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296 results on '"Teh, Bin T."'

1. Functional and genetic characterization of three cell lines derived from a single tumor of an Opisthorchis viverrini-associated cholangiocarcinoma patient

Author

Sripa, Banchob, Seubwai, Wunchana, Vaeteewoottacharn, Kulthida, Sawanyawisuth, Kanlayanee, Silsirivanit, Atit, Kaewkong, Worasak, Muisuk, Kanha, Dana, Paweena, Phoomak, Chatchai, Lert-itthiporn, Worachart, Luvira, Vor, Pairojkul, Chawalit, Teh, Bin T., Wongkham, Sopit, Okada, Seiji, and Chamgramol, Yaovalux

Published
2020
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4. Gene profiling suggests a common evolution of bladder cancer subtypes

Author

Hansel, Donna E, Zhang, Zhongfa, Petillo, David, and Teh, Bin T

Abstract

Abstract Background Bladder cancer exists as several distinct subtypes, including urothelial carcinoma (UCa), squamous cell carcinoma (SCCa), adenocarcinoma and small cell carcinoma. These entities, despite showing distinct morphology and clinical behavior, arise from the urothelial lining and are often accompanied by similar precursor/in situ findings. The relationship between these subtypes has not been explored in detail. Methods We compared gene expression analysis of the two most common subtypes of bladder cancer, UCa (n = 10) and SCCa (n = 9), with an additional comparison to normal urothelium from non-cancer patients (n = 8) using Affymetrix GeneChip Human genome arrays (Affymetrix, Santa Clara, CA). The results were stratified by supervised and unsupervised clustering analysis, as well as by overall fold change in gene expression. Results When compared to normal urothelium, UCa showed differential expression of 155 genes using a 5-fold cut-off. Examples of differentially regulated genes included topoisomerases, cancer-related transcription factors and cell cycle mediators. A second comparison of normal urothelium to SCCa showed differential expression of 503 genes, many of which were related to squamous-specific morphology (desmosomal complex, intermediate filaments present within squamous epithelium, squamous cornifying proteins, and molecules upregulated in squamous carcinomas from other anatomic sites). When compared, 137 genes were commonly dysregulated in both UCa and SCCa as compared to normal urothelium. All dysregulated genes in UCa were shared in common with SCCa, with the exception of only 18 genes. Supervised clustering analysis yielded correct classification of lesions in 26/27 (96%) of cases and unsupervised clustering analysis yielded correct classification in 25/27 (92.6%) of cases. Conclusions The results from this analysis suggest that bladder SCCa shares a significant number of gene expression changes with conventional UCa, but also demonstrates an additional set of alterations that is unique to this entity that defines the squamous phenotype. The similarity in deregulated gene products suggests that SCCa may be a much more closely related entity at the molecular level to conventional UCa than previously hypothesized.

Published
2013

6. Supplementary Table 1 from Next-Generation Sequencing of Translocation Renal Cell Carcinoma Reveals Novel RNA Splicing Partners and Frequent Mutations of Chromatin-Remodeling Genes

Author

Malouf, Gabriel G., primary, Su, Xiaoping, primary, Yao, Hui, primary, Gao, Jianjun, primary, Xiong, Liangwen, primary, He, Qiuming, primary, Compérat, Eva, primary, Couturier, Jérôme, primary, Molinié, Vincent, primary, Escudier, Bernard, primary, Camparo, Philippe, primary, Doss, Denaha J., primary, Thompson, Erika J., primary, Khayat, David, primary, Wood, Christopher G., primary, Yu, Willie, primary, Teh, Bin T., primary, Weinstein, John, primary, and Tannir, Nizar M., primary

Published
2023
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7. Supplementary Methods from Next-Generation Sequencing of Translocation Renal Cell Carcinoma Reveals Novel RNA Splicing Partners and Frequent Mutations of Chromatin-Remodeling Genes

Author

Malouf, Gabriel G., primary, Su, Xiaoping, primary, Yao, Hui, primary, Gao, Jianjun, primary, Xiong, Liangwen, primary, He, Qiuming, primary, Compérat, Eva, primary, Couturier, Jérôme, primary, Molinié, Vincent, primary, Escudier, Bernard, primary, Camparo, Philippe, primary, Doss, Denaha J., primary, Thompson, Erika J., primary, Khayat, David, primary, Wood, Christopher G., primary, Yu, Willie, primary, Teh, Bin T., primary, Weinstein, John, primary, and Tannir, Nizar M., primary

