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2. Management of classical Philadelphia chromosome-negative myeloproliferative neoplasms in Asia: consensus of the Asian Myeloid Working Group

Author

Gill, Harinder, Leung, Garret M. K., Ooi, Melissa G. M., Teo, Winnie Z. Y., Wong, Chieh-Lee, Choi, Chul Won, Wong, Gee-Chuan, Lao, Zhentang, Rojnuckarin, Ponlapat, Castillo, Ma. Rosario Irene D., Xiao, Zhijian, Hou, Hsin-An, Kuo, Ming-Chung, Shih, Lee-Yung, Gan, Gin-Gin, Lin, Chien-Chin, Chng, Wee-Joo, and Kwong, Yok-Lam

Published
2023
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4. Molecular taxonomy of myelodysplastic syndromes and its clinical implications

Author

Bernard, Elsa, Hasserjian, Robert P., Greenberg, Peter L., Arango Ossa, Juan E., Creignou, Maria, Tuechler, Heinz, Gutierrez-Abril, Jesus, Domenico, Dylan, Medina-Martinez, Juan S., Levine, Max, Liosis, Konstantinos, Farnoud, Noushin, Sirenko, Maria, Jädersten, Martin, Germing, Ulrich, Sanz, Guillermo, van de Loosdrecht, Arjan A., Nannya, Yasuhito, Kosmider, Olivier, Follo, Matilde Y., Thol, Felicitas, Zamora, Lurdes, Pinheiro, Ronald F., Pellagatti, Andrea, Elias, Harold K., Haase, Detlef, Ganster, Christina, Ades, Lionel, Tobiasson, Magnus, Palomo, Laura, Della Porta, Matteo Giovanni, Fenaux, Pierre, Belickova, Monika, Savona, Michael R., Klimek, Virginia M., Santos, Fabio P. S., Boultwood, Jacqueline, Kotsianidis, Ioannis, Santini, Valeria, Solé, Francesc, Platzbecker, Uwe, Heuser, Michael, Valent, Peter, Finelli, Carlo, Voso, Maria Teresa, Shih, Lee-Yung, Fontenay, Michaela, Jansen, Joop H., Cervera, José, Gattermann, Norbert, Ebert, Benjamin L., Bejar, Rafael, Malcovati, Luca, Ogawa, Seishi, Cazzola, Mario, Hellström-Lindberg, Eva, and Papaemmanuil, Elli

Published
2024
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8. Children with chronic myeloid leukaemia treated with front-line imatinib have a slower molecular response and comparable survival compared with adults: a multicenter experience in Taiwan

Author

Liu, Hsi-Che, Kuo, Ming-Chung, Wu, Kang-Hsi, Chen, Tsai-Yun, Chen, Jiann-Shiuh, Wang, Ming-Chung, Lin, Tung-Liang, Yang, YoungSen, Ma, Ming-Chun, Wang, Po-Nan, Sheen, Jiunn-Ming, Wang, Shih-Chung, Chen, Shih-Hsiang, Jaing, Tang-Her, Cheng, Chao-Neng, Yeh, Ting-Chi, Lin, Tung-Huei, and Shih, Lee-Yung

Published
2023
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9. Clinical characteristics and outcomes of B-cell precursor ALL with MEF2D rearrangements: a retrospective study by the Ponte di Legno Childhood ALL Working Group

Author

Ohki, Kentaro, Butler, Ellie R., Kiyokawa, Nobutaka, Hirabayashi, Shinsuke, Bergmann, Anke K., Möricke, Anja, Boer, Judith M., Cavé, Hélène, Cazzaniga, Giovanni, Yeoh, Allen Eng Juh, Sanada, Masashi, Imamura, Toshihiko, Inaba, Hiroto, Mullighan, Charles G., Loh, Mignon L., Norén-Nyström, Ulrika, Shih, Lee-Yung, Zaliova, Marketa, Pui, Ching-Hon, Haas, Oskar A., Harrison, Christine J., Moorman, Anthony V., and Manabe, Atsushi

Published
2023
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10. Implications of TP53 allelic state for genome stability, clinical presentation and outcomes in myelodysplastic syndromes

Author

Bernard, Elsa, Nannya, Yasuhito, Hasserjian, Robert P, Devlin, Sean M, Tuechler, Heinz, Medina-Martinez, Juan S, Yoshizato, Tetsuichi, Shiozawa, Yusuke, Saiki, Ryunosuke, Malcovati, Luca, Levine, Max F, Arango, Juan E, Zhou, Yangyu, Solé, Francesc, Cargo, Catherine A, Haase, Detlef, Creignou, Maria, Germing, Ulrich, Zhang, Yanming, Gundem, Gunes, Sarian, Araxe, van de Loosdrecht, Arjan A, Jädersten, Martin, Tobiasson, Magnus, Kosmider, Olivier, Follo, Matilde Y, Thol, Felicitas, Pinheiro, Ronald F, Santini, Valeria, Kotsianidis, Ioannis, Boultwood, Jacqueline, Santos, Fabio PS, Schanz, Julie, Kasahara, Senji, Ishikawa, Takayuki, Tsurumi, Hisashi, Takaori-Kondo, Akifumi, Kiguchi, Toru, Polprasert, Chantana, Bennett, John M, Klimek, Virginia M, Savona, Michael R, Belickova, Monika, Ganster, Christina, Palomo, Laura, Sanz, Guillermo, Ades, Lionel, Della Porta, Matteo Giovanni, Elias, Harold K, Smith, Alexandra G, Werner, Yesenia, Patel, Minal, Viale, Agnès, Vanness, Katelynd, Neuberg, Donna S, Stevenson, Kristen E, Menghrajani, Kamal, Bolton, Kelly L, Fenaux, Pierre, Pellagatti, Andrea, Platzbecker, Uwe, Heuser, Michael, Valent, Peter, Chiba, Shigeru, Miyazaki, Yasushi, Finelli, Carlo, Voso, Maria Teresa, Shih, Lee-Yung, Fontenay, Michaela, Jansen, Joop H, Cervera, José, Atsuta, Yoshiko, Gattermann, Norbert, Ebert, Benjamin L, Bejar, Rafael, Greenberg, Peter L, Cazzola, Mario, Hellström-Lindberg, Eva, Ogawa, Seishi, and Papaemmanuil, Elli

