutjnl-2016-313334
      Issue No: Vol. 67, No. 4 (2018)
  • Long-term use of antibiotics and risk of colorectal adenoma
    • Authors: Cao, Y; Wu, K, Mehta, R, Drew, D. A, Song, M, Lochhead, P, Nguyen, L. H, Izard, J, Fuchs, C. S, Garrett, W. S, Huttenhower, C, Ogino, S, Giovannucci, E. L, Chan, A. T.
      Pages: 672 - 678
      Abstract: ObjectiveRecent evidence suggests that antibiotic use, which alters the gut microbiome, is associated with an increased risk of colorectal cancer. However, the association between antibiotic use and risk of colorectal adenoma, the precursor for the majority of colorectal cancers, has not been investigated.DesignWe prospectively evaluated the association between antibiotic use at age 20–39 and 40–59 (assessed in 2004) and recent antibiotic use (assessed in 2008) with risk of subsequent colorectal adenoma among 16 642 women aged ≥60 enrolled in the Nurses' Health Study who underwent at least one colonoscopy through 2010. We used multivariate logistic regression to calculate ORs and 95% CIs.ResultsWe documented 1195 cases of adenoma. Increasing duration of antibiotic use at age 20–39 (ptrend=0.002) and 40–59 (ptrend=0.001) was significantly associated with an increased risk of colorectal adenoma. Compared with non-users, women who used antibiotics for ≥2 months between age 20 and 39 had a multivariable OR of 1.36 (95% CI 1.03 to 1.79). Women who used ≥2 months of antibiotics between age 40 and 59 had a multivariable OR of 1.69 (95% CI 1.24 to 2.31). The associations were similar for low-risk versus high-risk adenomas (size ≥1 cm, or with tubulovillous/villous histology, or ≥3 detected lesions), but appeared modestly stronger for proximal compared with distal adenomas. In contrast, recent antibiotic use within the past four years was not associated with risk of adenoma (ptrend=0.44).ConclusionsLong-term antibiotic use in early-to-middle adulthood was associated with increased risk of colorectal adenoma.
      Keywords: Press releases
      PubDate: 2018-03-08T07:15:46-08:00
      DOI: 10.1136/gutjnl-2016-313413
      Issue No: Vol. 67, No. 4 (2018)
  • Socioeconomic and ethnic inequities within organised colorectal cancer
           screening programmes worldwide
    • Authors: de Klerk, C; Gupta, S, Dekker, E, Essink-Bot, M, on behalf of the Expert Working Group 'Coalition to reduce inequities in colorectal cancer screening of the World Endoscopy Organization
      Pages: 679 - 687
      Abstract: ObjectiveColorectal cancer (CRC) screening programmes can reduce CRC mortality. However, the implementation of a screening programme may create or exacerbate socioeconomic and ethnic health inequities if participation varies by subgroup. We determined which organised programmes characterise participation inequities by socioeconomic and ethnic subgroups, and assessed the variation in subgroup participation among programmes collecting group-specific data.DesignEmploying a literature review and survey among leaders of national or regional screening programmes, this study identified published and unpublished data on participation by socioeconomic status and ethnicity. We assessed programmes offering faecal occult blood tests (FOBT) for screening. Primary outcome was screening participation rate.ResultsAcross 24 organised FOBT-screening programmes meeting the inclusion criteria, participation rates ranged from 21% to 73%. Most programmes (13/24, 54%) did not collect data on participation by socioeconomic status and ethnicity. Among the 11 programmes with data on participation by socioeconomic status, 90% (28/31 publications) reported lower participation among lower socioeconomic groups. Differences across socioeconomic gradients were moderate (66% vs 71%) to severe (35% vs 61%). Only six programmes reported participation results by ethnicity. Ethnic differences were moderate, though only limited data were available for evaluation.ConclusionsAcross organised CRC screening programmes worldwide, variation in participation by socioeconomic status and ethnicity is often not assessed. However, when measured, marked disparities in participation by socioeconomic status have been observed. Limited data were available to assess inequities by ethnicity. To avoid exacerbating health inequities, screening programmes should systematically monitor participation by socioeconomic status and ethnicity, and investigate and address determinants of low participation.