Published
2023
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8. Supplementary Figure S1 from The Investigational Aurora Kinase A Inhibitor MLN8237 Induces Defects in Cell Viability and Cell-Cycle Progression in Malignant Bladder Cancer Cells In Vitro and In Vivo

Author

Zhou, Ning, primary, Singh, Kamini, primary, Mir, Maria C., primary, Parker, Yvonne, primary, Lindner, Daniel, primary, Dreicer, Robert, primary, Ecsedy, Jeffrey A., primary, Zhang, Zhongfa, primary, Teh, Bin T., primary, Almasan, Alexandru, primary, and Hansel, Donna E., primary

Published
2023
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9. Supplementary Table 3 from Next-Generation Sequencing of Translocation Renal Cell Carcinoma Reveals Novel RNA Splicing Partners and Frequent Mutations of Chromatin-Remodeling Genes

Author

Malouf, Gabriel G., primary, Su, Xiaoping, primary, Yao, Hui, primary, Gao, Jianjun, primary, Xiong, Liangwen, primary, He, Qiuming, primary, Compérat, Eva, primary, Couturier, Jérôme, primary, Molinié, Vincent, primary, Escudier, Bernard, primary, Camparo, Philippe, primary, Doss, Denaha J., primary, Thompson, Erika J., primary, Khayat, David, primary, Wood, Christopher G., primary, Yu, Willie, primary, Teh, Bin T., primary, Weinstein, John, primary, and Tannir, Nizar M., primary

Published
2023
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10. Supplementary Table 2 from Next-Generation Sequencing of Translocation Renal Cell Carcinoma Reveals Novel RNA Splicing Partners and Frequent Mutations of Chromatin-Remodeling Genes

Author

Malouf, Gabriel G., primary, Su, Xiaoping, primary, Yao, Hui, primary, Gao, Jianjun, primary, Xiong, Liangwen, primary, He, Qiuming, primary, Compérat, Eva, primary, Couturier, Jérôme, primary, Molinié, Vincent, primary, Escudier, Bernard, primary, Camparo, Philippe, primary, Doss, Denaha J., primary, Thompson, Erika J., primary, Khayat, David, primary, Wood, Christopher G., primary, Yu, Willie, primary, Teh, Bin T., primary, Weinstein, John, primary, and Tannir, Nizar M., primary

Published
2023
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11. Supplementary Data from Prognostic Value of Tumor Necrosis Factor–Related Apoptosis-Inducing Ligand (TRAIL) and TRAIL Receptors in Renal Cell Cancer

Author

Macher-Goeppinger, Stephan, primary, Aulmann, Sebastian, primary, Tagscherer, Katrin E., primary, Wagener, Nina, primary, Haferkamp, Axel, primary, Penzel, Roland, primary, Brauckhoff, Antje, primary, Hohenfellner, Markus, primary, Sykora, Jaromir, primary, Walczak, Henning, primary, Teh, Bin T., primary, Autschbach, Frank, primary, Herpel, Esther, primary, Schirmacher, Peter, primary, and Roth, Wilfried, primary

Published
2023
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12. Supplementary Table 4 from Next-Generation Sequencing of Translocation Renal Cell Carcinoma Reveals Novel RNA Splicing Partners and Frequent Mutations of Chromatin-Remodeling Genes

Author

Malouf, Gabriel G., primary, Su, Xiaoping, primary, Yao, Hui, primary, Gao, Jianjun, primary, Xiong, Liangwen, primary, He, Qiuming, primary, Compérat, Eva, primary, Couturier, Jérôme, primary, Molinié, Vincent, primary, Escudier, Bernard, primary, Camparo, Philippe, primary, Doss, Denaha J., primary, Thompson, Erika J., primary, Khayat, David, primary, Wood, Christopher G., primary, Yu, Willie, primary, Teh, Bin T., primary, Weinstein, John, primary, and Tannir, Nizar M., primary

Published
2023
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13. Supplementary Table 5 from Next-Generation Sequencing of Translocation Renal Cell Carcinoma Reveals Novel RNA Splicing Partners and Frequent Mutations of Chromatin-Remodeling Genes

Author

Malouf, Gabriel G., primary, Su, Xiaoping, primary, Yao, Hui, primary, Gao, Jianjun, primary, Xiong, Liangwen, primary, He, Qiuming, primary, Compérat, Eva, primary, Couturier, Jérôme, primary, Molinié, Vincent, primary, Escudier, Bernard, primary, Camparo, Philippe, primary, Doss, Denaha J., primary, Thompson, Erika J., primary, Khayat, David, primary, Wood, Christopher G., primary, Yu, Willie, primary, Teh, Bin T., primary, Weinstein, John, primary, and Tannir, Nizar M., primary

