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14 results on '"Ong, Swee Hoe"'

2. Organismal metabolism regulates the expansion of oncogenic PIK3CA mutant clones in normal esophagus

Author

Herms, Albert, Colom, Bartomeu, Piedrafita, Gabriel, Kalogeropoulou, Argyro, Banerjee, Ujjwal, King, Charlotte, Abby, Emilie, Murai, Kasumi, Caseda, Irene, Fernandez-Antoran, David, Ong, Swee Hoe, Hall, Michael W. J., Bryant, Christopher, Sood, Roshan K., Fowler, Joanna C., Pol, Albert, Frezza, Christian, Vanhaesebroeck, Bart, and Jones, Philip H.

Published
2024
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3. Self-sustaining long-term 3D epithelioid cultures reveal drivers of clonal expansion in esophageal epithelium

Author

Herms, Albert, Fernandez-Antoran, David, Alcolea, Maria P., Kalogeropoulou, Argyro, Banerjee, Ujjwal, Piedrafita, Gabriel, Abby, Emilie, Valverde-Lopez, Jose Antonio, Ferreira, Inês S., Caseda, Irene, Bejar, Maria T., Dentro, Stefan C., Vidal-Notari, Sara, Ong, Swee Hoe, Colom, Bartomeu, Murai, Kasumi, King, Charlotte, Mahbubani, Krishnaa, Saeb-Parsy, Kourosh, Lowe, Alan R., Gerstung, Moritz, and Jones, Philip H.

Published
2024
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5. AKT-mTORC1 reactivation is the dominant resistance driver for PI3Kβ/AKT inhibitors in PTEN-null breast cancer and can be overcome by combining with Mcl-1 inhibitors

Author

Dunn, Shanade, Eberlein, Cath, Yu, Jason, Gris-Oliver, Albert, Ong, Swee Hoe, Yelland, Urs, Cureton, Natalie, Staniszewska, Anna, McEwen, Robert, Fox, Millie, Pilling, James, Hopcroft, Philip, Coker, Elizabeth A., Jaaks, Patricia, Garnett, Mathew J., Isherwood, Beverley, Serra, Violeta, Davies, Barry R., Barry, Simon T., Lynch, James T., and Yusa, Kosuke

Published
2022
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7. Organismal metabolism regulates the expansion of oncogenic PIK3CAmutant clones in normal esophagus

Author

Herms, Albert, Colom, Bartomeu, Piedrafita, Gabriel, Kalogeropoulou, Argyro, Banerjee, Ujjwal, King, Charlotte, Abby, Emilie, Murai, Kasumi, Caseda, Irene, Fernandez-Antoran, David, Ong, Swee Hoe, Hall, Michael W. J., Bryant, Christopher, Sood, Roshan K., Fowler, Joanna C., Pol, Albert, Frezza, Christian, Vanhaesebroeck, Bart, and Jones, Philip H.

Abstract

Oncogenic PIK3CAmutations generate large clones in aging human esophagus. Here we investigate the behavior of Pik3camutant clones in the normal esophageal epithelium of transgenic mice. Expression of a heterozygous Pik3caH1047Rmutation drives clonal expansion by tilting cell fate toward proliferation. CRISPR screening and inhibitor treatment of primary esophageal keratinocytes confirmed the PI3K–mTOR pathway increased mutant cell competitive fitness. The antidiabetic drug metformin reduced mutant cell advantage in vivo and in vitro. Conversely, metabolic conditions such as type 1 diabetes or diet-induced obesity enhanced the competitive fitness of Pik3caH1047Rcells. Consistently, we found a higher density of PIK3CAgain-of-function mutations in the esophagus of individuals with high body mass index compared with those with normal weight. We conclude that the metabolic environment selectively influences the evolution of the normal epithelial mutational landscape. Clinically feasible interventions to even out signaling imbalances between wild-type and mutant cells may limit the expansion of oncogenic mutants in normal tissues.