Subjects
Biomedical and Clinical Sciences, Oncology and Carcinogenesis, Hematology, Stem Cell Research, Cancer, Clinical Research, Rare Diseases, Genetics, 2.1 Biological and endogenous factors, Aetiology, Alleles, Cohort Studies, DNA Copy Number Variations, DNA Mutational Analysis, Female, Gene Frequency, Genomic Instability, Humans, Loss of Heterozygosity, Male, Mutation, Myelodysplastic Syndromes, Phenotype, Prognosis, Survival Analysis, Treatment Outcome, Tumor Suppressor Protein p53, Medical and Health Sciences, Immunology, Biomedical and clinical sciences, Health sciences
Abstract

Tumor protein p53 (TP53) is the most frequently mutated gene in cancer1,2. In patients with myelodysplastic syndromes (MDS), TP53 mutations are associated with high-risk disease3,4, rapid transformation to acute myeloid leukemia (AML)5, resistance to conventional therapies6-8 and dismal outcomes9. Consistent with the tumor-suppressive role of TP53, patients harbor both mono- and biallelic mutations10. However, the biological and clinical implications of TP53 allelic state have not been fully investigated in MDS or any other cancer type. We analyzed 3,324 patients with MDS for TP53 mutations and allelic imbalances and delineated two subsets of patients with distinct phenotypes and outcomes. One-third of TP53-mutated patients had monoallelic mutations whereas two-thirds had multiple hits (multi-hit) consistent with biallelic targeting. Established associations with complex karyotype, few co-occurring mutations, high-risk presentation and poor outcomes were specific to multi-hit patients only. TP53 multi-hit state predicted risk of death and leukemic transformation independently of the Revised International Prognostic Scoring System (IPSS-R)11. Surprisingly, monoallelic patients did not differ from TP53 wild-type patients in outcomes and response to therapy. This study shows that consideration of TP53 allelic state is critical for diagnostic and prognostic precision in MDS as well as in future correlative studies of treatment response.

Published
2020

12. TP53 mutation status divides myelodysplastic syndromes with complex karyotypes into distinct prognostic subgroups.

Author

Haase, Detlef, Stevenson, Kristen E, Neuberg, Donna, Maciejewski, Jaroslaw P, Nazha, Aziz, Sekeres, Mikkael A, Ebert, Benjamin L, Garcia-Manero, Guillermo, Haferlach, Claudia, Haferlach, Torsten, Kern, Wolfgang, Ogawa, Seishi, Nagata, Yasunobu, Yoshida, Kenichi, Graubert, Timothy A, Walter, Matthew J, List, Alan F, Komrokji, Rami S, Padron, Eric, Sallman, David, Papaemmanuil, Elli, Campbell, Peter J, Savona, Michael R, Seegmiller, Adam, Adès, Lionel, Fenaux, Pierre, Shih, Lee-Yung, Bowen, David, Groves, Michael J, Tauro, Sudhir, Fontenay, Michaela, Kosmider, Olivier, Bar-Natan, Michal, Steensma, David, Stone, Richard, Heuser, Michael, Thol, Felicitas, Cazzola, Mario, Malcovati, Luca, Karsan, Aly, Ganster, Christina, Hellström-Lindberg, Eva, Boultwood, Jacqueline, Pellagatti, Andrea, Santini, Valeria, Quek, Lynn, Vyas, Paresh, Tüchler, Heinz, Greenberg, Peter L, Bejar, Rafael, and International Working Group for MDS Molecular Prognostic Committee

Subjects
International Working Group for MDS Molecular Prognostic Committee, Humans, Myelodysplastic Syndromes, Chromosome Aberrations, Prognosis, Combined Modality Therapy, Survival Rate, Follow-Up Studies, Karyotyping, Mutation, Aged, Aged, 80 and over, Middle Aged, Female, Male, Tumor Suppressor Protein p53, Biomarkers, Tumor, Hematology, Rare Diseases, Genetics, Clinical Sciences, Oncology and Carcinogenesis, Immunology
Abstract

Risk stratification is critical in the care of patients with myelodysplastic syndromes (MDS). Approximately 10% have a complex karyotype (CK), defined as more than two cytogenetic abnormalities, which is a highly adverse prognostic marker. However, CK-MDS can carry a wide range of chromosomal abnormalities and somatic mutations. To refine risk stratification of CK-MDS patients, we examined data from 359 CK-MDS patients shared by the International Working Group for MDS. Mutations were underrepresented with the exception of TP53 mutations, identified in 55% of patients. TP53 mutated patients had even fewer co-mutated genes but were enriched for the del(5q) chromosomal abnormality (p 10%), abnormal 3q, abnormal 9, and monosomy 7 as having the greatest survival risk. The poor risk associated with CK-MDS is driven by its association with prognostically adverse TP53 mutations and can be refined by considering clinical and karyotype features.

Published
2019

13. ASXL2 regulates hematopoiesis in mice and its deficiency promotes myeloid expansion

Author

Madan, Vikas, Han, Lin, Hattori, Norimichi, Teoh, Weoi Woon, Mayakonda, Anand, Sun, Qiao-Yang, Ding, Ling-Wen, Nordin, Hazimah Binte Mohd, Lim, Su Lin, Shyamsunder, Pavithra, Dakle, Pushkar, Sundaresan, Janani, Doan, Ngan B, Sanada, Masashi, Sato-Otsubo, Aiko, Meggendorfer, Manja, Yang, Henry, Said, Jonathan W, Ogawa, Seishi, Haferlach, Torsten, Liang, Der-Cherng, Shih, Lee-Yung, Nakamaki, Tsuyoshi, Wang, Q Tian, and Koeffler, H Phillip

Subjects
Rare Diseases, Human Genome, Childhood Leukemia, Cancer, Pediatric, Hematology, Pediatric Cancer, Genetics, 2.1 Biological and endogenous factors, Aetiology, Acute Disease, Animals, Cell Differentiation, Cell Proliferation, Gene Expression Profiling, Hematopoiesis, Humans, Leukemia, Myeloid, Mice, 129 Strain, Mice, Inbred C57BL, Mice, Knockout, Myeloid Cells, Myelopoiesis, Repressor Proteins, Immunology
Abstract

Chromosomal translocation t(8;21)(q22;q22) which leads to the generation of oncogenic RUNX1-RUNX1T1 (AML1-ETO) fusion is observed in approximately 10% of acute myelogenous leukemia (AML). To identify somatic mutations that co-operate with t(8;21)-driven leukemia, we performed whole and targeted exome sequencing of an Asian cohort at diagnosis and relapse. We identified high frequency of truncating alterations in ASXL2 along with recurrent mutations of KIT, TET2, MGA, FLT3, and DHX15 in this subtype of AML. To investigate in depth the role of ASXL2 in normal hematopoiesis, we utilized a mouse model of ASXL2 deficiency. Loss of ASXL2 caused progressive hematopoietic defects characterized by myeloid hyperplasia, splenomegaly, extramedullary hematopoiesis, and poor reconstitution ability in transplantation models. Parallel analyses of young and >1-year old Asxl2-deficient mice revealed age-dependent perturbations affecting, not only myeloid and erythroid differentiation, but also maturation of lymphoid cells. Overall, these findings establish a critical role for ASXL2 in maintaining steady state hematopoiesis, and provide insights into how its loss primes the expansion of myeloid cells.

