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1. 223 IMMUNE CELL PHENOTYPING IN BARRETT'S ESOPHAGUS IN PATIENTS PRIOR AND AT TIME OF PROGRESSION

Author

Lin, Meng-Lay, Hickey, John W, Schürch, Christian M, Passman, Adam M, Carlotti, Emanuela, Devkumar, Shruthi, Hackett, Richard J, Rodriguez-Justo, Manuel, Novelli, Marco, Jansen, Marnix, Gascard, Philippe D, Tlsty, Thea D, and McDonald, Stuart A

Subjects
Biomedical and Clinical Sciences, Clinical Sciences, Nutrition and Dietetics, Neurosciences, Paediatrics and Reproductive Medicine, Gastroenterology & Hepatology, Clinical sciences, Nutrition and dietetics
Published
2023

2. The co-evolution of the genome and epigenome in colorectal cancer

Author

Heide, Timon, Househam, Jacob, Cresswell, George D., Spiteri, Inmaculada, Lynn, Claire, Mossner, Maximilian, Kimberley, Chris, Fernandez-Mateos, Javier, Chen, Bingjie, Zapata, Luis, James, Chela, Barozzi, Iros, Chkhaidze, Ketevan, Nichol, Daniel, Gunasri, Vinaya, Berner, Alison, Schmidt, Melissa, Lakatos, Eszter, Baker, Ann-Marie, Costa, Helena, Mitchinson, Miriam, Piazza, Rocco, Jansen, Marnix, Caravagna, Giulio, Ramazzotti, Daniele, Shibata, Darryl, Bridgewater, John, Rodriguez-Justo, Manuel, Magnani, Luca, Graham, Trevor A., and Sottoriva, Andrea

Published
2022
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3. Phenotypic plasticity and genetic control in colorectal cancer evolution

Author

Househam, Jacob, Heide, Timon, Cresswell, George D., Spiteri, Inmaculada, Kimberley, Chris, Zapata, Luis, Lynn, Claire, James, Chela, Mossner, Maximilian, Fernandez-Mateos, Javier, Vinceti, Alessandro, Baker, Ann-Marie, Gabbutt, Calum, Berner, Alison, Schmidt, Melissa, Chen, Bingjie, Lakatos, Eszter, Gunasri, Vinaya, Nichol, Daniel, Costa, Helena, Mitchinson, Miriam, Ramazzotti, Daniele, Werner, Benjamin, Iorio, Francesco, Jansen, Marnix, Caravagna, Giulio, Barnes, Chris P., Shibata, Darryl, Bridgewater, John, Rodriguez-Justo, Manuel, Magnani, Luca, Sottoriva, Andrea, and Graham, Trevor A.

Published
2022
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4. Immunosuppressive niche engineering at the onset of human colorectal cancer

Author

Gatenbee, Chandler D., Baker, Ann-Marie, Schenck, Ryan O., Strobl, Maximilian, West, Jeffrey, Neves, Margarida P., Hasan, Sara Yakub, Lakatos, Eszter, Martinez, Pierre, Cross, William C. H., Jansen, Marnix, Rodriguez-Justo, Manuel, Whelan, Christopher J., Sottoriva, Andrea, Leedham, Simon, Robertson-Tessi, Mark, Graham, Trevor A., and Anderson, Alexander R. A.

Published
2022
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6. Abstract 4539: Tumor evolution and immune microenvironment dynamics define response to neoadjuvant treatment of esophageal adenocarcinoma

Author

Barroux, Melissa, primary, Househam, Jacob, additional, Lakatos, Eszter, additional, Ronel, Tahel, additional, Baker, Ann-Marie, additional, Salié, Henrike, additional, Mossner, Max, additional, Smith, Kane, additional, Kimberley, Chris, additional, Nowinski, Salpie, additional, Berner, Alison, additional, Gunasri, Vinaya, additional, Jansen, Marnix, additional, Caravagna, Giulio, additional, Slotta-Huspenina, Julia, additional, Weichert, Wilko, additional, Alberstmeier, Markus, additional, Chain, Benny, additional, Friess, Helmut, additional, Bengsch, Bertram, additional, Schmid, Roland M., additional, Siveke, Jens T., additional, Quante, Michael, additional, and Graham, Trevor A., additional

Published
2023
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9. Pan-cancer analysis of the extent and consequences of intratumor heterogeneity

Author

Andor, Noemi, Graham, Trevor A., Jansen, Marnix, Xia, Li.C., Aktipis, C.Athena, Petritsch, Claudia, Ji, Hanlee P., and Maley, Carlo C.