Published
2024
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8. Data from Selection of Oncogenic Mutant Clones in Normal Human Skin Varies with Body Site

Author

Fowler, Joanna C., primary, King, Charlotte, primary, Bryant, Christopher, primary, Hall, Michael W.J., primary, Sood, Roshan, primary, Ong, Swee Hoe, primary, Earp, Eleanor, primary, Fernandez-Antoran, David, primary, Koeppel, Jonas, primary, Dentro, Stefan C., primary, Shorthouse, David, primary, Durrani, Amer, primary, Fife, Kate, primary, Rytina, Edward, primary, Milne, Doreen, primary, Roshan, Amit, primary, Mahububani, Krishnaa, primary, Saeb-Parsy, Kourosh, primary, Hall, Benjamin A., primary, Gerstung, Moritz, primary, and Jones, Philip H., primary

Published
2023
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9. Supplementary Data from Selection of Oncogenic Mutant Clones in Normal Human Skin Varies with Body Site

Author

Fowler, Joanna C., primary, King, Charlotte, primary, Bryant, Christopher, primary, Hall, Michael W.J., primary, Sood, Roshan, primary, Ong, Swee Hoe, primary, Earp, Eleanor, primary, Fernandez-Antoran, David, primary, Koeppel, Jonas, primary, Dentro, Stefan C., primary, Shorthouse, David, primary, Durrani, Amer, primary, Fife, Kate, primary, Rytina, Edward, primary, Milne, Doreen, primary, Roshan, Amit, primary, Mahububani, Krishnaa, primary, Saeb-Parsy, Kourosh, primary, Hall, Benjamin A., primary, Gerstung, Moritz, primary, and Jones, Philip H., primary

Published
2023
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10. Epithelioids: Self-sustaining 3D epithelial cultures to study long-term processes

Author

Herms, Albert, primary, Fernandez-Antoran, David, additional, Alcolea, Maria P., additional, Kalogeropoulou, Argyro, additional, Banerjee, Ujjwal, additional, Piedrafita, Gabriel, additional, Abby, Emilie, additional, Valverde-Lopez, Jose Antonio, additional, Ferreira, Inês S., additional, Dentro, Stefan C., additional, Ong, Swee Hoe, additional, Colom, Bartomeu, additional, Murai, Kasumi, additional, King, Charlotte, additional, Mahbubani, Krishnaa, additional, Saeb-Parsy, Kourosh, additional, Lowe, Alan R, additional, Gerstung, Moritz, additional, and Jones, Philip H, additional

Published
2023
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11. HIV-phyloTSI: Subtype-independent estimation of time since HIV-1 infection for cross-sectional measures of population incidence using deep sequence data

Author

Golubchik, Tanya, Abeler-Dörner, Lucie, Hall, Matthew, Wymant, Chris, Bonsall, David, Macintyre-Cockett, George, Thomson, Laura, Baeten, Jared, Celum, Connie, Galiwango, Ronald, Kosloff, Barry, Limbada, Mohammed, Mujugira, Andrew, Mugo, Nelly, Gall, Astrid, Blanquart, François, Bakker, Margreet, Bezemer, Daniela, Ong, Swee Hoe, Albert, Jan, Bannert, Norbert, Fellay, Jacques, Gunsenheimer-Bartmeyer, Barbara, Günthard, Huldrych, Kivelä, Pia, Kouyos, Roger, Meyer, Laurence, Porter, Kholoud, van Sighem, Ard, van der Valk, Mark, Berkhout, Ben, Kellam, Paul, Cornelissen, Marion, Reiss, Peter, Ayles, Helen, Burns, David, Fidler, Sarah, Grabowski, Mary Kate, Hayes, Richard, Herbeck, Joshua, Kagaayi, Joseph, Kaleebu, Pontiano, Lingappa, Jairam, Ssemwanga, Deogratius, Eshleman, Susan, Cohen, Myron, Ratmann, Oliver, Laeyendecker, Oliver, Fraser, Christophe, Blanquart, François, Centre interdisciplinaire de recherche en biologie (CIRB), Labex MemoLife, École normale supérieure - Paris (ENS-PSL), Université Paris sciences et lettres (PSL)-Université Paris sciences et lettres (PSL)-Collège de France (CdF (institution))-Ecole Superieure de Physique et de Chimie Industrielles de la Ville de Paris (ESPCI Paris), Université Paris sciences et lettres (PSL)-École normale supérieure - Paris (ENS-PSL), Université Paris sciences et lettres (PSL)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Infection, Anti-microbiens, Modélisation, Evolution (IAME (UMR_S_1137 / U1137)), Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Paris Cité (UPCité)-Université Sorbonne Paris Nord, Centre de recherche en épidémiologie et santé des populations (CESP), Université de Versailles Saint-Quentin-en-Yvelines (UVSQ)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Hôpital Paul Brousse-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Paris-Saclay, and On behalf of the HPTN 071 (PopART) Phylogenetics protocol team, the BEEHIVE collaboration and the PANGEA consortium