Published
2018

14. Real-world study of children and young adults with myeloproliferative neoplasms: identifying risks and unmet needs

Author

Sobas, Marta, Kiladjian, Jean-Jacques, Beauverd, Yan, Curto-Garcia, Natalia, Sadjadian, Parvis, Shih, Lee Yung, Devos, Timothy, Krochmalczyk, Dorota, Galli, Serena, Bieniaszewska, Maria, Seferynska, Ilona, McMullin, Mary Frances, Armatys, Anna, Spalek, Adrianna, Waclaw, Joanna, Zdrenghea, Mihnea, Legros, Laurence, Girodon, François, Lewandowski, Krzysztof, Angona Figueras, Anna, Samuelsson, Jan, Abuin Blanco, Aitor, Cony-Makhoul, Pascale, Collins, Angela, James, Chloé, Kusec, Rajko, Lauermannova, Marie, Noya, Maria Sol, Skowronek, Malgorzata, Szukalski, Lukasz, Szmigielska-Kaplon, Anna, Wondergem, Marielle, Dudchenko, Iryna, Gora Tybor, Joanna, Laribi, Kamel, Kulikowska de Nalecz, Anna, Demory, Jean-Loup, Le Du, Katell, Zweegman, Sonja, Besses Raebel, Carlos, Skoda, Radek, Giraudier, Stéphane, Griesshammer, Martin, Harrison, Claire N., and Ianotto, Jean-Christophe

Published
2022
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16. Pathobiological Pseudohypoxia as a Putative Mechanism Underlying Myelodysplastic Syndromes.

Author

Hayashi, Yoshihiro, Zhang, Yue, Yokota, Asumi, Yan, Xiaomei, Liu, Jinqin, Choi, Kwangmin, Li, Bing, Sashida, Goro, Peng, Yanyan, Xu, Zefeng, Huang, Rui, Zhang, Lulu, Freudiger, George M, Wang, Jingya, Dong, Yunzhu, Zhou, Yile, Wang, Jieyu, Wu, Lingyun, Bu, Jiachen, Chen, Aili, Zhao, Xinghui, Sun, Xiujuan, Chetal, Kashish, Olsson, Andre, Watanabe, Miki, Romick-Rosendale, Lindsey E, Harada, Hironori, Shih, Lee-Yung, Tse, William, Bridges, James P, Caligiuri, Michael A, Huang, Taosheng, Zheng, Yi, Witte, David P, Wang, Qian-Fei, Qu, Cheng-Kui, Salomonis, Nathan, Grimes, H Leighton, Nimer, Stephen D, Xiao, Zhijian, and Huang, Gang

Subjects
Animals, Mice, Knockout, Humans, Mice, Myelodysplastic Syndromes, Histone-Lysine N-Methyltransferase, Gene Expression Regulation, Neoplastic, Core Binding Factor Alpha 2 Subunit, Myeloid-Lymphoid Leukemia Protein, Hypoxia-Inducible Factor 1, alpha Subunit, Metabolome, Hypoxia, Rare Diseases, Hematology, Genetics, Cancer, Stem Cell Research, Aging, 2.1 Biological and endogenous factors, Aetiology, Oncology and Carcinogenesis
Abstract

Myelodysplastic syndromes (MDS) are heterogeneous hematopoietic disorders that are incurable with conventional therapy. Their incidence is increasing with global population aging. Although many genetic, epigenetic, splicing, and metabolic aberrations have been identified in patients with MDS, their clinical features are quite similar. Here, we show that hypoxia-independent activation of hypoxia-inducible factor 1α (HIF1A) signaling is both necessary and sufficient to induce dysplastic and cytopenic MDS phenotypes. The HIF1A transcriptional signature is generally activated in MDS patient bone marrow stem/progenitors. Major MDS-associated mutations (Dnmt3a, Tet2, Asxl1, Runx1, and Mll1) activate the HIF1A signature. Although inducible activation of HIF1A signaling in hematopoietic cells is sufficient to induce MDS phenotypes, both genetic and chemical inhibition of HIF1A signaling rescues MDS phenotypes in a mouse model of MDS. These findings reveal HIF1A as a central pathobiologic mediator of MDS and as an effective therapeutic target for a broad spectrum of patients with MDS.Significance: We showed that dysregulation of HIF1A signaling could generate the clinically relevant diversity of MDS phenotypes by functioning as a signaling funnel for MDS driver mutations. This could resolve the disconnection between genotypes and phenotypes and provide a new clue as to how a variety of driver mutations cause common MDS phenotypes. Cancer Discov; 8(11); 1438-57. ©2018 AACR. See related commentary by Chen and Steidl, p. 1355 This article is highlighted in the In This Issue feature, p. 1333.