Subjects
Tumors -- Genetic aspects -- Research, Cancer -- Genetic aspects, Biological sciences, Health
Abstract

Intratumor heterogeneity (ITH) drives neoplastic progression and therapeutic resistance. We used the bioinformatics tools 'expanding ploidy and allele frequency on nested subpopulations' (EXPANDS) and PyClone to detect clones that are present at a ≥ 10% frequency in 1,165 exome sequences from tumors in The Cancer Genome Atlas. 86% of tumors across 12 cancer types had at least two clones. ITH in the morphology of nuclei was associated with genetic ITH (Spearman's correlation coefficient, ρ = 0.24-0.41; P < 0.001). Mutation of a driver gene that typically appears in smaller clones was a survival risk factor (hazard ratio (HR) = 2.15, 95% confidence interval (CI): 1.71-2.69). The risk of mortality also increased when >2 clones coexisted in the same tumor sample (HR = 1.49, 95% CI: 1.20-1.87). In two independent data sets, copy-number alterations affecting either 75% of a tumor's genome predicted reduced risk (HR = 0.15, 95% CI: 0.08-0.29). Mortality risk also declined when >4 clones coexisted in the sample, suggesting a trade-off between the costs and benefits of genomic instability. ITH and genomic instability thus have the potential to be useful measures that can universally be applied to all cancers., Cancers are a mosaic of clones with varying population sizes, different genetic makeups and distinct phenotypic characteristics (1-4). This intratumor heterogeneity provides the fuel for the engine of natural selection [...]

Published
2016
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10. Mo1164: UTILISATION OF THE CYTOSPONGE DEVICE AS A TOOL FOR RISK STRATIFICATION IN PATIENTS WITH BARRETT'S OESOPHAGUS WHO ARE OVERDUE ENDOSCOPIC SURVEILLANCE DUE TO THE COVID-19 PANDEMIC

Author

Sehgal, Vinay, primary, Aslam, Nasar, additional, Mcguire, Joshua, additional, Telese, Andrea, additional, Hussein, Mohamed, additional, Bassett, Paul, additional, Naidoo, Dashnee, additional, Coates, Olivia, additional, Thorpe, Sally, additional, Brogden, Sara E., additional, Makahamadze, Christwishes, additional, Sesay, Michael, additional, Mitchison, Miriam, additional, Jansen, Marnix, additional, Sami, Sarmed S., additional, Sweis, Rami, additional, Banks, Matthew, additional, Graham, David, additional, Lovat, Laurence B., additional, and Haidry, Rehan, additional

Published
2022
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11. Clonal Transitions and Phenotypic Evolution in Barrett’s Esophagus

Author

Evans, James A., primary, Carlotti, Emanuela, additional, Lin, Meng-Lay, additional, Hackett, Richard J., additional, Haughey, Magnus J., additional, Passman, Adam M., additional, Dunn, Lorna, additional, Elia, George, additional, Porter, Ross J., additional, McLean, Mairi H., additional, Hughes, Frances, additional, ChinAleong, Joanne, additional, Woodland, Philip, additional, Preston, Sean L., additional, Griffin, S. Michael, additional, Lovat, Laurence, additional, Rodriguez-Justo, Manuel, additional, Huang, Weini, additional, Wright, Nicholas A., additional, Jansen, Marnix, additional, and McDonald, Stuart A.C., additional

Published
2022
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14. The natural history of low‐grade dysplasia in Barrett's esophagus and risk factors for progression

Author

Hussein, Mohamed, primary, Sehgal, Vinay, additional, Sami, Sarmed, additional, Bassett, Paul, additional, Sweis, Rami, additional, Graham, David, additional, Telese, Andrea, additional, Morris, Danielle, additional, Rodriguez‐Justo, Manuel, additional, Jansen, Marnix, additional, Novelli, Marco, additional, Banks, Matthew, additional, Lovat, Laurence B, additional, and Haidry, Rehan, additional

Published
2021
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15. Poor-prognosis colon cancer is defined by a molecularly distinct subtype and develops from serrated precursor lesions