Subjects
[SDV] Life Sciences [q-bio], [SDV]Life Sciences [q-bio]
Abstract

Estimating the time since HIV infection (TSI) at population level is essential for tracking changes in the global HIV epidemic. Most methods for determining duration of infection classify samples into recent and non-recent and are unable to give more granular TSI estimates. These binary classifications have a limited recency time window of several months, therefore requiring large sample sizes, and cannot assess the cumulative impact of an intervention. We developed a Random Forest Regression model, HIV-phyloTSI, that combines measures of within-host diversity and divergence to generate TSI estimates from viral deep-sequencing data, with no need for additional variables. HIV-phyloTSI provides a continuous measure of TSI up to 9 years, with a mean absolute error of less than 12 months overall and less than 5 months for infections with a TSI of up to a year. It performed equally well for all major HIV subtypes based on data from African and European cohorts. We demonstrate how HIV-phyloTSI can be used for incidence estimates on a population level.

Published
2022
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12. Notch1mutations drive clonal expansion in normal esophageal epithelium but impair tumor growth

Author

Abby, Emilie, Dentro, Stefan C., Hall, Michael W. J., Fowler, Joanna C., Ong, Swee Hoe, Sood, Roshan, Herms, Albert, Piedrafita, Gabriel, Abnizova, Irina, Siebel, Christian W., Gerstung, Moritz, Hall, Benjamin A., and Jones, Philip H.

Abstract

NOTCH1mutant clones occupy the majority of normal human esophagus by middle age but are comparatively rare in esophageal cancers, suggesting NOTCH1mutations drive clonal expansion but impede carcinogenesis. Here we test this hypothesis. Sequencing NOTCH1mutant clones in aging human esophagus reveals frequent biallelic mutations that block NOTCH1signaling. In mouse esophagus, heterozygous Notch1mutation confers a competitive advantage over wild-type cells, an effect enhanced by loss of the second allele. Widespread Notch1loss alters transcription but has minimal effects on the epithelial structure and cell dynamics. In a carcinogenesis model, Notch1mutations were less prevalent in tumors than normal epithelium. Deletion of Notch1reduced tumor growth, an effect recapitulated by anti-NOTCH1 antibody treatment. Notch1null tumors showed reduced proliferation. We conclude that Notch1mutations in normal epithelium are beneficial as wild-type Notch1favors tumor expansion. NOTCH1 blockade may have therapeutic potential in preventing esophageal squamous cancer.