Published
2018

17. Molecular and clinical presentation of UBA1-mutated myelodysplastic syndromes

Author

Sirenko, Maria, primary, Bernard, Elsa, additional, Creignou, Maria, additional, Domenico, Dylan, additional, Farina, Andrea, additional, Arango Ossa, Juan Esteban, additional, Kosmider, Olivier, additional, Hasserjian, Robert P, additional, Jädersten, Martin, additional, Germing, Ulrich, additional, Sanz, Guillermo F., additional, van de Loosdrecht, Arjan A., additional, Gurnari, Carmelo, additional, Follo, Matilde Y, additional, Thol, Felicitas R., additional, Zamora, Lurdes, additional, Pellagatti, Andrea, additional, Elias, Harold Kunal, additional, Haase, Detlef Thomas, additional, Sander, Birgitta, additional, Orna, Elisa, additional, Zoldan, Katharina, additional, Eder, Lea Naomi, additional, Sperr, Wolfgang R, additional, Thalhammer, Renate, additional, Ganster, Christina, additional, Adès, Lionel, additional, Tobiasson, Magnus, additional, Palomo, Laura, additional, Della Porta, Matteo Giovanni, additional, Huberman, Kety H, additional, Fenaux, Pierre, additional, Belickova, Monika, additional, Savona, Michael R., additional, Klimek, Virginia, additional, Santos, Fabio P S, additional, Boultwood, Jacqueline, additional, Kotsianidis, Ioannis, additional, Santini, Valeria, additional, Sole, Francesc, additional, Platzbecker, Uwe, additional, Heuser, Michael, additional, Valent, Peter, additional, Finelli, Carlo, additional, Voso, Maria Teresa, additional, Shih, Lee Yung, additional, Ogawa, Seishi, additional, Fontenay, Michaela, additional, Jansen, Joop H, additional, Cervera, José, additional, Ebert, Benjamin L, additional, Bejar, Rafael, additional, Greenberg, Peter L., additional, Gattermann, Norbert, additional, Malcovati, Luca, additional, Cazzola, Mario, additional, Beck, David B., additional, Hellstrom-Lindberg, Eva S, additional, Papaemmanuil, Elli, additional, and Pinheiro, Ronald Feitosa, additional

Published
2024
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18. Refining risk stratification in paediatric B‐acute lymphoblastic leukaemia: Combining IKZF1plus and Day 15 MRD positivity

Author

Liu, Hsi‐Che, primary, Huang, Ying‐Jung, additional, Jaing, Tang‐Her, additional, Wu, Kang‐Hsi, additional, Chen, Shih‐Hsiang, additional, Wang, Shih‐Chung, additional, Yeh, Ting‐Chi, additional, Hsiao, Chih‐Cheng, additional, Chang, Te‐Kau, additional, Yen, Hsiu‐Ju, additional, Huang, Fang‐Liang, additional, Lin, Pei‐Chin, additional, Hou, Jen‐Yin, additional, Sheen, Jiunn‐Ming, additional, Liao, Yu‐Mei, additional, Chang, Tsung‐Yen, additional, Chen, Yu‐Chieh, additional, Chiou, Shyh‐Shin, additional, Yang, Chao‐Ping, additional, Pui, Ching‐Hon, additional, Liang, Der‐Cherng, additional, and Shih, Lee‐Yung, additional

Published
2024
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19. Clinical characteristics and outcomes of B-ALL with ZNF384 rearrangements: a retrospective analysis by the Ponte di Legno Childhood ALL Working Group

Author

Hirabayashi, Shinsuke, Butler, Ellie R., Ohki, Kentaro, Kiyokawa, Nobutaka, Bergmann, Anke K., Möricke, Anja, Boer, Judith M., Cavé, Hélène, Cazzaniga, Giovanni, Yeoh, Allen Eng Juh, Sanada, Masashi, Imamura, Toshihiko, Inaba, Hiroto, Mullighan, Charles, Loh, Mignon L., Norén-Nyström, Ulrika, Pastorczak, Agata, Shih, Lee-Yung, Zaliova, Marketa, Pui, Ching-Hon, Haas, Oskar A., Harrison, Christine J., Moorman, Anthony V., and Manabe, Atsushi

Published
2021
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20. Mutational Landscape of Pediatric Acute Lymphoblastic Leukemia

Author

Ding, Ling-Wen, Sun, Qiao-Yang, Tan, Kar-Tong, Chien, Wenwen, Thippeswamy, Anand Mayakonda, Yeoh, Allen Eng Juh, Kawamata, Norihiko, Nagata, Yasunobu, Xiao, Jin-Fen, Loh, Xin-Yi, Lin, De-Chen, Garg, Manoj, Jiang, Yan-Yi, Xu, Liang, Lim, Su-Lin, Liu, Li-Zhen, Madan, Vikas, Sanada, Masashi, Fernández, Lucia Torres, Preethi, Hema, Lill, Michael, Kantarjian, Hagop M, Kornblau, Steven M, Miyano, Satoru, Liang, Der-Cherng, Ogawa, Seishi, Shih, Lee-Yung, Yang, Henry, and Koeffler, H Phillip

Subjects
Biological Sciences, Biomedical and Clinical Sciences, Genetics, Oncology and Carcinogenesis, Cancer, Rare Diseases, Clinical Research, Childhood Leukemia, Pediatric Research Initiative, Pediatric Cancer, Biotechnology, Hematology, Pediatric, Aetiology, 2.1 Biological and endogenous factors, Good Health and Well Being, Adolescent, Animals, Blotting, Western, Child, Child, Preschool, DNA Mutational Analysis, Female, High-Throughput Nucleotide Sequencing, Humans, Infant, Male, Mice, Mutation, Precursor Cell Lymphoblastic Leukemia-Lymphoma, Oncology & Carcinogenesis, Biochemistry and cell biology, Oncology and carcinogenesis
Abstract

Current standard of care for patients with pediatric acute lymphoblastic leukemia (ALL) is mainly effective, with high remission rates after treatment. However, the genetic perturbations that give rise to this disease remain largely undefined, limiting the ability to address resistant tumors or develop less toxic targeted therapies. Here, we report the use of next-generation sequencing to interrogate the genetic and pathogenic mechanisms of 240 pediatric ALL cases with their matched remission samples. Commonly mutated genes fell into several categories, including RAS/receptor tyrosine kinases, epigenetic regulators, transcription factors involved in lineage commitment, and the p53/cell-cycle pathway. Unique recurrent mutational hotspots were observed in epigenetic regulators CREBBP (R1446C/H), WHSC1 (E1099K), and the tyrosine kinase FLT3 (K663R, N676K). The mutant WHSC1 was established as a gain-of-function oncogene, while the epigenetic regulator ARID1A and transcription factor CTCF were functionally identified as potential tumor suppressors. Analysis of 28 diagnosis/relapse trio patients plus 10 relapse cases revealed four evolutionary paths and uncovered the ordering of acquisition of mutations in these patients. This study provides a detailed mutational portrait of pediatric ALL and gives insights into the molecular pathogenesis of this disease. Cancer Res; 77(2); 390-400. ©2016 AACR.

