Author
Peter A. Bampton
Other affiliations: Repatriation General Hospital, St George's Hospital, Royal Adelaide Hospital ...read more
Bio: Peter A. Bampton is an academic researcher from Flinders University. The author has contributed to research in topics: Inflammatory bowel disease & Colonoscopy. The author has an hindex of 36, co-authored 124 publications receiving 7588 citations. Previous affiliations of Peter A. Bampton include Repatriation General Hospital & St George's Hospital.
Papers published on a yearly basis
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Wellcome Trust Sanger Institute1, Broad Institute2, University of Groningen3, University of Pittsburgh4, Cedars-Sinai Medical Center5, Yale University6, University of Cambridge7, University of Chicago8, Harvard University9, Katholieke Universiteit Leuven10, University of Liège11, King's College London12, Université de Montréal13, New Jersey Institute of Technology14, Cleveland Clinic15, Peninsula College of Medicine and Dentistry16, Université libre de Bruxelles17, Aarhus University18, University of Adelaide19, University of Kiel20, Flinders University21, McGill University22, Ludwig Maximilian University of Munich23, Charité24, Icahn School of Medicine at Mount Sinai25, University of Bonn26, Karolinska Institutet27, Torbay Hospital28, University of Auckland29, Christchurch Hospital30, Imperial College London31, Queen's University32, University of Oslo33, Lithuanian University of Health Sciences34, Emory University35, Casa Sollievo della Sofferenza36, Ghent University37, University of Western Australia38, University of Edinburgh39, Queensland Health40, Newcastle University41, University of Dundee42, University of Manchester43, University of Amsterdam44, University of Maribor45, Royal Hospital for Sick Children46, Guy's and St Thomas' NHS Foundation Trust47, QIMR Berghofer Medical Research Institute48, Norfolk and Norwich University Hospital49, Leiden University50, Technische Universität München51, University of Toronto52, University of Pennsylvania53, Johns Hopkins University54, University of Queensland55
TL;DR: A meta-analysis of Crohn’s disease and ulcerative colitis genome-wide association scans is undertaken, followed by extensive validation of significant findings, with a combined total of more than 75,000 cases and controls.
Abstract: Crohn's disease and ulcerative colitis, the two common forms of inflammatory bowel disease (IBD), affect over 2.5 million people of European ancestry, with rising prevalence in other populations. Genome-wide association studies and subsequent meta-analyses of these two diseases as separate phenotypes have implicated previously unsuspected mechanisms, such as autophagy, in their pathogenesis and showed that some IBD loci are shared with other inflammatory diseases. Here we expand on the knowledge of relevant pathways by undertaking a meta-analysis of Crohn's disease and ulcerative colitis genome-wide association scans, followed by extensive validation of significant findings, with a combined total of more than 75,000 cases and controls. We identify 71 new associations, for a total of 163 IBD loci, that meet genome-wide significance thresholds. Most loci contribute to both phenotypes, and both directional (consistently favouring one allele over the course of human history) and balancing (favouring the retention of both alleles within populations) selection effects are evident. Many IBD loci are also implicated in other immune-mediated disorders, most notably with ankylosing spondylitis and psoriasis. We also observe considerable overlap between susceptibility loci for IBD and mycobacterial infection. Gene co-expression network analysis emphasizes this relationship, with pathways shared between host responses to mycobacteria and those predisposing to IBD.
4,094 citations
St. Vincent's Health System1, University of Melbourne2, Imperial College London3, University of Western Australia4, Royal Adelaide Hospital5, Flinders Medical Centre6, Monash University7, University of New South Wales8, University of Queensland9, University of Otago10, Royal Brisbane and Women's Hospital11, Royal Melbourne Hospital12, Royal Prince Alfred Hospital13
TL;DR: Treatment according to clinical risk of recurrence, with early colonoscopy and treatment step-up for recurrence), is better than conventional drug therapy alone for prevention of postoperative Crohn's disease recurrence.
446 citations
University of Melbourne1, St. Vincent's Health System2, University of New South Wales3, University of Western Australia4, Fremantle Hospital5, Royal Adelaide Hospital6, University of Adelaide7, Flinders Medical Centre8, Flinders University9, Monash University10, Mater Health Services11, Royal Melbourne Hospital12, QIMR Berghofer Medical Research Institute13, Royal Prince Alfred Hospital14, University of Otago15
TL;DR: In this analysis of data from a prospective clinical trial, FC measurement has sufficient sensitivity and NPV values to monitor for CD recurrence after intestinal resection and its predictive value might be used to identify patients most likely to relapse.