      PubDate: 2018-03-08T07:15:46-08:00
      DOI: 10.1136/gutjnl-2016-313311
      Issue No: Vol. 67, No. 4 (2018)
  • Development and external validation of a nomogram and online tool to
           predict bowel dysfunction following restorative rectal cancer resection:
           the POLARS score
    • Authors: Battersby; N. J., Bouliotis, G., Emmertsen, K. J., Juul, T., Glynne-Jones, R., Branagan, G., Christensen, P., Laurberg, S., Moran, B. J., on behalf of the UK Danish LARS Study Groups, Khan*, Kurasz, Waldron, Janjau, Shahir, Chan, Hughes*, Kelly, Evans, Smith, Heath, Leinhardt*, Norton, Jayne*, Moriarty, Laing, Mawdsley*, Bourner, Narula*, Ward, Lacy-Colson*, Moore, Potts, Bell, Chave, Carter, Mirza*, Pereira, Williams, Last*, Todd, Woodcock*
      Pages: 688 - 696
      Abstract: ObjectiveBowel dysfunction is common following a restorative rectal cancer resection, but symptom severity and the degree of quality of life impairment is highly variable. An internationally validated patient-reported outcome measure, Low Anterior Resection Syndrome (LARS) score, now enables these symptoms to be measured. The study purpose was: (1) to develop a model that predicts postoperative bowel function; (2) externally validate the model and (3) incorporate these findings into a nomogram and online tool in order to individualise patient counselling and aid preoperative consent.DesignPatients more than 1 year after curative restorative anterior resection (UK, median 54 months; Denmark (DK), 56 months since surgery) were invited to complete The European Organisation for Research and Treatment of Cancer Quality of Life Questionnaire - Core 30 version3 (EORTC QLQ-C30 v3), LARS and Wexner incontinence scores. Demographics, tumour characteristics, preoperative/postoperative treatment and surgical procedures were recorded. Using transparent reporting of a multivariable prediction model for individual prognosis or diagnosis (TRIPOD) guidelines, risk factors for bowel dysfunction were independently assessed by advanced linear regression shrinkage techniques for each dataset (UK:DK).ResultsPatients in the development (UK, n=463) and validation (DK, n=938) datasets reported mean (SD) LARS scores of 26 (11) and 24 (11), respectively. Key predictive factors for LARS were: age (at surgery); tumour height, total versus partial mesorectal excision, stoma and preoperative radiotherapy, with satisfactory model calibration and a Mallow's Cp of 7.5 and 5.5, respectively.ConclusionsThe Pre-Operative LARS score (POLARS) is the first nomogram and online tool to predict bowel dysfunction severity prior to anterior resection. Colorectal surgeons, gastroenterologist and nurse specialists may use POLARS to help patients understand their risk of bowel dysfunction and to preoperatively highlight patients who may require additional postoperative support.
      PubDate: 2018-03-08T07:15:46-08:00
      DOI: 10.1136/gutjnl-2016-312695
      Issue No: Vol. 67, No. 4 (2018)
  • Minimally invasive and endoscopic versus open necrosectomy for necrotising
           pancreatitis: a pooled analysis of individual data for 1980 patients
    • Authors: van Brunschot, S; Hollemans, R. A, Bakker, O. J, Besselink, M. G, Baron, T. H, Beger, H. G, Boermeester, M. A, Bollen, T. L, Bruno, M. J, Carter, R, French, J. J, Coelho, D, Dahl, B, Dijkgraaf, M. G, Doctor, N, Fagenholz, P. J, Farkas, G, Castillo, C. F. d, Fockens, P, Freeman, M. L, Gardner, T. B, Goor, H. v, Gooszen, H. G, Hannink, G, Lochan, R, McKay, C. J, Neoptolemos, J. P, Olah, A, Parks, R. W, Peev, M. P, Raraty, M, Rau, B, Rösch, T, Rovers, M, Seifert, H, Siriwardena, A. K, Horvath, K. D, van Santvoort, H. C.