Published
2017

21. Genetic risk of extranodal natural killer T-cell lymphoma: a genome-wide association study in multiple populations

Author

Au, Wing-Yan, Chiu, Brian, Fan, Lei, Li, Zheng, LAM, Tai Hing, Liang, Raymond, Yeh, Su-Peng, Xu, Jun, Ip, Dennis Kai Ming, Li, Gandi, Xu, Gang, Wang, Xiaodong, Bai, Ou, Cai, Qing-Qing, Xia, Yi, Chen, Jie-Rong, Luo, Chun-Ling, Xiong, Xiang-Yu, Zeng, Yanni, Wei, Pan-Pan, Liu, Chu-Jun, Liu, Yu-Xiang, Cao, Yu-Lu, He, Shuai, Liu, Yang, Ha, Jeslin Chian Hung, Khoo, Lay Poh, Kee, Rebecca Xiangpin, Tan, Jing, Liu, Yanhui, Zhang, Fen, Feng, Yanfen, Rao, Huilan, Chng, Wee Joo, Chan, Jason Yong Sheng, Somasundaram, Nagavalli D/O, Tao, Miriam, Ras, Mohamad Farid Bin Harunal, Yeoh, Kheng-Wei, Goh, Yeow Tee, Ong, Shin Yeu, Grigoropoulos, Nicholas Francis, Wong, Esther Kam Yin, Pang, Jane Wan Lu, Lim, Jing Quan, Chia, Burton Kuan Hui, Kim, Seok Jin, Yoon, Sang Eun, Choi, Seungkyu, Kuo, Ching-Yuan, Chen, Tsai-Yun, Su, Yu-Chieh, Huang, Wen-Tsung, Lee, Ming-Yang, Yao, Wenxiu, Ngan, Kai-Cheong, Liu, Herman, Lee, Harold, Yip, Sze-Fai, Liu, Jie, Li, Jianyong, Rabkin, Charles S., Berndt, Sonja, Bassig, Bryan, Hu, Wei, Zhao, Mingfeng, Li, Yuming, Zhai, Qiongli, Shao, Zonghong, Qiu, Lugui, Wang, Jianxiang, Xu, Fu-Ping, Chen, Ling, Hou, Yu, Xu, Shuangnian, Huang, Zhen, Xie, Mingling, Li, Ming, Zhong, Shilong, Zhang, Yan, Gu, Dongqing, Wang, Xin, Foo, Jia Nee, Li, Zhiqiang, Dai, Juncheng, Sun, Liangdan, Wang, Zhenzhen, Liu, Hong, Zhou, Hui, Sun, Yonghu, Koh, Woon-Puay, Heng, Chew-Kiat, Hong, Chew Soo, Ahn, Jeeyun, Park, Kyu Hyung, Tin, Aung, Gu, Jieruo, Xia, Xiaojun, Li, Bo, Yu, Xueqing, Lin, Guo-Wang, Xu, Caigang, Chen, Kexin, Huang, Hui-Qiang, Chen, Jieping, Song, Bao, Chan, John K C, Li, Wenyu, Liu, Weiping, Shih, Lee-Yung, Chuang, Wen-Yu, Kim, Won Seog, Tan, Wen, Peng, Rou-Jun, Laurensia, Yurike, Cheah, Daryl Ming Zhe, Huang, DaChuan, Cheng, Chee Leong, Su, Yi-Jiun, Tan, Soo-Yong, Ng, Siok-Bian, Tang, Tiffany Pooi Ling, Han, Kyudong, Wang, Vivien Ya-Fan, Jia, Wei-Hua, Pei, Zhong, Li, Ya-Jun, Gao, Song, Shi, Yongyong, Hu, Zhibin, Zhang, Furen, Zhang, Ben, Zeng, Yi-Xin, Shen, Hongbing, He, Lin, Ong, Choon Kiat, Lim, Soon Thye, Chanock, Stephen, Kwong, Yok-Lam, Lin, Dongxin, Rothman, Nathaniel, Khor, Chiea Chuen, Lan, Qing, and Bei, Jin-Xin

Published
2020
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23. Clonal evolution and clinical implications of genetic abnormalities in blastic transformation of chronic myeloid leukaemia

Author

Ochi, Yotaro, Yoshida, Kenichi, Huang, Ying-Jung, Kuo, Ming-Chung, Nannya, Yasuhito, Sasaki, Ko, Mitani, Kinuko, Hosoya, Noriko, Hiramoto, Nobuhiro, Ishikawa, Takayuki, Branford, Susan, Shanmuganathan, Naranie, Ohyashiki, Kazuma, Takahashi, Naoto, Takaku, Tomoiku, Tsuchiya, Shun, Kanemura, Nobuhiro, Nakamura, Nobuhiko, Ueda, Yasunori, Yoshihara, Satoshi, Bera, Rabindranath, Shiozawa, Yusuke, Zhao, Lanying, Takeda, June, Watatani, Yosaku, Okuda, Rurika, Makishima, Hideki, Shiraishi, Yuichi, Chiba, Kenichi, Tanaka, Hiroko, Sanada, Masashi, Takaori-Kondo, Akifumi, Miyano, Satoru, Ogawa, Seishi, and Shih, Lee-Yung

Published
2021
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25. Treatment outcome and germline predictive factors of ropeginterferon alpha‐2b in myeloproliferative neoplasm patients.

Author

Chen, Chih‐Cheng, Kuo, Ming‐Chung, Wang, Ying‐Hsuan, Pei, Sung‐Nan, Huang, Ming‐Lih, Chen, Chiu‐Chen, Huang, Cih‐En, Chen, Yi‐Yang, and Shih, Lee‐Yung

Subjects
MYELOPROLIFERATIVE neoplasms, SINGLE nucleotide polymorphisms, TREATMENT effectiveness, HAPLOTYPES, MYELOFIBROSIS, GERM cells
Abstract

Background: Studies have shown that some single nucleotide polymorphisms (SNPs) could serve as excellent markers in foretelling the treatment outcome of interferon (IFN) in myeloproliferative neoplasms (MPN). However, most work originated from western countries, and data from different ethnic populations have been lacking. Methods: To gain insights, targeted sequencing was performed to detect myeloid‐associated mutations and SNPs in eight loci across three genes (IFNL4, IFN‐γ, and inosine triphosphate pyrophosphatase [ITPA]) to explore their predictive roles in our cohort of 21 ropeginterferon alpha‐2b (ROPEG)‐treated MPN patients, among whom real‐time quantitative PCR was also performed periodically to monitor the JAK2V617F allele burden in 19 JAK2V617F‐mutated cases. Results: ELN response criteria were adopted to designate patients as good responders if they achieved complete hematological responses (CHR) within 1 year (CHR1) or attained major molecular responses (MMR), which occurred in 70% and 45% of the patients, respectively. IFNL4 and IFN‐γ gene SNPs were infrequent in our population and were thus excluded from further analysis. Two ITPA SNPs rs6051702 A>C and rs1127354 C>A were associated with an inferior CHR1 rate and MMR rate, respectively. The former seemed to be linked to grade 2 or worse hepatotoxicity as well, although the comparison was of borderline significance only (50%, vs. 6.7% in those with common haplotype, p = 0.053). Twelve patients harbored 19 additional somatic mutations in 12 genes, but the trajectory of these mutations varied considerably and was not predictive of any response. Conclusions: Overall, this study provided valuable information on the ethnics‐ and genetics‐based algorithm in the treatment of MPN. [ABSTRACT FROM AUTHOR]

