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10 results on '"Ko, Tun Kiat"'

1. Single-cell landscape of idiopathic multicentric Castleman disease in identical twins

Author

Chan, Jason Yongsheng, primary, Loh, Jui Wan, additional, Lim, Jing Quan, additional, Liany, Herty, additional, Lee, Elizabeth Chun Yong, additional, Lee, Jing Yi, additional, Kannan, Bavani, additional, Lim, Boon Yee, additional, Guo, Zexi, additional, Lim, Kerry, additional, Ha, Jeslin Chian Hung, additional, Ng, Cedric Chuan-Young, additional, Ko, Tun Kiat, additional, Huang, Dachuan, additional, Seow, Dominique Yuan Bin, additional, Cheng, Chee Leong, additional, Chan, Sock Hoai, additional, Ngeow, Joanne, additional, Teh, Bin Tean, additional, Lim, Soon Thye, additional, and Ong, Choon Kiat, additional

Published
2024
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2. An integrative model of pathway convergence in genetically heterogeneous blast crisis chronic myeloid leukemia

Author

Ko, Tun Kiat, Javed, Asif, Lee, Kian Leong, Pathiraja, Thushangi N., Liu, Xingliang, Malik, Simeen, Soh, Sheila Xinxuan, Heng, Xiu Ting, Takahashi, Naoto, Tan, Joanna H.J., Bhatia, Ravi, Khng, Alexis J., Chng, Wee-Joo, Sia, Yee Yen, Fruman, David A., Ng, King Pan, Chan, Zhu En, Xie, Kim Jiajing, Hoi, Qiangze, Chan, Cheryl Xueli, Teo, Audrey S.M., Velazquez Camacho, Oscar, Meah, Wee Yang, Khor, Chiea Chuen, Ong, Chin Thing J., Soon, Wei Jia W., Tan, Patrick, Ng, Pauline C., Chuah, Charles, Hillmer, Axel M., and Ong, S. Tiong

Published
2020
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3. Therapeutic Repurposing of Brincidofovir in Natural Killer/T-Cell Lymphoma Reveals Potent Induction of Replication Stress, Sting Pathway Activation and Immunogenic Cell Death

Author

Chan, Jason Yongsheng, primary, Lee, Elizabeth Chun Yong, additional, Chai, Kelila Xin Ye, additional, Lee, Jing Yi, additional, Kannan, Bavani, additional, Lim, Boon Yee, additional, Kok, Jessica Sook-Ting, additional, Li, Zhimei, additional, Loh, Jui Wan, additional, Ko, Tun Kiat, additional, Lim, Kah Suan, additional, Ng, Cedric Chuan-Young, additional, Lim, Kerry, additional, Huang, Dachuan, additional, Lim, Jing Quan, additional, Hazama, Masatoshi, additional, Fukushima, Koji, additional, Teh, Bin Tean, additional, Lim, Soon Thye, additional, and Ong, Choon Kiat, additional

Published
2022
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4. Functional Analysis of the CML Blast Crisis Transcriptome and Epigenome Using Crispr-CAS9 and Pharmacologic Approaches

Author

Ko, Tun Kiat, primary, Soh, Xin Xuan Sheila, additional, Yu, Willie, additional, Winter, Peter S., additional, Pathiraja, Thushangi, additional, Javed, Asif, additional, Malik, Simeen, additional, Tan, Joanna H.J., additional, Chuah, Charles, additional, Takahashi, Naoto, additional, Bhatia, Ravi, additional, Chng, Wee Joo, additional, Valent, Peter, additional, Cerny-Reiterer, Sabine, additional, Ng, King Pan, additional, Tennakoon, Chandana, additional, Hoi, Qiangze, additional, Guan, Peiyong, additional, Teo, Audrey S.M., additional, Lee, Wah Heng, additional, Tan, Patrick, additional, Sung, Win Kin, additional, Ng, Pauline, additional, Hillmer, Axel, additional, Wood, Kris C., additional, Rozen, Steve, additional, and Ong, S. Tiong, additional

Published
2015
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5. The Genomic and Epigenomic Landscapes of Blast Crisis Transformation in Chronic Myeloid Leukemia

Author

Ong, S. Tiong, primary, Pathiraja, Thushangi, additional, Javed, Asif, additional, Soh, Xin Xuan Sheila, additional, Malik, Simeen, additional, Tan, Joanna H.J., additional, Ko, Tun Kiat, additional, Chuah, Charles, additional, Takahashi, Naoto, additional, Bhatia, Ravi, additional, Ng, King Pan, additional, Chng, Wee Joo, additional, Tennakoon, Chandana, additional, Hoi, Qiangze, additional, Guan, Peiyong, additional, Teo, Audrey S.M., additional, Lee, Wah Heng, additional, Tan, Patrick, additional, Sung, Win Kin, additional, Ng, Pauline, additional, and Hillmer, Axel, additional