      Pages: 697 - 706
      Abstract: ObjectiveMinimally invasive surgical necrosectomy and endoscopic necrosectomy, compared with open necrosectomy, might improve outcomes in necrotising pancreatitis, especially in critically ill patients. Evidence from large comparative studies is lacking.DesignWe combined original and newly collected data from 15 published and unpublished patient cohorts (51 hospitals; 8 countries) on pancreatic necrosectomy for necrotising pancreatitis. Death rates were compared in patients undergoing open necrosectomy versus minimally invasive surgical or endoscopic necrosectomy. To adjust for confounding and to study effect modification by clinical severity, we performed two types of analyses: logistic multivariable regression and propensity score matching with stratification according to predicted risk of death at baseline (low:
      Keywords: Surgery, Gut
      PubDate: 2018-03-08T07:15:46-08:00
      DOI: 10.1136/gutjnl-2016-313341
      Issue No: Vol. 67, No. 4 (2018)
  • c-Myc downregulation is required for preacinar to acinar maturation and
           pancreatic homeostasis
    • Authors: Sanchez-Arevalo Lobo, V. J; Fernandez, L. C, Carrillo-de-Santa-Pau, E, Richart, L, Cobo, I, Cendrowski, J, Moreno, U, del Pozo, N, Megias, D, Breant, B, Wright, C. V, Magnuson, M, Real, F. X.
      Pages: 707 - 718
      Abstract: Background and aimsc-Myc is highly expressed in pancreatic multipotent progenitor cells (MPC) and in pancreatic cancer. The transition from MPC to unipotent acinar progenitors is associated with c-Myc downregulation; a role for c-Myc in this process, and its possible relationship to a role in cancer, has not been established.DesignUsing coimmunoprecipitation assays, we demonstrate that c-Myc and Ptf1a interact. Using reverse transcriptase qPCR, western blot and immunofluorescence, we show the erosion of the acinar programme. To analyse the genomic distribution of c-Myc and Ptf1a and the global transcriptomic profile, we used ChIP-seq and RNA-seq, respectively; validation was performed with ChIP-qPCR and RT-qPCR. Lineage-tracing experiments were used to follow the effect of c-Myc overexpression in preacinar cells on acinar differentiation.Resultsc-Myc binds and represses the transcriptional activity of Ptf1a. c-Myc overexpression in preacinar cells leads to a massive erosion of differentiation. In adult Ela1-Myc mice: (1) c-Myc binds to Ptf1a, and Tcf3 is downregulated; (2) Ptf1a and c-Myc display partially overlapping chromatin occupancy but do not bind the same E-boxes; (3) at the proximal promoter of genes coding for digestive enzymes, we find reduced PTF1 binding and increased levels of repressive chromatin marks and PRC2 complex components. Lineage tracing of committed acinar precursors reveals that c-Myc overexpression does not restore multipotency but allows the persistence of a preacinar-like cell population. In addition, mutant KRas can lead to c-Myc overexpression and acinar dysregulation.Conclusionsc-Myc repression during development is crucial for the maturation of preacinar cells, and c-Myc overexpression can contribute to pancreatic carcinogenesis through the induction of a dedifferentiated state.
      PubDate: 2018-03-08T07:15:46-08:00
      DOI: 10.1136/gutjnl-2016-312306
      Issue No: Vol. 67, No. 4 (2018)
  • Annexin A11 is targeted by IgG4 and IgG1 autoantibodies in IgG4-related
    • Authors: Hubers, L. M; Vos, H, Schuurman, A. R, Erken, R, Oude Elferink, R. P, Burgering, B, van de Graaf, S. F. J, Beuers, U.
      Pages: 728 - 735
      Abstract: ObjectiveImmunoglobulin G4-related disease (IgG4-RD) is a multiorgan immune-mediated disease that predominantly affects the biliary tract (IgG4-associated cholangitis, IAC) and pancreas (autoimmune pancreatitis, AIP). We recently identified highly expanded IgG4+ B-cell receptor clones in blood and affected tissues of patients with IAC/AIP suggestive of specific (auto)antigenic stimuli involved in initiating and/or maintaining the inflammatory response. This study aimed to identify (auto)antigen(s) that are responsible for the clonal expansion of IgG4+ B cells in IgG4-RD.DesignWe screened sera of patients with IAC/AIP (n=50), in comparison to control sera of patients with primary sclerosing cholangitis (PSC) and pancreatobiliary malignancies (n=47), for reactivity against human H69 cholangiocyte lysates on immunoblot. Subsequently, target antigens were immunoprecipitated and analysed by mass spectrometry.ResultsProminent reactivity against a 56 kDa protein was detected in human H69 cholangiocyte lysates exposed to sera of nine patients with IAC/AIP. Affinity purification and mass spectrometry analysis identified annexin A11, a calcium-dependent phospholipid-binding protein. Annexin A11-specific IgG4 and IgG1 antibodies were only detected in serum of patients with IgG4-RD of the biliary tract/pancreas/salivary glands and not in disease mimickers with PSC and pancreatobiliary malignancies. Epitope analysis showed that two annexin A11 epitopes targeted by IgG1 and IgG4 autoantibodies were shared between patients with IAC/AIP and IgG4 antibodies blocked binding of IgG1 antibodies to the shared annexin A11 epitopes.ConclusionOur data suggest that IgG1-mediated pro-inflammatory autoreactivity against annexin A11 in patients with IgG4-RD may be attenuated by formation of annexin A11-specific IgG4 antibodies supporting an anti-inflammatory role of IgG4 in IgG4-RD.