Published
2024
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33. Supplementary Table from Amplified EPOR/JAK2 Genes Define a Unique Subtype of Acute Erythroid Leukemia

Author

Takeda, June, primary, Yoshida, Kenichi, primary, Nakagawa, Masahiro M., primary, Nannya, Yasuhito, primary, Yoda, Akinori, primary, Saiki, Ryunosuke, primary, Ochi, Yotaro, primary, Zhao, Lanying, primary, Okuda, Rurika, primary, Qi, Xingxing, primary, Mori, Takuto, primary, Kon, Ayana, primary, Chiba, Kenichi, primary, Tanaka, Hiroko, primary, Shiraishi, Yuichi, primary, Kuo, Ming-Chung, primary, Kerr, Cassandra M., primary, Nagata, Yasunobu, primary, Morishita, Daisuke, primary, Hiramoto, Nobuhiro, primary, Hangaishi, Akira, primary, Nakazawa, Hideyuki, primary, Ishiyama, Ken, primary, Miyano, Satoru, primary, Chiba, Shigeru, primary, Miyazaki, Yasushi, primary, Kitano, Toshiyuki, primary, Usuki, Kensuke, primary, Sezaki, Nobuo, primary, Tsurumi, Hisashi, primary, Miyawaki, Shuichi, primary, Maciejewski, Jaroslaw P., primary, Ishikawa, Takayuki, primary, Ohyashiki, Kazuma, primary, Ganser, Arnold, primary, Heuser, Michael, primary, Thol, Felicitas, primary, Shih, Lee-Yung, primary, Takaori-Kondo, Akifumi, primary, Makishima, Hideki, primary, and Ogawa, Seishi, primary

Published
2023
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34. Supplementary Figure from Amplified EPOR/JAK2 Genes Define a Unique Subtype of Acute Erythroid Leukemia

Author

Takeda, June, primary, Yoshida, Kenichi, primary, Nakagawa, Masahiro M., primary, Nannya, Yasuhito, primary, Yoda, Akinori, primary, Saiki, Ryunosuke, primary, Ochi, Yotaro, primary, Zhao, Lanying, primary, Okuda, Rurika, primary, Qi, Xingxing, primary, Mori, Takuto, primary, Kon, Ayana, primary, Chiba, Kenichi, primary, Tanaka, Hiroko, primary, Shiraishi, Yuichi, primary, Kuo, Ming-Chung, primary, Kerr, Cassandra M., primary, Nagata, Yasunobu, primary, Morishita, Daisuke, primary, Hiramoto, Nobuhiro, primary, Hangaishi, Akira, primary, Nakazawa, Hideyuki, primary, Ishiyama, Ken, primary, Miyano, Satoru, primary, Chiba, Shigeru, primary, Miyazaki, Yasushi, primary, Kitano, Toshiyuki, primary, Usuki, Kensuke, primary, Sezaki, Nobuo, primary, Tsurumi, Hisashi, primary, Miyawaki, Shuichi, primary, Maciejewski, Jaroslaw P., primary, Ishikawa, Takayuki, primary, Ohyashiki, Kazuma, primary, Ganser, Arnold, primary, Heuser, Michael, primary, Thol, Felicitas, primary, Shih, Lee-Yung, primary, Takaori-Kondo, Akifumi, primary, Makishima, Hideki, primary, and Ogawa, Seishi, primary

Published
2023
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35. Data from Amplified EPOR/JAK2 Genes Define a Unique Subtype of Acute Erythroid Leukemia

Author

Takeda, June, primary, Yoshida, Kenichi, primary, Nakagawa, Masahiro M., primary, Nannya, Yasuhito, primary, Yoda, Akinori, primary, Saiki, Ryunosuke, primary, Ochi, Yotaro, primary, Zhao, Lanying, primary, Okuda, Rurika, primary, Qi, Xingxing, primary, Mori, Takuto, primary, Kon, Ayana, primary, Chiba, Kenichi, primary, Tanaka, Hiroko, primary, Shiraishi, Yuichi, primary, Kuo, Ming-Chung, primary, Kerr, Cassandra M., primary, Nagata, Yasunobu, primary, Morishita, Daisuke, primary, Hiramoto, Nobuhiro, primary, Hangaishi, Akira, primary, Nakazawa, Hideyuki, primary, Ishiyama, Ken, primary, Miyano, Satoru, primary, Chiba, Shigeru, primary, Miyazaki, Yasushi, primary, Kitano, Toshiyuki, primary, Usuki, Kensuke, primary, Sezaki, Nobuo, primary, Tsurumi, Hisashi, primary, Miyawaki, Shuichi, primary, Maciejewski, Jaroslaw P., primary, Ishikawa, Takayuki, primary, Ohyashiki, Kazuma, primary, Ganser, Arnold, primary, Heuser, Michael, primary, Thol, Felicitas, primary, Shih, Lee-Yung, primary, Takaori-Kondo, Akifumi, primary, Makishima, Hideki, primary, and Ogawa, Seishi, primary

Published
2023
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36. Abstract 6168: Implementation and adoption of a web tool to support precision diagnostic and treatment decisions for patient with myelodysplastic syndromes