Author

De Sousa E. Melo, Felipe, Wang, Xin, Jansen, Marnix, Fessler, Evelyn, Trinh, Anne, de Rooij, Laura P M H, de Jong, Joan H., de Boer, Onno J., van Leersum, Ronald, Bijlsma, Maarten F., Rodermond, Hans, van der Heijden, Maartje, van Noesel, Carel J.M., Tuynman, Jurriaan B., Dekker, Evelien, Markowetz, Florian, Markowetz, Jan Paul, and Vermeulen, Louis

Subjects
Gene mutations -- Physiological aspects -- Genetic aspects -- Research, Colon cancer -- Prognosis -- Genetic aspects -- Care and treatment -- Research, Cancer -- Genetic aspects, Biological sciences, Health
Abstract

Colon cancer is a clinically diverse disease. This heterogeneity makes it difficult to determine which patients will benefit most from adjuvant therapy and impedes the development of new targeted agents [...]

Published
2013
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17. Stain-free identification of tissue pathology using a generative adversarial network to infer nanomechanical signatures

Author

Neary-Zajiczek, Lydia, primary, Essmann, Clara, additional, Rau, Anita, additional, Bano, Sophia, additional, Clancy, Neil, additional, Jansen, Marnix, additional, Heptinstall, Lauren, additional, Miranda, Elena, additional, Gander, Amir, additional, Pawar, Vijay, additional, Fernandez-Reyes, Delmiro, additional, Shaw, Michael, additional, Davidson, Brian, additional, and Stoyanov, Danail, additional

Published
2021
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18. 253e IMMUNE EDITING IN THE INVASIVE MARGIN AND NODE DEPOSITS OF COLORECTAL CANCER SELECTS FOR CELLULAR NEIGHBOURHOODS ENRICHED IN PDL1+ CANCER CELLS

Author

Gunasri, Vinaya, Lakatos, Eszter, Trahearn, Nick, Cisneros, Luis, Househam, Jacob, Heide, Timon, Cresswell, George D., Spiteri, Inmaculada, Mossner, Maximilian, Kimberley, Christopher, Ortiz, Luis Zapata, James, Chela, Lynn, Claire, Berner, Alison A., Costa, Helena, Mitchison, Miriam, Jansen, Marnix, Caravagna, Giulio, Rodriguez-Justo, Manuel, Shibata, Darryl, Bridgewater, John, Baker, Ann-Marie, Sottoriva, Andrea, and Graham, Trevor A.

Published
2023
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22. Tu1277 UTILISATION OF THE CYTOSPONGE DEVICE AS A TOOL FOR NON-ENDOSCOPIC SURVEILLANCE IN PATIENTS WITH BARRETT'S OESOPHAGUS

Author

Sehgal, Vinay, Alkandari, Ameenah, McGuire, Joshua, Aslam, Nasar, Telese, Andrea, Hussein, Mohamed, Naidoo, Dashnee, Coates, Olivia, Thorpe, Sally, Brogden, Sara E., Makahamadze, Christwishes, Duku, Margaret, Sesay, Michael, Mitchison, Miriam, Jansen, Marnix, Sweis, Rami, Banks, Matthew, Graham, David, Lovat, Laurence B., and Haidry, Rehan

Published
2023
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23. 225 MITOTIC AGE OF NON-DYSPLASTIC BARRETT'S ESOPHAGUS DEFINES RISK OF PROGRESSION TO ESOPHAGEAL ADENOCARCINOMA USING A NOVEL TARGETED ALLELE SPECIFIC METHYLATION SEQUENCING ARRAY

Author

Hackett, Richard J., Carlotti, Emanuela, Passman, Adam M., Devkumar, Shruthi, Lin, Meng-Lay, Mossner, Maximilian, Whiting, Freddie, Chin-Aleong, Joanne, Rodriguez-Justo, Manuel, Jansen, Marnix, Lovat, Laurence B., Preston, Sean L., Woodland, Philip J., Graham, Trevor A., Wright, Nicholas A., and McDonald, Stuart A.

Published
2023
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26. 30 TRACING SPATIAL CLONAL EVOLUTION OF INTESTINAL METAPLASIA IN THE CHRONICALLY INFLAMED STOMACH, A QUANTITATIVE MODEL OF PRE-TUMOUR PROGRESSION.