      Keywords: Gut
      PubDate: 2018-03-08T07:15:46-08:00
      DOI: 10.1136/gutjnl-2017-314548
      Issue No: Vol. 67, No. 4 (2018)
  • Humanisation of a claudin-1-specific monoclonal antibody for clinical
           prevention and cure of HCV infection without escape
    • Authors: Colpitts, C. C; Tawar, R. G, Mailly, L, Thumann, C, Heydmann, L, Durand, S. C, Xiao, F, Robinet, E, Pessaux, P, Zeisel, M. B, Baumert, T. F.
      Pages: 736 - 745
      Abstract: ObjectiveHCV infection is a leading cause of chronic liver disease and a major indication for liver transplantation. Although direct-acting antivirals (DAAs) have much improved the treatment of chronic HCV infection, alternative strategies are needed for patients with treatment failure. As an essential HCV entry factor, the tight junction protein claudin-1 (CLDN1) is a promising antiviral target. However, genotype-dependent escape via CLDN6 and CLDN9 has been described in some cell lines as a possible limitation facing CLDN1-targeted therapies. Here, we evaluated the clinical potential of therapeutic strategies targeting CLDN1.DesignWe generated a humanised anti-CLDN1 monoclonal antibody (mAb) (H3L3) suitable for clinical development and characterised its anti-HCV activity using cell culture models, a large panel of primary human hepatocytes (PHH) from 12 different donors, and human liver chimeric mice.ResultsH3L3 pan-genotypically inhibited HCV pseudoparticle entry into PHH, irrespective of donor. Escape was likely precluded by low surface expression of CLDN6 and CLDN9 on PHH. Co-treatment of a panel of PHH with a CLDN6-specific mAb did not enhance the antiviral effect of H3L3, confirming that CLDN6 does not function as an entry factor in PHH from multiple donors. H3L3 also inhibited DAA-resistant strains of HCV and synergised with current DAAs. Finally, H3L3 cured persistent HCV infection in human-liver chimeric uPA-SCID mice in monotherapy.ConclusionsOverall, these findings underscore the clinical potential of CLDN1-targeted therapies and describe the functional characterisation of a humanised anti-CLDN1 antibody suitable for further clinical development to complement existing therapeutic strategies for HCV.
      Keywords: Open access
      PubDate: 2018-03-08T07:15:46-08:00
      DOI: 10.1136/gutjnl-2016-312577
      Issue No: Vol. 67, No. 4 (2018)
  • ERK activation and autophagy impairment are central mediators of
           irinotecan-induced steatohepatitis
    • Authors: Mahli, A; Saugspier, M, Koch, A, Sommer, J, Dietrich, P, Lee, S, Thasler, R, Schulze-Luehrmann, J, Luehrmann, A, Thasler, W. E, Müller, M, Bosserhoff, A, Hellerbrand, C.