Author

Bernard, Elsa, primary, Ossa, Juan E. Arango, additional, Tuechler, Heinz, additional, Greenberg, Peter L., additional, Hasserjian, Robert P., additional, Nannya, Yasuhito, additional, Devlin, Sean M., additional, Creignou, Maria, additional, Pinel, Philippe, additional, Monier, Lily, additional, Medina-Martinez, Juan S., additional, Domenico, Dylan, additional, Jädersten, Martin, additional, Germing, Ulrich, additional, Sanz, Guillermo, additional, van de Loosdrecht, Arjan A., additional, Kosmider, Olivier, additional, Follo, Matilde Y., additional, Thol, Felicitas, additional, Zamora, Lurdes, additional, Pinheiro, Ronald F., additional, Pellagatti, Andrea, additional, Haase, Detlef, additional, Fenaux, Pierre, additional, Belickova, Monika, additional, Savona, Michael R., additional, Klimek, Virginia M., additional, Santos, Fabio P., additional, Boultwood, Jacqueline, additional, Kotsianidis, Ioannis, additional, Santini, Valeria, additional, Solé, Francesc, additional, Platzbecker, Uwe, additional, Heuser, Michael, additional, Valent, Peter, additional, Ohyashiki, Kazuma, additional, Finelli, Carlo, additional, Voso, Maria Teresa, additional, Shih, Lee-Yung, additional, Fontenay, Michaela, additional, Jansen, Joop H., additional, Cervera, José, additional, Gattermann, Norbert, additional, Ebert, Benjamin L., additional, Bejar, Rafael, additional, Malcovati, Luca, additional, Cazzola, Mario, additional, Ogawa, Seishi, additional, Hellström-Lindberg, Eva, additional, and Papaemmanuil, Elli, additional

Published
2023
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37. Data from Pathobiological Pseudohypoxia as a Putative Mechanism Underlying Myelodysplastic Syndromes

Author

Hayashi, Yoshihiro, primary, Zhang, Yue, primary, Yokota, Asumi, primary, Yan, Xiaomei, primary, Liu, Jinqin, primary, Choi, Kwangmin, primary, Li, Bing, primary, Sashida, Goro, primary, Peng, Yanyan, primary, Xu, Zefeng, primary, Huang, Rui, primary, Zhang, Lulu, primary, Freudiger, George M., primary, Wang, Jingya, primary, Dong, Yunzhu, primary, Zhou, Yile, primary, Wang, Jieyu, primary, Wu, Lingyun, primary, Bu, Jiachen, primary, Chen, Aili, primary, Zhao, Xinghui, primary, Sun, Xiujuan, primary, Chetal, Kashish, primary, Olsson, Andre, primary, Watanabe, Miki, primary, Romick-Rosendale, Lindsey E., primary, Harada, Hironori, primary, Shih, Lee-Yung, primary, Tse, William, primary, Bridges, James P., primary, Caligiuri, Michael A., primary, Huang, Taosheng, primary, Zheng, Yi, primary, Witte, David P., primary, Wang, Qian-fei, primary, Qu, Cheng-Kui, primary, Salomonis, Nathan, primary, Grimes, H. Leighton, primary, Nimer, Stephen D., primary, Xiao, Zhijian, primary, and Huang, Gang, primary

Published
2023
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38. Supplementary Methods from Pathobiological Pseudohypoxia as a Putative Mechanism Underlying Myelodysplastic Syndromes

Author

Hayashi, Yoshihiro, primary, Zhang, Yue, primary, Yokota, Asumi, primary, Yan, Xiaomei, primary, Liu, Jinqin, primary, Choi, Kwangmin, primary, Li, Bing, primary, Sashida, Goro, primary, Peng, Yanyan, primary, Xu, Zefeng, primary, Huang, Rui, primary, Zhang, Lulu, primary, Freudiger, George M., primary, Wang, Jingya, primary, Dong, Yunzhu, primary, Zhou, Yile, primary, Wang, Jieyu, primary, Wu, Lingyun, primary, Bu, Jiachen, primary, Chen, Aili, primary, Zhao, Xinghui, primary, Sun, Xiujuan, primary, Chetal, Kashish, primary, Olsson, Andre, primary, Watanabe, Miki, primary, Romick-Rosendale, Lindsey E., primary, Harada, Hironori, primary, Shih, Lee-Yung, primary, Tse, William, primary, Bridges, James P., primary, Caligiuri, Michael A., primary, Huang, Taosheng, primary, Zheng, Yi, primary, Witte, David P., primary, Wang, Qian-fei, primary, Qu, Cheng-Kui, primary, Salomonis, Nathan, primary, Grimes, H. Leighton, primary, Nimer, Stephen D., primary, Xiao, Zhijian, primary, and Huang, Gang, primary

Published
2023
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39. Supplementary Table S2 from Pathobiological Pseudohypoxia as a Putative Mechanism Underlying Myelodysplastic Syndromes

Author

Hayashi, Yoshihiro, primary, Zhang, Yue, primary, Yokota, Asumi, primary, Yan, Xiaomei, primary, Liu, Jinqin, primary, Choi, Kwangmin, primary, Li, Bing, primary, Sashida, Goro, primary, Peng, Yanyan, primary, Xu, Zefeng, primary, Huang, Rui, primary, Zhang, Lulu, primary, Freudiger, George M., primary, Wang, Jingya, primary, Dong, Yunzhu, primary, Zhou, Yile, primary, Wang, Jieyu, primary, Wu, Lingyun, primary, Bu, Jiachen, primary, Chen, Aili, primary, Zhao, Xinghui, primary, Sun, Xiujuan, primary, Chetal, Kashish, primary, Olsson, Andre, primary, Watanabe, Miki, primary, Romick-Rosendale, Lindsey E., primary, Harada, Hironori, primary, Shih, Lee-Yung, primary, Tse, William, primary, Bridges, James P., primary, Caligiuri, Michael A., primary, Huang, Taosheng, primary, Zheng, Yi, primary, Witte, David P., primary, Wang, Qian-fei, primary, Qu, Cheng-Kui, primary, Salomonis, Nathan, primary, Grimes, H. Leighton, primary, Nimer, Stephen D., primary, Xiao, Zhijian, primary, and Huang, Gang, primary

Published
2023
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40. Supplementary Figure S1-13 and Supplementary Table S1,3 from Pathobiological Pseudohypoxia as a Putative Mechanism Underlying Myelodysplastic Syndromes

Author

Hayashi, Yoshihiro, primary, Zhang, Yue, primary, Yokota, Asumi, primary, Yan, Xiaomei, primary, Liu, Jinqin, primary, Choi, Kwangmin, primary, Li, Bing, primary, Sashida, Goro, primary, Peng, Yanyan, primary, Xu, Zefeng, primary, Huang, Rui, primary, Zhang, Lulu, primary, Freudiger, George M., primary, Wang, Jingya, primary, Dong, Yunzhu, primary, Zhou, Yile, primary, Wang, Jieyu, primary, Wu, Lingyun, primary, Bu, Jiachen, primary, Chen, Aili, primary, Zhao, Xinghui, primary, Sun, Xiujuan, primary, Chetal, Kashish, primary, Olsson, Andre, primary, Watanabe, Miki, primary, Romick-Rosendale, Lindsey E., primary, Harada, Hironori, primary, Shih, Lee-Yung, primary, Tse, William, primary, Bridges, James P., primary, Caligiuri, Michael A., primary, Huang, Taosheng, primary, Zheng, Yi, primary, Witte, David P., primary, Wang, Qian-fei, primary, Qu, Cheng-Kui, primary, Salomonis, Nathan, primary, Grimes, H. Leighton, primary, Nimer, Stephen D., primary, Xiao, Zhijian, primary, and Huang, Gang, primary