Author

Waddingham, William, primary, Cross, William, additional, Shutkever, Oliver, additional, Curtius, Kit, additional, dawas, khaled, additional, Mohammadi, borzoueh, additional, Jenkinson, Andrew, additional, Graham, David, additional, Banks, Matthew, additional, Sekine, Shigeki, additional, and Jansen, Marnix, additional

Published
2020
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27. VEROnA Protocol: A Pilot, Open-Label, Single-Arm, Phase 0, Window-of-Opportunity Study of Vandetanib-Eluting Radiopaque Embolic Beads (BTG-002814) in Patients With Resectable Liver Malignancies

Author

Beaton, Laura, primary, Tregidgo, Henry F J, additional, Znati, Sami A, additional, Forsyth, Sharon, additional, Clarkson, Matthew J, additional, Bandula, Steven, additional, Chouhan, Manil, additional, Lowe, Helen L, additional, Zaw Thin, May, additional, Hague, Julian, additional, Sharma, Dinesh, additional, Pollok, Joerg-Matthias, additional, Davidson, Brian R, additional, Raja, Jowad, additional, Munneke, Graham, additional, Stuckey, Daniel J, additional, Bascal, Zainab A, additional, Wilde, Paul E, additional, Cooper, Sarah, additional, Ryan, Samantha, additional, Czuczman, Peter, additional, Boucher, Eveline, additional, Hartley, John A, additional, Lewis, Andrew L, additional, Jansen, Marnix, additional, Meyer, Tim, additional, and Sharma, Ricky A, additional

Published
2019
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28. Histopathologist Features Predictive of Diagnostic Concordance at Expert Level Amongst a Large International Sample of Pathologists Diagnosing Barrett’s Dysplasia Using Digital Pathology

Author

Coleman, Helen, van der Wel, Myrtle, Jansen, Marnix, Bergman, Jacques, and Meijer, Sybren

Subjects
education, digestive system diseases
Abstract

Introduction Histopathological diagnosis of dysplasia in Barrett’s oesophagus (BO) is the gold standard for patient risk stratification, but is subject to significant interobserver variation. We investigated histopathologist features that predict diagnostic performance amongst a large international cohort of gastrointestinal (GI) pathologists.Methods An online scoring environment was developed for GI-pathologists (n=55) from over 20 countries to grade a case set of 55 digitalised BO biopsies encompassing the complete spectrum from non-dysplastic Barrett’s oesophagus (NDBO), indefinite, low and high-grade dysplasia (IND/LGD/HGD). Case interpretations were recorded before and after revealing P53 immunohistochemistry. Detailed histopathologist demographic data (experience, centre volume, fellowship training etc.) was obtained through an online questionnaire. A consensus gold standard diagnosis was obtained for the entire case set through a reference panel of four expert pathologists. Multivariate regression analyses was conducted to identify pathologist predictors of concordance.Results We recorded over 6000 case diagnoses. Of 2,805 hour and E diagnoses, we found excellent concordance for NDBO (643 of 816 diagnoses; 79%) and HGD (544 of 765 diagnoses; 71%) and intermediate concordance for LGD (382 of 918; 42%) and IND (70 of 306; 23%), replicating known glass slide test characteristics. Major over or under-interpretations (i.e. NDBO overstaged as LGD/HGD, or LGD/HGD understaged as NDBO) were reported in 248 diagnoses (8.8%). Addition of p53 staining further improved diagnostic consensus, but had limited impact on major over or under-interpretations. Multivariate regression analyses revealed independent histopathologist predictors of expert level diagnostic performance, including; at least 5 years of experience, working within a teaching hospital, viewing 5–20 Barrett’s cases per week, adherence to major guidelines, and an interest in digital pathology.ConclusionsUsing this rich dataset representing a heterogeneous group of gastrointestinal pathologists working globally, we have quantified diagnostic performance for BO dysplasia diagnosis using digital case review. Our results reveal predictors of diagnostic performance at expert level, and will aid formulation of quality assurance criteria for guideline development.

