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14 results on '"Jansen, Marnix"'

2. The stem cell organisation, and the proliferative and gene expression profile of Barrettʼs epithelium, replicates pyloric-type gastric glands

Author

Lavery, Danielle L, Nicholson, Anna M, Poulsom, Richard, Jeffery, Rosemary, Hussain, Alia, Gay, Laura J, Jankowski, Janusz A, Zeki, Sebastian S, Barr, Hugh, Harrison, Rebecca, Going, James, Kadirkamanathan, Sritharan, Davis, Peter, Underwood, Timothy, Novelli, Marco R, Rodriguez-Justo, Manuel, Shepherd, Neil, Jansen, Marnix, Wright, Nicholas A, and McDonald, Stuart A C

Published
2014
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6. Evolution of oesophageal adenocarcinoma from metaplastic columnar epithelium without goblet cells in Barrett's oesophagus

Author

Lavery, Danielle L., Martinez, Pierre, Gay, Laura J., Cereser, Biancastella, Novelli, Marco R., Rodriguez-Justo, Manuel, Meijer, Sybren L., Graham, Trevor A., McDonald, Stuart A. C., Wright, Nicholas A., Jansen, Marnix, Pathology, and Other departments

Subjects
BARRETT'S CARCINOMA, Metaplasia, Gastroenterology & Hepatology, Esophageal Neoplasms, Biopsy, 1103 Clinical Sciences, BARRETT'S METAPLASIA, Sequence Analysis, DNA, Adenocarcinoma, Middle Aged, digestive system, digestive system diseases, Epithelium, Mitochondria, Electron Transport Complex IV, Oesophagus, Barrett Esophagus, Mutation, 1114 Paediatrics And Reproductive Medicine, Humans, Exome, Female, Goblet Cells, BARRETT'S OESOPHAGUS
Abstract

OBJECTIVE: Barrett's oesophagus commonly presents as a patchwork of columnar metaplasia with and without goblet cells in the distal oesophagus. The presence of metaplastic columnar epithelium with goblet cells on oesophageal biopsy is a marker of cancer progression risk, but it is unclear whether clonal expansion and progression in Barrett's oesophagus is exclusive to columnar epithelium with goblet cells. DESIGN: We developed a novel method to trace the clonal ancestry of an oesophageal adenocarcinoma across an entire Barrett's segment. Clonal expansions in Barrett's mucosa were identified using cytochrome c oxidase enzyme histochemistry. Somatic mutations were identified through mitochondrial DNA sequencing and single gland whole exome sequencing. RESULTS: By tracing the clonal origin of an oesophageal adenocarcinoma across an entire Barrett's segment through a combination of histopathological spatial mapping and clonal ordering, we find that this cancer developed from a premalignant clonal expansion in non-dysplastic ('cardia-type') columnar metaplasia without goblet cells. CONCLUSION: Our data demonstrate the premalignant potential of metaplastic columnar epithelium without goblet cells in the context of Barrett's oesophagus.

Published
2015

7. British Society of Gastroenterology guidelines on the diagnosis and management of patients at risk of gastric adenocarcinoma

Author

Banks, Matthew, primary, Graham, David, additional, Jansen, Marnix, additional, Gotoda, Takuji, additional, Coda, Sergio, additional, di Pietro, Massimiliano, additional, Uedo, Noriya, additional, Bhandari, Pradeep, additional, Pritchard, D Mark, additional, Kuipers, Ernst J, additional, Rodriguez-Justo, Manuel, additional, Novelli, Marco R, additional, Ragunath, Krish, additional, Shepherd, Neil, additional, and Dinis-Ribeiro, Mario, additional

Published
2019
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8. Crypt fusion as a homeostatic mechanism in the human colon

Author

Baker, Ann-Marie, primary, Gabbutt, Calum, additional, Williams, Marc J, additional, Cereser, Biancastella, additional, Jawad, Noor, additional, Rodriguez-Justo, Manuel, additional, Jansen, Marnix, additional, Barnes, Chris P, additional, Simons, Benjamin D, additional, McDonald, Stuart AC, additional, Graham, Trevor A, additional, and Wright, Nicholas A, additional

Published
2019
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10. Evolutionary history of human colitis-associated colorectal cancer

Author

Baker, Ann-Marie, primary, Cross, William, additional, Curtius, Kit, additional, Al Bakir, Ibrahim, additional, Choi, Chang-Ho Ryan, additional, Davis, Hayley Louise, additional, Temko, Daniel, additional, Biswas, Sujata, additional, Martinez, Pierre, additional, Williams, Marc J, additional, Lindsay, James O, additional, Feakins, Roger, additional, Vega, Roser, additional, Hayes, Stephen J, additional, Tomlinson, Ian P M, additional, McDonald, Stuart A C, additional, Moorghen, Morgan, additional, Silver, Andrew, additional, East, James E, additional, Wright, Nicholas A, additional, Wang, Lai Mun, additional, Rodriguez-Justo, Manuel, additional, Jansen, Marnix, additional, Hart, Ailsa L, additional, Leedham, Simon J, additional, and Graham, Trevor A, additional

Published
2018
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11. Evolutionary history of human colitis-associated colorectal cancer