      Pages: 746 - 756
      Abstract: ObjectivePreoperative chemotherapy with irinotecan is associated with the development of steatohepatitis, which increases the risk of perioperative morbidity and mortality for liver surgery. The molecular mechanisms of this chemotherapeutic complication are widely unknown.DesignMechanisms of irinotecan-induced steatohepatitis were studied in primary human hepatocytes in vitro, in mice treated with irinotecan and in liver specimens from irinotecan-treated compared with control patients.ResultsIrinotecan dose-dependently induced lipid accumulation and pro-inflammatory gene expression in hepatocytes. This was accompanied by an impairment of mitochondrial function with reduced expression of carnitine palmitoyltransferase I and an induction of acyl-coenzyme A oxidase-1 (ACOX1), oxidative stress and extracellular signal-regulated kinase (ERK) activation. ERK inhibition prevented irinotecan-induced pro-inflammatory gene expression but had only a slight effect on lipid accumulation. However, irinotecan also induced an impairment of the autophagic flux mediated by alkalisation of lysosomal pH. Re-acidification of lysosomal pH abolished irinotecan-induced autophagy impairment and lipid accumulation. Also in mice, irinotecan treatment induced hepatic ACOX1 expression, ERK phosphorylation and inflammation, as well as impairment of autophagy and significant steatosis. Furthermore, irinotecan-treated patients revealed higher hepatic ERK activity, expression of pro-inflammatory genes and markers indicative for a shift to peroxisomal fatty acid oxidation and an impaired autophagic flux. Pretreatment with the multityrosine kinase inhibitor sorafenib did not affect autophagy impairment and steatosis but significantly reduced ERK phosphorylation and inflammatory response in irinotecan-treated hepatocytes and murine livers.ConclusionsIrinotecan induces hepatic steatosis via autophagy impairment and inflammation via ERK activation. Sorafenib appears as a novel therapeutic option for the prevention and treatment of irinotecan-induced inflammation.
      PubDate: 2018-03-08T07:15:46-08:00
      DOI: 10.1136/gutjnl-2016-312485
      Issue No: Vol. 67, No. 4 (2018)
  • Tears of colonoscopy
    • Authors: McFarlane, M; Disney, B, Eaden, J.
      Pages: 756 - 756
      Abstract: Clinical presentation A 72-year-old woman was referred to the gastroenterology outpatient clinic reporting an 18-month history of loose and watery stools up to 10 times per day with nocturnal episodes. She also presented with urgency, occasional faecal incontinence, excessive bloating and flatulence. She had lost 14 kg in weight over the same period. There was no blood or mucus in her stools. Her symptoms began after she underwent an emergency appendicectomy for suspected appendicitis. The histology revealed a carcinoid tumour, but with clear resection margins and a subsequent CT scan showed no distal spread. She smoked 10 cigarettes per day and consumed 20 units of alcohol per week. There was no significant family history or history of foreign travel. On examination her abdomen was soft and non-tender and there were no palpable masses or organomegaly, rectal examination was unremarkable. Laboratory investigations including full blood count, renal and liver function...
      Keywords: GUT Snapshot
      PubDate: 2018-03-08T07:15:46-08:00
      DOI: 10.1136/gutjnl-2017-313846
      Issue No: Vol. 67, No. 4 (2018)
  • Genome-wide association study identifies HLA-DR variants conferring risk
           of HBV-related acute-on-chronic liver failure
    • Authors: Tan, W; Xia, J, Dan, Y, Li, M, Lin, S, Pan, X, Wang, H, Tang, Y, Liu, N, Tan, S, Liu, M, He, W, Zhang, W, Mao, Q, Wang, Y, Deng, G.
      Pages: 757 - 766
      Abstract: ObjectiveAcute-on-chronic liver failure (ACLF) is an extreme condition after severe acute exacerbation of chronic hepatitis B; however, the underlying genetic factors involved in its onset and progression are currently unclear.DesignWe carried out a genome-wide association study among 399 HBV-related ACLFs (cases) and 401 asymptomatic HBV carriers (AsCs, as controls) without antiviral treatment. The initial findings were replicated in four independent case–control sets (a total of 901 ACLFs and 1686 AsCs). The roles of risk variants on clinical traits of ACLF were also analysed.ResultsAmong 1300 ACLFs and 2087 AsCs, we identified rs3129859 at human leucocyte antigen (HLA) class II region (chromosome 6p21.32) associated with HBV-related ACLF (combined Pdominant=2.64x10–20, OR=1.83). Analysis identified HLA-DRB1*12:02 as the top susceptible HLA allele associated with ACLF (p=3.94x10–6, OR=2.05). The association of rs3129859 was robust in ACLF subgroups (ACLFs with liver cirrhosis, p=1.36x10–16; ACLFs without liver cirrhosis, p=1.52x10–7), and patients at low-replicative phase (p=6.36x10–11, OR=2.29) or HBV e antigen-negative chronic hepatitis B phase (p=1.51x10–14, OR=1.86). Clinical traits analysis in patients with ACLF showed that the risky rs3129859*C allele was also associated with prolonged prothrombin time, faster progression to ascites development and higher 28-day mortality.ConclusionsOur genome-wide association study identified HLA-DR as the major locus for susceptibility to HBV-related ACLF. Our findings highlight the importance of HLA class II restricted CD4+ T-cell pathway on the immunopathogenesis of HBV-related ACLF.