Published
2019

29. Undifferentiated sarcomas develop through distinct evolutionary pathways

Author

Steele, Christopher D., Tarabichi, Maxime, Oukrif, Dahmane, Webster, Amy P., Ye, Hongtao, Fittall, Matthew, Lombard, Patrick, Martincorena, Iñigo, Tarpey, Patrick S., Collord, Grace, Haase, Kerstin, Strauss, Sandra J., Berisha, Fitim, Vaikkinen, Heli, Dhami, Pawan, Jansen, Marnix, Behjati, Sam, Amary, M. Fernanda, Tirabosco, Roberto, Feber, Andrew, Campbell, Peter J., Alexandrov, Ludmil B., Van Loo, Peter, Flanagan, Adrienne M., and Pillay, Nischalan

Subjects
Human Biology & Physiology, Ploidies, sarcoma, cancer evolution, tumor mutational burden, Gene Expression Profiling, mutational signatures, Sequence Analysis, DNA, DNA Methylation, Tumour Biology, Prognosis, copy-number signatures, Article, Evolution, Molecular, Ecology,Evolution & Ethology, Gene Duplication, Mutation, genomics, Humans, immuno-oncology, Genetics & Genomics, Computational & Systems Biology
Abstract

Summary Undifferentiated sarcomas (USARCs) of adults are diverse, rare, and aggressive soft tissue cancers. Recent sequencing efforts have confirmed that USARCs exhibit one of the highest burdens of structural aberrations across human cancer. Here, we sought to unravel the molecular basis of the structural complexity in USARCs by integrating DNA sequencing, ploidy analysis, gene expression, and methylation profiling. We identified whole genome duplication as a prevalent and pernicious force in USARC tumorigenesis. Using mathematical deconvolution strategies to unravel the complex copy-number profiles and mutational timing models we infer distinct evolutionary pathways of these rare cancers. In addition, 15% of tumors exhibited raised mutational burdens that correlated with gene expression signatures of immune infiltration, and good prognosis., Graphical Abstract, Highlights • Undifferentiated sarcomas contain biologically relevant molecular subgroups • Identification of mismatch repair deficiency open up alternate avenues for therapy • Pseudohaploidization is a recurrent event in undifferentiated sarcomas • Copy-number signatures are useful for inferring states of sarcoma evolution, Steele et al. determine the molecular landscape of undifferentiated sarcomas. They identify tumors with high mutation burdens, which are enriched for activation of immune pathways and have good prognoses, and deduce four tumorigenic routes, all of which begin with driver mutations before whole genome duplication.

Published
2019
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31. 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

32. 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

Subjects
Male, Colonoscopy/methods, colorectal cancer, Polymorphism, Single Nucleotide, Risk Assessment, Severity of Illness Index, dysplasia, Humans, Colitis, Ulcerative/genetics, Phylogeny, Manchester Cancer Research Centre, ResearchInstitutes_Networks_Beacons/mcrc, Inflammatory Bowel Disease, Cell Transformation, Neoplastic/genetics, Colonoscopy, Middle Aged, Polymorphism, Single Nucleotide/genetics, Colorectal Neoplasms/genetics, digestive system diseases, Gene Expression Regulation, Neoplastic, Cell Transformation, Neoplastic, IBD - genetics, Disease Progression, Colitis, Ulcerative, Female, Colorectal Neoplasms
Abstract

OBJECTIVE: IBD 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.DESIGN: Exome 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.RESULTS: 10/12 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.CONCLUSIONS: Evolutionary 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
2018

33. Accuracy of endoscopic staging and targeted biopsies for routine gastric intestinal metaplasia and gastric atrophy evaluation study protocol of a prospective, cohort study: the estimate study

Author

Nieuwenburg, Stella A V, primary, Waddingham, William W, additional, Graham, David, additional, Rodriguez-Justo, Manuel, additional, Biermann, Katharina, additional, Kuipers, Ernst J, additional, Banks, Matthew, additional, Jansen, Marnix, additional, and Spaander, Manon C W, additional

Published
2019
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34. Quality indicators for Barrett’s endotherapy (QBET): UK consensus statements for patients undergoing endoscopic therapy for Barrett’s neoplasia

Author

Alzoubaidi, Durayd, primary, Ragunath, Krish, additional, Wani, Sachin, additional, Penman, Ian D, additional, Trudgill, Nigel John, additional, Jansen, Marnix, additional, Banks, Matthew, additional, Bhandari, Pradeep, additional, Morris, Allan John, additional, Willert, Robert, additional, Boger, Phil, additional, Smart, Howard L, additional, Ravi, Narayanasamy, additional, Dunn, Jason, additional, Gordon, Charles, additional, Mannath, Jayan, additional, Mainie, Inder, additional, di Pietro, Massi, additional, Veitch, Andrew M, additional, Thorpe, Sally, additional, Magee, Cormac, additional, Everson, Martin, additional, Sami, Sarmed, additional, Bassett, Paul, additional, Graham, David, additional, Attwood, Stephen, additional, Pech, Oliver, additional, Sharma, Prateek, additional, Lovat, Laurence B, additional, and Haidry, Rehan, additional