219 citations
TL;DR: Whether IBD patients' perceptions of the issues surrounding IBD, pregnancy, and childbearing influence their reproductive behavior is determined and specific patient concerns included IBD heritability, the risk of congenital abnormalities, and medication teratogenicity.
Abstract: BACKGROUND: Smaller family size and voluntary childlessness has been reported in IBD; however the disease-related reasons for this from a patient viewpoint are not described. The aims were to 1) determine whether IBD patients perceptions of the issues surrounding IBD pregnancy and childbearing influence their reproductive behavior and 2) describe these specific perceptions and concerns related to fertility and pregnancy. METHODS: All contactable subjects between 18-50 years of age from a hospital-based IBD database were surveyed by postal questionnaire. Data were obtained regarding age gender IBD diagnosis and treatment body image and sexual relationships as well as both objective and subjective data regarding fertility and pregnancy. Comparisons were made to community norms where data were available. Contingency tables with Fishers exact test were used. RESULTS: Of 365 subjects 255 responded (70%). The mean age was 35.5 years overall 34.7 years for women. In all 34% of participants were male 127 had Crohns disease (CD) 85 ulcerative colitis (UC) and 5 indeterminate colitis (IC). The average fertility rate was no different between women with CD and UC (1.0 and 1.2 births/woman respectively; P = 0.553) compared with 1.81 for all Australian women. Although 42.7% of IBD patients reported a fear of infertility patients only sought medical fertility advice at the same rate as the general population. Fear of infertility was most evident in women those with CD and those reporting previous surgery. Specific patient concerns which appear to have decreased patients family size included IBD heritability the risk of congenital abnormalities and medication teratogenicity. CONCLUSIONS: The unusually high response rate indicates the centrality of reproductive issues to IBD patients. "Voluntary" childlessness in this group appears to result from concerns about adverse reproductive outcomes that may not be justified. Patients require accurate counseling addressing fertility and pregnancy outcomes in IBD to assist in their decision making.
209 citations
TL;DR: A paired comparison of a sensitive guaiac FOBT with a brush‐sampling FIT is conducted to determine whether this FIT improves detection of significant neoplasia.
Abstract: BACKGROUND.
Fecal immunochemical tests (FIT) are an advanced fecal occult blood test (FOBT) technology that reduces barriers to population screening by simplifying the logistics of stool-sampling. The current study was conducted to undertake a paired comparison of a sensitive guaiac FOBT (GFOBT; Hemoccult II Sensa, Beckman Coulter, Fullerton, CA) with a brush-sampling FIT (InSure; Enterix, North Ryde, NSW, Australia), to determine whether this FIT improves detection of significant neoplasia.
METHODS.
Individuals sampled consecutive stools, at home, with both FIT and GFOBT sampling devices while following dietary restrictions appropriate for GFOBT. Study populations included a screening cohort (n = 2351) and a symptomatic diagnostic group (n = 161). Paired comparison of positivity rates was undertaken in those found to have cancer and/or significant adenoma (high-grade dysplasia, villous change, ≥10 mm, serrated histology or ≥3 polyps), benign pathology, or no pathology.
RESULTS.
Combined results for both cohorts showed that the FIT returned a true-positive result significantly more often in cancer (n = 24; 87.5% vs. 54.2%) and in significant adenomas (n = 61; 42.6% vs. 23.0%). Of all UICC Stage I cancers, the FIT was positive in 12 of 13 compared with 4 of 13 with the GFOBT (P = .002). In analyses of just the screening cohort, the FIT remained significantly better at detecting cancers and significant adenomas; the false-positive rate for any neoplasia was marginally higher with the FIT than the GFOBT (3.4% vs. 2.5%; 95% CI of difference, 0–1.8%), whereas positive predictive values were 41.9% and 40.4%, respectively.
CONCLUSIONS.
This brush-sampling FIT is more sensitive for cancers and significant adenomas than a sensitive GFOBT. As such, it should deliver greater reductions in colorectal cancer mortality and incidence than the GFOBT. Cancer 2006; © 2006 American Cancer Society.
187 citations
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01 Jan 2016
TL;DR: The using multivariate statistics is universally compatible with any devices to read, allowing you to get the most less latency time to download any of the authors' books like this one.