Published
2023
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13. Notch1 mutations drive clonal expansion in normal esophageal epithelium but impair tumor growth

Author

Emilie Abby, Stefan C. Dentro, Michael W. J. Hall, Joanna C. Fowler, Swee Hoe Ong, Roshan Sood, Albert Herms, Gabriel Piedrafita, Irina Abnizova, Christian W. Siebel, Moritz Gerstung, Benjamin A. Hall, Philip H. Jones, Dentro, Stefan C [0000-0002-0478-9729], Hall, Michael WJ [0000-0003-2904-6902], Ong, Swee Hoe [0000-0002-3629-5387], Sood, Roshan [0000-0002-1318-7025], Herms, Albert [0000-0003-2999-8196], Piedrafita, Gabriel [0000-0001-8701-1084], Gerstung, Moritz [0000-0001-6709-963X], Hall, Benjamin A [0000-0003-0355-2946], Jones, Philip H [0000-0002-5904-795X], and Apollo - University of Cambridge Repository

Subjects
45/91, 64, Esophageal Neoplasms, 631/67/1504/1477, 45, Carcinogenesis, 45/41, article, 45/23, 64/110, Middle Aged, Epithelium, 38, 631/208/514/1948, Mice, 631/532/7, Mutation, 14/63, Genetics, Animals, Humans, Receptor, Notch1, 14/19
Abstract

NOTCH1 mutant clones occupy the majority of normal human esophagus by middle age but are comparatively rare in esophageal cancers, suggesting NOTCH1 mutations drive clonal expansion but impede carcinogenesis. Here we test this hypothesis. Sequencing NOTCH1 mutant clones in aging human esophagus reveals frequent biallelic mutations that block NOTCH1 signaling. In mouse esophagus, heterozygous Notch1 mutation confers a competitive advantage over wild-type cells, an effect enhanced by loss of the second allele. Widespread Notch1 loss alters transcription but has minimal effects on the epithelial structure and cell dynamics. In a carcinogenesis model, Notch1 mutations were less prevalent in tumors than normal epithelium. Deletion of Notch1 reduced tumor growth, an effect recapitulated by anti-NOTCH1 antibody treatment. Notch1 null tumors showed reduced proliferation. We conclude that Notch1 mutations in normal epithelium are beneficial as wild-type Notch1 favors tumor expansion. NOTCH1 blockade may have therapeutic potential in preventing esophageal squamous cancer.

Published
2023

14. Phylogenetic estimation of the viral fitness landscape of HIV-1 set-point viral load.

Author

Zhao L, Wymant C, Blanquart F, Golubchik T, Gall A, Bakker M, Bezemer D, Hall M, Ong SH, Albert J, Bannert N, Fellay J, Grabowski MK, Gunsenheimer-Bartmeyer B, Günthard HF, Kivelä P, Kouyos RD, Laeyendecker O, Meyer L, Porter K, van Sighem A, van der Valk M, Berkhout B, Kellam P, Cornelissen M, Reiss P, Fraser C, and Ferretti L

Abstract

Set-point viral load (SPVL), a common measure of human immunodeficiency virus (HIV)-1 virulence, is partially determined by viral genotype. Epidemiological evidence suggests that this viral property has been under stabilising selection, with a typical optimum for the virus between 10 4 and 10 5 copies of viral RNA per ml. Here we aimed to detect transmission fitness differences between viruses from individuals with different SPVLs directly from phylogenetic trees inferred from whole-genome sequences. We used the local branching index (LBI) as a proxy for transmission fitness. We found that LBI is more sensitive to differences in infectiousness than to differences in the duration of the infectious state. By analysing subtype-B samples from the Bridging the Evolution and Epidemiology of HIV in Europe project, we inferred a significant positive relationship between SPVL and LBI up to approximately 10 5 copies/ml, with some evidence for a peak around this value of SPVL. This is evidence of selection against low values of SPVL in HIV-1 subtype-B strains, likely related to lower infectiousness, and perhaps a peak in the transmission fitness in the expected range of SPVL. The less prominent signatures of selection against higher SPVL could be explained by an inherent limit of the method or the deployment of antiretroviral therapy., (© The Author(s) 2022. Published by Oxford University Press.)

Published
2022
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