      PubDate: 2018-03-08T07:15:46-08:00
      DOI: 10.1136/gutjnl-2016-313035
      Issue No: Vol. 67, No. 4 (2018)
  • Liver sampling: a vital window into HBV pathogenesis on the path to
           functional cure
    • Authors: Gill, U. S; Pallett, L. J, Kennedy, P. T. F, Maini, M. K.
      Pages: 767 - 775
      Abstract: In order to optimally refine the multiple emerging drug targets for hepatitis B virus (HBV), it is vital to evaluate virological and immunological changes at the site of infection. Traditionally liver biopsy has been the mainstay of HBV disease assessment, but with the emergence of non-invasive markers of liver fibrosis, there has been a move away from tissue sampling. Here we argue that liver biopsy remains an important tool, not only for the clinical assessment of HBV but also for research progress and evaluation of novel agents. The importance of liver sampling has been underscored by recent findings of specialised subsets of tissue-resident immune subsets capable of efficient pathogen surveillance, compartmentalised in the liver and not sampled in the blood. Importantly, the assessment of virological parameters, such as cccDNA quantitation, also requires access to liver tissue. We discuss strategies to maximise information obtained from the site of infection and disease pathology. Fine needle aspirates of the liver may allow longitudinal sampling of the local virus/host landscape. The careful utilisation of liver tissue and aspirates in conjunction with blood will provide critical information in the assessment of new therapeutics for the functional cure of HBV.
      Keywords: GUT Recent advances in basic science, Open access, Gut
      PubDate: 2018-03-08T07:15:46-08:00
      DOI: 10.1136/gutjnl-2017-314873
      Issue No: Vol. 67, No. 4 (2018)
  • GI highlights from the literature
    • Authors: McLean M. H.
      Pages: 776 - 777
      Abstract: Basic scienceThe role of the microbiota in hypertension: take it with a pinch of salt' Wilck N, Matus MG, Kearney SM et al. Salt-responsive commensal modulates TH17 axis and disease. Nature 2017;551:585–589. A high salt diet predisposes to hypertension and cardiovascular disease. This paper proposes that the microbiome and immune system bring about these effects of a high salt diet. High salt intake induces proinflammatory Th17 cells, which have been linked to hypertension and autoimmune disease. To find a link between salt intake and microbiota, mice were fed a high-salt diet made up of 4% salt, as compared with a normal-salt diet of 0.5% salt. After 2 weeks, faecal pellets were sequenced to reveal microbiota populations. There were clear differences between the two groups, but the most marked change was a reduction in Lactobacillus murinus in the high-salt group. L. murinus was cultured in the lab and growth...
      Keywords: Gut
      PubDate: 2018-03-08T07:15:46-08:00
      DOI: 10.1136/gutjnl-2018-316129
      Issue No: Vol. 67, No. 4 (2018)
  • Faecal microbiota composition associates with abdominal pain in the
           general population
    • Authors: Hadizadeh, F; Bonfiglio, F, Belheouane, M, Vallier, M, Sauer, S, Bang, C, Bujanda, L, Andreasson, A, Agreus, L, Engstrand, L, Talley, N. J, Rafter, J, Baines, J. F, Walter, S, Franke, A, DAmato, M.
      Pages: 778 - 779
      Abstract: We read with great interest the recent communication by Simrén et al,1 reporting a correlation between visceral hypersensitivity and GI symptom severity in functional GI disorders (FGID). Previously, it has been shown that visceral hypersensitivity can be modulated or even induced in animal models, by altering the composition of their gut microbiota with antibiotics or faecal transplantation from IBS donors.2 3 Hence, while a direct link between gut microbiota composition and visceral pain may need to be conclusively established, this holds great potential for translational exploitation in the treatment of IBS and other FGID. Thus far, the potential association between microbiota and abdominal pain in humans has only been investigated in one study that included 15 individuals.4 For this purpose, we studied 159 individuals (average age 59.1, 39.6% men) from the Swedish Population-based Colonoscopy (PopCol) cohort, previously described and with faecal microbiota...