Published
2023
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14. Supplementary Figure Legends from The Investigational Aurora Kinase A Inhibitor MLN8237 Induces Defects in Cell Viability and Cell-Cycle Progression in Malignant Bladder Cancer Cells In Vitro and In Vivo

Author

Zhou, Ning, primary, Singh, Kamini, primary, Mir, Maria C., primary, Parker, Yvonne, primary, Lindner, Daniel, primary, Dreicer, Robert, primary, Ecsedy, Jeffrey A., primary, Zhang, Zhongfa, primary, Teh, Bin T., primary, Almasan, Alexandru, primary, and Hansel, Donna E., primary

Published
2023
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15. Supplementary Table 6 from Next-Generation Sequencing of Translocation Renal Cell Carcinoma Reveals Novel RNA Splicing Partners and Frequent Mutations of Chromatin-Remodeling Genes

Author

Malouf, Gabriel G., primary, Su, Xiaoping, primary, Yao, Hui, primary, Gao, Jianjun, primary, Xiong, Liangwen, primary, He, Qiuming, primary, Compérat, Eva, primary, Couturier, Jérôme, primary, Molinié, Vincent, primary, Escudier, Bernard, primary, Camparo, Philippe, primary, Doss, Denaha J., primary, Thompson, Erika J., primary, Khayat, David, primary, Wood, Christopher G., primary, Yu, Willie, primary, Teh, Bin T., primary, Weinstein, John, primary, and Tannir, Nizar M., primary

Published
2023
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16. Supplementary Figure 1 from Next-Generation Sequencing of Translocation Renal Cell Carcinoma Reveals Novel RNA Splicing Partners and Frequent Mutations of Chromatin-Remodeling Genes

Author

Malouf, Gabriel G., primary, Su, Xiaoping, primary, Yao, Hui, primary, Gao, Jianjun, primary, Xiong, Liangwen, primary, He, Qiuming, primary, Compérat, Eva, primary, Couturier, Jérôme, primary, Molinié, Vincent, primary, Escudier, Bernard, primary, Camparo, Philippe, primary, Doss, Denaha J., primary, Thompson, Erika J., primary, Khayat, David, primary, Wood, Christopher G., primary, Yu, Willie, primary, Teh, Bin T., primary, Weinstein, John, primary, and Tannir, Nizar M., primary

Published
2023
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23. 6 Supplementary Tables from Gene Expression of Parathyroid Tumors

Author

Haven, Carola J., primary, Howell, Viive M., primary, Eilers, Paul H. C., primary, Dunne, Robert, primary, Takahashi, Masayuki, primary, van Puijenbroek, Marjo, primary, Furge, Kyle, primary, Kievit, Job, primary, Tan, Min-Han, primary, Fleuren, Gert Jan, primary, Robinson, Bruce G., primary, Delbridge, Leigh W., primary, Philips, Jeanette, primary, Nelson, Anne E., primary, Krause, Ulf, primary, Dralle, Henning, primary, Hoang-Vu, Cuong, primary, Gimm, Oliver, primary, Morreau, Hans, primary, Marsh, Deborah J., primary, and Teh, Bin T., primary

Published
2023
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28. Clear cell sarcomas of the kidney are characterised by BCOR gene abnormalities, including exon 15 internal tandem duplications and BCOR–CCNB3 gene fusion

Author

Wong, Meng K, Ng, Cedric C Y, Kuick, Chik H, Aw, Sze J, Rajasegaran, Vikneswari, Lim, Jing Q, Sudhanshi, Jain, Loh, Eva, Yin, Minzhi, Ma, Jing, Zhang, Zhongde, Iyer, Prasad, Loh, Amos H P, Lian, Derrick W Q, Wang, Shi, Goh, Shaun G H, Lim, Tse H, Lim, Alvin S T, Ng, Tony, Goytain, Angela, Loh, Alwin H L, Tan, Puay H, Teh, Bin T, and Chang, Kenneth T E

Published
2018
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36. A germline mutation in PBRM1 predisposes to renal cell carcinoma

Author

Benusiglio, Patrick R, Couvé, Sophie, Gilbert-Dussardier, Brigitte, Deveaux, Sophie, Le Jeune, Hélène, Da Costa, Mélanie, Fromont, Gaëlle, Memeteau, Françoise, Yacoub, Mokrane, Coupier, Isabelle, Leroux, Dominique, Méjean, Arnaud, Escudier, Bernard, Giraud, Sophie, Gimenez-Roqueplo, Anne-Paule, Blondel, Christophe, Frouin, Eric, Teh, Bin T, Ferlicot, Sophie, Bressac-de Paillerets, Brigitte, Richard, Stéphane, and Gad, Sophie