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14,604 citations
TL;DR: Associations at DRD2 and several genes involved in glutamatergic neurotransmission highlight molecules of known and potential therapeutic relevance to schizophrenia, and are consistent with leading pathophysiological hypotheses.
Abstract: Schizophrenia is a highly heritable disorder. Genetic risk is conferred by a large number of alleles, including common alleles of small effect that might be detected by genome-wide association studies. Here we report a multi-stage schizophrenia genome-wide association study of up to 36,989 cases and 113,075 controls. We identify 128 independent associations spanning 108 conservatively defined loci that meet genome-wide significance, 83 of which have not been previously reported. Associations were enriched among genes expressed in brain, providing biological plausibility for the findings. Many findings have the potential to provide entirely new insights into aetiology, but associations at DRD2 and several genes involved in glutamatergic neurotransmission highlight molecules of known and potential therapeutic relevance to schizophrenia, and are consistent with leading pathophysiological hypotheses. Independent of genes expressed in brain, associations were enriched among genes expressed in tissues that have important roles in immunity, providing support for the speculated link between the immune system and schizophrenia.
6,809 citations
Massachusetts Institute of Technology1, Broad Institute2, University of California, Los Angeles3, University of British Columbia4, Baylor College of Medicine5, Howard Hughes Medical Institute6, University of Washington7, Ludwig Institute for Cancer Research8, University of California, San Francisco9, University of Connecticut10, University of Zagreb11, University of Texas at Austin12, Washington University in St. Louis13, University of Queensland14, Harvard University15, Cold Spring Harbor Laboratory16, University of Southern California17, University of California, Santa Cruz18, Simon Fraser University19, Morgridge Institute for Research20, University of Texas at Dallas21, National Institutes of Health22
TL;DR: It is shown that disease- and trait-associated genetic variants are enriched in tissue-specific epigenomic marks, revealing biologically relevant cell types for diverse human traits, and providing a resource for interpreting the molecular basis of human disease.
Abstract: The reference human genome sequence set the stage for studies of genetic variation and its association with human disease, but epigenomic studies lack a similar reference. To address this need, the NIH Roadmap Epigenomics Consortium generated the largest collection so far of human epigenomes for primary cells and tissues. Here we describe the integrative analysis of 111 reference human epigenomes generated as part of the programme, profiled for histone modification patterns, DNA accessibility, DNA methylation and RNA expression. We establish global maps of regulatory elements, define regulatory modules of coordinated activity, and their likely activators and repressors. We show that disease- and trait-associated genetic variants are enriched in tissue-specific epigenomic marks, revealing biologically relevant cell types for diverse human traits, and providing a resource for interpreting the molecular basis of human disease. Our results demonstrate the central role of epigenomic information for understanding gene regulation, cellular differentiation and human disease.
5,037 citations
TL;DR: The landscape of gene expression across tissues is described, thousands of tissue-specific and shared regulatory expression quantitative trait loci (eQTL) variants are cataloged, complex network relationships are described, and signals from genome-wide association studies explained by eQTLs are identified.
Abstract: Understanding the functional consequences of genetic variation, and how it affects complex human disease and quantitative traits, remains a critical challenge for biomedicine. We present an analysi...
4,418 citations
01 Feb 2015
TL;DR: In this article, the authors describe the integrative analysis of 111 reference human epigenomes generated as part of the NIH Roadmap Epigenomics Consortium, profiled for histone modification patterns, DNA accessibility, DNA methylation and RNA expression.
Abstract: The reference human genome sequence set the stage for studies of genetic variation and its association with human disease, but epigenomic studies lack a similar reference. To address this need, the NIH Roadmap Epigenomics Consortium generated the largest collection so far of human epigenomes for primary cells and tissues. Here we describe the integrative analysis of 111 reference human epigenomes generated as part of the programme, profiled for histone modification patterns, DNA accessibility, DNA methylation and RNA expression. We establish global maps of regulatory elements, define regulatory modules of coordinated activity, and their likely activators and repressors. We show that disease- and trait-associated genetic variants are enriched in tissue-specific epigenomic marks, revealing biologically relevant cell types for diverse human traits, and providing a resource for interpreting the molecular basis of human disease. Our results demonstrate the central role of epigenomic information for understanding gene regulation, cellular differentiation and human disease.
4,409 citations