Published
2019
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35. Sa1160 – The Natural History of Low Grade Dysplasia in Patients with Barrett's Esophagus: 12 Year Retrospective Analysis from a Tertiary Centre

Author

Hussein, Mohamed, primary, Sehgal, Vinay, additional, Magee, Cormac, additional, Sami, Sarmed S., additional, Banks, Matthew, additional, Sweis, Rami, additional, Graham, David G., additional, Morris, Danielle, additional, Rodriguez-Justo, Manuel, additional, Jansen, Marnix, additional, Novelli, Marco, additional, Lovat, Laurence, additional, and Haidry, Rehan, additional

Published
2019
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36. Quantification of Crypt and Stem Cell Evolution in the Normal and Neoplastic Human Colon

Author

Baker, Ann-Marie, primary, Cereser, Biancastella, additional, Melton, Samuel, additional, Fletcher, Alexander G., additional, Rodriguez-Justo, Manuel, additional, Tadrous, Paul J., additional, Humphries, Adam, additional, Elia, George, additional, McDonald, Stuart A.C., additional, Wright, Nicholas A., additional, Simons, Benjamin D., additional, Jansen, Marnix, additional, and Graham, Trevor A., additional

Published
2019
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37. 781 – Quantifying Evolution of Early Dysplastic Lesions in Ulcerative Colitis Predicts Future Colorectal Cancer Risk

Author

Curtius, Kit, primary, Al Bakir, Ibrahim, additional, Baker, Ann-Marie, additional, Clarke, Theo, additional, Nasreddin, Nadia, additional, Kopczynska, Maja, additional, Agnew, Meghan, additional, Smith, Kane, additional, Moorghen, Morgan, additional, Rodriguez-Justo, Manuel, additional, Jansen, Marnix, additional, East, James, additional, Wang, Lai Mun, additional, Hart, Ailsa, additional, and Graham, Trevor A., additional

Published
2019
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39. Undifferentiated Sarcomas Develop through Distinct Evolutionary Pathways

Author

Steele, Christopher D., primary, Tarabichi, Maxime, additional, Oukrif, Dahmane, additional, Webster, Amy P., additional, Ye, Hongtao, additional, Fittall, Matthew, additional, Lombard, Patrick, additional, Martincorena, Iñigo, additional, Tarpey, Patrick S., additional, Collord, Grace, additional, Haase, Kerstin, additional, Strauss, Sandra J., additional, Berisha, Fitim, additional, Vaikkinen, Heli, additional, Dhami, Pawan, additional, Jansen, Marnix, additional, Behjati, Sam, additional, Amary, M. Fernanda, additional, Tirabosco, Roberto, additional, Feber, Andrew, additional, Campbell, Peter J., additional, Alexandrov, Ludmil B., additional, Van Loo, Peter, additional, Flanagan, Adrienne M., additional, and Pillay, Nischalan, additional

Published
2019
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40. Risk of lymph node metastases in patients with T1b oesophageal adenocarcinoma: A retrospective single centre experience

Author

Graham, David, primary, Sever, Nejc, additional, Magee, Cormac, additional, Waddingham, William, additional, Banks, Matthew, additional, Sweis, Rami, additional, Al-Yousuf, Hannah, additional, Mitchison, Miriam, additional, Alzoubaidi, Durayd, additional, Rodriguez-Justo, Manuel, additional, Lovat, Laurence, additional, Novelli, Marco, additional, Jansen, Marnix, additional, and Haidry, Rehan, additional

Published
2018
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41. Quality indicators for Barrett's endotherapy (QBeT): UK consensus statements for patients undergoing endoscopic therapy for Barrett's neoplasia.