Published
2015
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8. A Common Deletion Polymorphism in the BIM Gene Contributes to Intrinsic Imatinib Resistance in Chronic Myelogenous Leukemia

Author

Hillmer, Axel M, primary, Ng, King-Pan, additional, Chuah, Charles, additional, Juan, Wen Chun, additional, Ko, Tun-Kiat, additional, Teo, Audrey S.M., additional, Ariyaratne, Pramila N, additional, Takahashi, Naoto, additional, Sawada, Kenichi, additional, Fei, Yao, additional, Lee, Wah Heng, additional, Huang, Weijie, additional, Allen, John C, additional, Woo, Xing Yi, additional, Nagarajan, Niranjan, additional, Kumar, Vikrant, additional, Thalamuthu, Anbupalam, additional, Poh, Wan Ting, additional, Ang, Ai Leen, additional, Mya, Hae Tha, additional, How, Gee Fung, additional, Yang, Li Yi, additional, Koh, Liang Piu, additional, Nadarajan, Veera S, additional, Chng, Wee-Joo, additional, Than, Hein, additional, Lim, Lay Cheng, additional, Goh, Yeow-Tee, additional, Nöthen, Markus M, additional, Wong, Tien Y, additional, Shahab, Atif, additional, Ruan, Xiaoan, additional, Cacheux-Rataboul, Valère, additional, Sung, Wing-Kin, additional, Ruan, Yijun, additional, and Ong, S. Tiong, additional

Published
2011
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9. The BIMDeletion Polymorphism: A Paradigm Of a Permissive Interaction Between Germline and Acquired TKI Resistance Factors In Chronic Myeloid Leukemia

Author

Ko, Tun Kiat, Chuah, Charles, Huang, John W.J., Ng, King-Pan, and Ong, S. Tiong

Abstract

Germline polymorphisms and tumor-specific genetic mutations together contribute to the behavior of human cancers, including the response to therapy. However, few specific models allow for the detailed study of how inherited and acquired genetic factors interact to cause clinical drug resistance, nor how their interaction can be prevented or overcome. We recently reported a germline deletion polymorphism in the BIMgene that was sufficient to mediate intrinsic resistance to targeted therapies in cancer, including the example of imatinib in chronic myeloid leukemia (CML) (Ng et al. Nature Medicine, 2012). Mechanistically, the deletion polymorphism led to the generation of BIMsplice forms that lacked the pro-apoptotic BH3 domain, and that were incapable of activating apoptosis in response to targeted therapy. Clinically, we found that CML patients with the deletion polymorphism experienced inferior responses to imatinib. Furthermore, within the cohort of resistant patients harboring the BIMdeletion polymorphism, we found that the majority developed cross-resistance to second or third generation TKI (nilotinib, dasatinib, and bosutinib), and that TKI resistance-conferring BCR-ABL kinase domain mutations were less frequent in patients with the BIMdeletion polymorphism than those without. These observations suggested that the BIMdeletion polymorphism cooperates with both BCR-ABL-independent and -dependent TKI resistance mechanisms to produce broad resistance to TKI.

Published
2013
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10. A Common Deletion Polymorphism in the BIMGene Contributes to Intrinsic Imatinib Resistance in Chronic Myelogenous Leukemia

Author

Hillmer, Axel M, Ng, King-Pan, Chuah, Charles, Juan, Wen Chun, Ko, Tun-Kiat, Teo, Audrey S.M., Ariyaratne, Pramila N, Takahashi, Naoto, Sawada, Kenichi, Fei, Yao, Lee, Wah Heng, Huang, Weijie, Allen, John C, Woo, Xing Yi, Nagarajan, Niranjan, Kumar, Vikrant, Thalamuthu, Anbupalam, Poh, Wan Ting, Ang, Ai Leen, Mya, Hae Tha, How, Gee Fung, Yang, Li Yi, Koh, Liang Piu, Nadarajan, Veera S, Chng, Wee-Joo, Than, Hein, Lim, Lay Cheng, Goh, Yeow-Tee, Nöthen, Markus M, Wong, Tien Y, Shahab, Atif, Ruan, Xiaoan, Cacheux-Rataboul, Valère, Sung, Wing-Kin, Ruan, Yijun, and Ong, S. Tiong

Abstract

Abstract 1666

Published
2011
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