Published
2015
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37. Whole-Exome Sequencing Studies of Parathyroid Carcinomas Reveal Novel PRUNE2 Mutations, Distinctive Mutational Spectra Related to APOBEC-Catalyzed DNA Mutagenesis and Mutational Enrichment in Kinases Associated With Cell Migration and Invasion

Author

Yu, Willie, McPherson, John R, Stevenson, Mark, van Eijk, Ronald, Heng, Hong Lee, Newey, Paul, Gan, Anna, Ruano, Dina, Huang, Dachuan, Poon, Song Ling, Ong, Choon Kiat, van Wezel, Tom, Cavaco, Branca, Rozen, Steven G, Tan, Patrick, Teh, Bin T, Thakker, Rajesh V, and Morreau, Hans

Published
2015

39. Signatures of mutation and selection in the cancer genome

Author

Bignell, Graham R., Greenman, Chris D., Davies, Helen, Butler, Adam P., Edkins, Sarah, Andrews, Jenny M., Buck, Gemma, Chen, Lina, Beare, David, Latimer, Calli, Widaa, Sara, Hinton, Jonathon, Fahey, Ciara, Fu, Beiyuan, Swamy, Sajani, Dalgliesh, Gillian L., Teh, Bin T., Deloukas, Panos, Yang, Fengtang, Campbell, Peter J., Futreal, P. Andrew, and Stratton, Michael R.

Subjects
Gene mutations -- Health aspects -- Research, Carcinogenesis -- Risk factors -- Genetic aspects -- Research, Cancer -- Genetic aspects, Environmental issues, Science and technology, Zoology and wildlife conservation
Abstract

The cancer genome is moulded by the dual processes of somatic mutation and selection. Homozygous deletions in cancer genomes occur over recessive cancer genes, where they can confer selective growth advantage, and over fragile sites, where they are thought to reflect an increased local rate of DNA breakage. However, most homozygous deletions in cancer genomes are unexplained. Here we identified 2,428 somatic homozygous deletions in 746 cancer cell lines. These overlie 11% of protein-coding genes that, therefore, are not mandatory for survival of human cells. We derived structural signatures that distinguish between homozygous deletions over recessive cancer genes and fragile sites. Application to clusters of unexplained homozygous deletions suggests that many are in regions of inherent fragility, whereas a small subset overlies recessive cancer genes. The results illustrate how structural signatures can be used to distinguish between the influences of mutation and selection in cancer genomes. The extensive copy number, genotyping, sequence and expression data available for this large series of publicly available cancer cell lines renders them informative reagents for future studies of cancer biology and drug discovery., The genome of a cancer cell usually carries several somatic changes (1). A subset, termed 'driver' mutations, confer clonal growth advantage, are positively selected and are causally implicated in cancer [...]

Published
2010
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43. Whole exome sequencing identifies clinically relevant mutational signatures in resected hepatocellular carcinoma

Author

Chan, Jason Y., primary, Lim, Abner H., additional, Boot, Arnoud, additional, Lee, Elizabeth, additional, Ng, Cedric C.‐Y., additional, Lee, Jing Y., additional, Rajasegaran, Vikneswari, additional, Liu, Wei, additional, Goh, Shane, additional, Hong, Jing H., additional, Xu, Xiaoying, additional, Bharwani, Lavina D., additional, Chan, Chung Y., additional, Chung, Alexander Y. F., additional, Cheow, Peng C., additional, Tan, Chee‐Kiat, additional, Ho, Choon K., additional, Liau, Kui H., additional, Woon, Winston W. L., additional, Low, Jee K., additional, Chopra, Akhil, additional, Lopes, Gilberto, additional, Rozen, Steven G., additional, Teh, Bin T., additional, and Chang, Alex Y.‐C., additional

Published
2020
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46. Expression and chromosomal localization of the Requiem gene

Author

Gabig, Theodore G., Crean, Colin D., Klenk, Alison, Long, Haiyan, Copeland, Neal G., Gilbert, Debra J., Jenkins, Nancy A., Quincey, Danielle, Parente, Fabienne, Lespinasse, Françoise, Carle, Georges F., Gaudray, Patrick, Zhang, Chang X., Calender, Alain, Hoeppener, Jo, Kas, Koen, Thakker, Rajesh V., Farnebo, Filip, Teh, Bin T., Larsson, Catharina, Piehl, Fredrik, Lagercrantz, Jacob, Khodaei, Shideh, Carson, Emma, and Weber, Günther

Published
1998
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