Author

Alzoubaidi, Durayd, Ragunath, Krish, Wani, Sachin, Penman, Ian D., Trudgill, Nigel John, Jansen, Marnix, Banks, Matthew, Bhandari, Pradeep, Morris, Allan John, Willert, Robert, Boger, Phil, Smart, Howard L., Ravi, Narayanasamy, Dunn, Jason, Gordon, Charles, Mannath, Jayan, Mainie, Inder, di Pietro, Massi, Veitch, Andrew M., and Thorpe, Sally

Published
2020
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42. Abstract 5368: The evolutionary history of human colitis-associated colorectal cancer

Author

Baker, Ann-Marie, primary, Cross, William, additional, Curtius, Kathleen, additional, Choi, Chang-ho Ryan, additional, Al-Bakir, Ibrahim, additional, Temko, Daniel, additional, Martinez, Pierre, additional, Williams, Marc, additional, Davis, Hayley, additional, Biswas, Sujata, additional, Wright, Nicholas A., additional, Moorghen, Morgan, additional, Hayes, Stephen J., additional, Rodriguez-Justo, Manuel, additional, Silver, Andrew, additional, Wang, Lai Mun, additional, Jansen, Marnix, additional, Hart, Ailsa L., additional, Leedham, Simon J., additional, and Graham, Trevor A., additional

Published
2018
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45. 335 - Lineage Tracing in Barrett's Esophagus Reveals both its Origins and Evolution and Suggests that Gland Diversity may be an Important Biomarker for the Progression to Dysplasia in Patients

Author

Evans, James, primary, Carlotti, Emanuela, additional, Williams, Marc, additional, Preston, Sean L., additional, Rodriguez-Justo, Manuel, additional, Wright, Nicholas A., additional, Graham, Trevor A., additional, Jansen, Marnix, additional, and McDonald, Stuart A., additional

Published
2018
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47. Robust RNA-based in situ mutation detection delineates colorectal cancer subclonal evolution

Author

Baker, Ann-Marie, primary, Huang, Weini, additional, Wang, Xiao-Ming Mindy, additional, Jansen, Marnix, additional, Ma, Xiao-Jun, additional, Kim, Jeffrey, additional, Anderson, Courtney M., additional, Wu, Xingyong, additional, Pan, Liuliu, additional, Su, Nan, additional, Luo, Yuling, additional, Domingo, Enric, additional, Heide, Timon, additional, Sottoriva, Andrea, additional, Lewis, Annabelle, additional, Beggs, Andrew D., additional, Wright, Nicholas A., additional, Rodriguez-Justo, Manuel, additional, Park, Emily, additional, Tomlinson, Ian, additional, and Graham, Trevor A., additional

Published
2017
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48. Vitamin D3 suppresses morphological evolution of the cribriform cancerous phenotype

Author

Deevi, Ravi K., McClements, Jane, McCloskey, Karen D., Fatehullah, Aliya, Tkocz, Dorota, Javadi, Arman, Higginson, Robyn, Marsh Durban, Victoria, Jansen, Marnix, Clarke, Alan, Loughrey, Maurice B., and Campbell, Frederick C.

Subjects
RC0254
Abstract

Development of cribriform morphology (CM) heralds malignant change in human colon but lack of mechanistic understanding hampers preventive therapy. This study investigated CM pathobiology in three-dimensional (3D) Caco-2 culture models of colorectal glandular architecture, assessed translational relevance and tested effects of 1,25(OH)2D3, the active form of vitamin D. CM evolution was driven by oncogenic perturbation of the apical polarity (AP) complex comprising PTEN, CDC42 and PRKCZ (phosphatase and tensin homolog, cell division cycle 42 and protein kinase C zeta). Suppression of AP genes initiated a spatiotemporal cascade of mitotic spindle misorientation, apical membrane misalignment and aberrant epithelial configuration. Collectively, these events promoted “Swiss cheese-like” cribriform morphology (CM) comprising multiple abnormal “back to back” lumens surrounded by atypical stratified epithelium, in 3D colorectal gland models. Intestinal cancer driven purely by PTEN-deficiency in transgenic mice developed CM and in human CRC, CM associated with PTEN and PRKCZ readouts. Treatment of PTEN-deficient 3D cultures with 1,25(OH)2D3 upregulated PTEN, rapidly activated CDC42 and PRKCZ, corrected mitotic spindle alignment and suppressed CM development. Conversely, mutationally-activated KRAS blocked 1,25(OH)2D3 rescue of glandular architecture. We conclude that 1,25(OH)2D3 upregulates AP signalling to reverse CM in a KRAS wild type (wt), clinically predictive CRC model system. Vitamin D could be developed as therapy to suppress inception or progression of a subset of colorectal tumors.

Published
2016

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