      Keywords: Open access, Gut
      PubDate: 2018-03-08T07:15:46-08:00
      DOI: 10.1136/gutjnl-2017-314792
      Issue No: Vol. 67, No. 4 (2018)
  • Germline variation of circadian pathway genes and prognosis of gastric
           cancer patients
    • Authors: Rajendran, S; Benna, C, Monticelli, H, Spiro, G, Menin, C, Mocellin, S.
      Pages: 779 - 780
      Abstract: As we have summarised in this journal,1 germline DNA variation has been long recognised as a key component of the risk to develop to gastric carcinoma, the discovery pace being greatly accelerated by genome-wide association studies.2 More recently, growing evidence is accumulating also on the association between genetic variation and prognosis of patients with gastric cancer.3 4 Furthermore, investigators have demonstrated that alterations of the circadian rhythm can predispose to a variety of illnesses, including different types of malignancies and gastrointestinal diseases.5 6 Putting together these observations, we studied the relationship between circadian genes germline variation and the overall survival of 460 patients with TNM stage I to IV gastric carcinoma. We considered 21 single nucleotide polymorphisms (SNPs) of 14 circadian pathway genes. Genotyping was performed with real-time quantitative PCR using patient peripheral blood samples. Expression quantitative...
      Keywords: Gut
      PubDate: 2018-03-08T07:15:46-08:00
      DOI: 10.1136/gutjnl-2017-314740
      Issue No: Vol. 67, No. 4 (2018)
  • Combined effect of anti-BAG3 and anti-PD-1 treatment on macrophage
           infiltrate, CD8+ T cell number and tumour growth in pancreatic cancer
    • Authors: Iorio, V; Rosati, A, DAuria, R, De Marco, M, Marzullo, L, Basile, A, Festa, M, Pascale, M, Remondelli, P, Capunzo, M, Sala, G, Damiani, V, Amodio, G, Di Nicola, M, Lattanzio, R, Turco, M. C, De Laurenzi, V.
      Pages: 780 - 782
      Abstract: We read with great interest the article by Zhang et al1 showing that CD8+ cell infiltration in pancreatic tumours can be enhanced by depletion of myeloid cells (CD11b+ macrophages and myeloid-derived suppressor cells) and that the depletion of CD11b+ cells resulted in decreased PD-L1 expression on cancer cells thus impairing the triggering of the inhibitory receptor PD-1 on T cells.1 Recruitment and activation of CD8+ lymphocytes in tumours are suppressed by mechanisms only partially understood and rescuing CD8+ cell infiltrate in tumours is one of the objectives of immunotherapies.1 2 Tumour-associated macrophages (TAMs) play a crucial role in the relation between tumour cells and their environment.3 Here, we confirm the interplay between macrophages and CD8+ cells in pancreatic cancer and identify a potential way to exploit this enhancing effect of anti-PD-1 treatment. Indeed, we show that reduction of macrophage...
      Keywords: Open access, Gut
      PubDate: 2018-03-08T07:15:46-08:00
      DOI: 10.1136/gutjnl-2017-314225
      Issue No: Vol. 67, No. 4 (2018)
  • Correction: Discoidin domain receptor 2 deficiency predisposes hepatic
           tissue to colon carcinoma metastasis
    • Pages: 782 - 782
      Abstract: Badiola I, Olaso E, Crende O, et al. Discoidin domain receptor 2 deficiency predisposes hepatic tissue to colon carcinoma metastasis. Gut 2012;61:1465–72. doi: 10.1136/gutjnl-2011-300810.A second affiliation for the first author, Iker Badiola, has been added:Department of Cell Biology and Histology, University of the Basque Country, Leioa, Bizkaia, Spain
      Keywords: Gut
      PubDate: 2018-03-08T07:15:46-08:00
      DOI: 10.1136/gutjnl-2011-300810corr1
      Issue No: Vol. 67, No. 4 (2018)
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