Author

Baker, Ann-Marie, Cross, William, Curtius, Kit, Al Bakir, Ibrahim, Choi, Chang-Ho Ryan, Davis, Hayley Louise, Temko, Daniel, Biswas, Sujata, Martinez, Pierre, Williams, Marc J, Lindsay, James O, Feakins, Roger, Vega, Roser, Hayes, Stephen J, Tomlinson, Ian P M, McDonald, Stuart A C, Moorghen, Morgan, Silver, Andrew, East, James E, Wright, Nicholas A, Wang, Lai Mun, Rodriguez-Justo, Manuel, Jansen, Marnix, Hart, Ailsa L, Leedham, Simon J, and Graham, Trevor A

Abstract

ObjectiveIBD confers an increased lifetime risk of developing colorectal cancer (CRC), and colitis-associated CRC (CA-CRC) is molecularly distinct from sporadic CRC (S-CRC). Here we have dissected the evolutionary history of CA-CRC using multiregion sequencing.DesignExome sequencing was performed on fresh-frozen multiple regions of carcinoma, adjacent non-cancerous mucosa and blood from 12 patients with CA-CRC (n=55 exomes), and key variants were validated with orthogonal methods. Genome-wide copy number profiling was performed using single nucleotide polymorphism arrays and low-pass whole genome sequencing on archival non-dysplastic mucosa (n=9), low-grade dysplasia (LGD; n=30), high-grade dysplasia (HGD; n=13), mixed LGD/HGD (n=7) and CA-CRC (n=19). Phylogenetic trees were reconstructed, and evolutionary analysis used to reveal the temporal sequence of events leading to CA-CRC.Results10/12 tumours were microsatellite stable with a median mutation burden of 3.0 single nucleotide alterations (SNA) per Mb, ~20% higher than S-CRC (2.5 SNAs/Mb), and consistent with elevated ageing-associated mutational processes. Non-dysplastic mucosa had considerable mutation burden (median 47 SNAs), including mutations shared with the neighbouring CA-CRC, indicating a precancer mutational field. CA-CRCs were often near triploid (40%) or near tetraploid (20%) and phylogenetic analysis revealed that copy number alterations (CNAs) began to accrue in non-dysplastic bowel, but the LGD/HGD transition often involved a punctuated ‘catastrophic’ CNA increase.ConclusionsEvolutionary genomic analysis revealed precancer clones bearing extensive SNAs and CNAs, with progression to cancer involving a dramatic accrual of CNAs at HGD. Detection of the cancerised field is an encouraging prospect for surveillance, but punctuated evolution may limit the window for early detection.

Published
2019
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12. Aberrant intestinal stem cell lineage dynamics in Peutz–Jeghers syndrome and familial adenomatous polyposis consistent with protracted clonal evolution in the crypt

Author

Langeveld, Danielle, primary, Jansen, Marnix, additional, de Boer, D V, additional, van Sprundel, Mariska, additional, Brosens, Lodewijk A A, additional, Morsink, Folkert H, additional, Giardiello, Francis M, additional, Offerhaus, G Johan A, additional, and de Leng, Wendy W J, additional

Published
2011
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13. Aberrant intestinal stem cell lineage dynamics in PeutzeJeghers syndrome and familial adenomatous polyposis consistent with protracted clonal evolution in the crypt.

Author

Langeveld, Danielle, Jansen, Marnix, de Boer, D. V., van Sprundel, Mariska, Brosens, Lodewijk A. A., Morsink, Folkert H., Giardiello, Francis M., Offerhaus, G. Johan A., and de Leng, Wendy W. J.

Subjects
*GENETIC disorders, *INTESTINAL physiology, *ECTOPIC tissue, *STEM cells, *DISEASE susceptibility, *CANCER genetics, *HOMEOBOX genes, *METHYLATION
Abstract

Objective Genetic predisposition to cancer in PeutzeJeghers syndrome (PJS) and the role of germline serineethreonine kinase (LKB1) mutations are poorly understood. The authors studied the effect of germline LKB1 mutations on intestinal stem cell dynamics in unaffected flat PJS mucosa. Recent research has documented that the intestinal crypt houses multiple equipotent stem cell lineages. Lineages continuously compete through random drifts, while somatically inherited methylation patterns record clonal diversity. Design To study the effect of germline LKB1 mutations on clonal expansion, the authors performed quantitative analyses of cardiac-specific homeobox methylation pattern diversity in crypts isolated from unaffected colonic mucosa obtained from archival PJS patient material. The authors compared methylation density and methylation pattern diversity in patients with PJS to those in patients with familial adenomatous polyposis and age-matched controls. Results The percentage of total methylation is comparable between groups, but the number of unique methylation patterns is significantly increased for patients with familial adenomatous polyposis and patients with PJS compared to control subjects. Conclusions Monoallelic LKB1 loss is not silent and provokes a protracted clonal evolution in the crypt. The increased methylation pattern diversity observed in unaffected PJS mucosa predicts that premalignant lesions will arise at an accelerated pace compared to the general population. INSET: Significance of this study. [ABSTRACT FROM AUTHOR]

Published
2012
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