Published
2023
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41. Data from Mutational Landscape of Pediatric Acute Lymphoblastic Leukemia

Author

Ding, Ling-Wen, primary, Sun, Qiao-Yang, primary, Tan, Kar-Tong, primary, Chien, Wenwen, primary, Thippeswamy, Anand Mayakonda, primary, Eng Juh Yeoh, Allen, primary, Kawamata, Norihiko, primary, Nagata, Yasunobu, primary, Xiao, Jin-Fen, primary, Loh, Xin-Yi, primary, Lin, De-Chen, primary, Garg, Manoj, primary, Jiang, Yan-Yi, primary, Xu, Liang, primary, Lim, Su-Lin, primary, Liu, Li-Zhen, primary, Madan, Vikas, primary, Sanada, Masashi, primary, Fernández, Lucia Torres, primary, Preethi, Hema, primary, Lill, Michael, primary, Kantarjian, Hagop M., primary, Kornblau, Steven M., primary, Miyano, Satoru, primary, Liang, Der-Cherng, primary, Ogawa, Seishi, primary, Shih, Lee-Yung, primary, Yang, Henry, primary, and Koeffler, H. Phillip, primary

Published
2023
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42. Supplementary Fig 3 from Mutational Landscape of Pediatric Acute Lymphoblastic Leukemia

Author

Ding, Ling-Wen, primary, Sun, Qiao-Yang, primary, Tan, Kar-Tong, primary, Chien, Wenwen, primary, Thippeswamy, Anand Mayakonda, primary, Eng Juh Yeoh, Allen, primary, Kawamata, Norihiko, primary, Nagata, Yasunobu, primary, Xiao, Jin-Fen, primary, Loh, Xin-Yi, primary, Lin, De-Chen, primary, Garg, Manoj, primary, Jiang, Yan-Yi, primary, Xu, Liang, primary, Lim, Su-Lin, primary, Liu, Li-Zhen, primary, Madan, Vikas, primary, Sanada, Masashi, primary, Fernández, Lucia Torres, primary, Preethi, Hema, primary, Lill, Michael, primary, Kantarjian, Hagop M., primary, Kornblau, Steven M., primary, Miyano, Satoru, primary, Liang, Der-Cherng, primary, Ogawa, Seishi, primary, Shih, Lee-Yung, primary, Yang, Henry, primary, and Koeffler, H. Phillip, primary

Published
2023
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43. Supplementary Fig 1 from Mutational Landscape of Pediatric Acute Lymphoblastic Leukemia

Author

Ding, Ling-Wen, primary, Sun, Qiao-Yang, primary, Tan, Kar-Tong, primary, Chien, Wenwen, primary, Thippeswamy, Anand Mayakonda, primary, Eng Juh Yeoh, Allen, primary, Kawamata, Norihiko, primary, Nagata, Yasunobu, primary, Xiao, Jin-Fen, primary, Loh, Xin-Yi, primary, Lin, De-Chen, primary, Garg, Manoj, primary, Jiang, Yan-Yi, primary, Xu, Liang, primary, Lim, Su-Lin, primary, Liu, Li-Zhen, primary, Madan, Vikas, primary, Sanada, Masashi, primary, Fernández, Lucia Torres, primary, Preethi, Hema, primary, Lill, Michael, primary, Kantarjian, Hagop M., primary, Kornblau, Steven M., primary, Miyano, Satoru, primary, Liang, Der-Cherng, primary, Ogawa, Seishi, primary, Shih, Lee-Yung, primary, Yang, Henry, primary, and Koeffler, H. Phillip, primary

Published
2023
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44. Supplementary Figure legends from Mutational Landscape of Pediatric Acute Lymphoblastic Leukemia

Author

Ding, Ling-Wen, primary, Sun, Qiao-Yang, primary, Tan, Kar-Tong, primary, Chien, Wenwen, primary, Thippeswamy, Anand Mayakonda, primary, Eng Juh Yeoh, Allen, primary, Kawamata, Norihiko, primary, Nagata, Yasunobu, primary, Xiao, Jin-Fen, primary, Loh, Xin-Yi, primary, Lin, De-Chen, primary, Garg, Manoj, primary, Jiang, Yan-Yi, primary, Xu, Liang, primary, Lim, Su-Lin, primary, Liu, Li-Zhen, primary, Madan, Vikas, primary, Sanada, Masashi, primary, Fernández, Lucia Torres, primary, Preethi, Hema, primary, Lill, Michael, primary, Kantarjian, Hagop M., primary, Kornblau, Steven M., primary, Miyano, Satoru, primary, Liang, Der-Cherng, primary, Ogawa, Seishi, primary, Shih, Lee-Yung, primary, Yang, Henry, primary, and Koeffler, H. Phillip, primary

Published
2023
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45. Supplementary Fig 4 from Mutational Landscape of Pediatric Acute Lymphoblastic Leukemia

Author

Ding, Ling-Wen, primary, Sun, Qiao-Yang, primary, Tan, Kar-Tong, primary, Chien, Wenwen, primary, Thippeswamy, Anand Mayakonda, primary, Eng Juh Yeoh, Allen, primary, Kawamata, Norihiko, primary, Nagata, Yasunobu, primary, Xiao, Jin-Fen, primary, Loh, Xin-Yi, primary, Lin, De-Chen, primary, Garg, Manoj, primary, Jiang, Yan-Yi, primary, Xu, Liang, primary, Lim, Su-Lin, primary, Liu, Li-Zhen, primary, Madan, Vikas, primary, Sanada, Masashi, primary, Fernández, Lucia Torres, primary, Preethi, Hema, primary, Lill, Michael, primary, Kantarjian, Hagop M., primary, Kornblau, Steven M., primary, Miyano, Satoru, primary, Liang, Der-Cherng, primary, Ogawa, Seishi, primary, Shih, Lee-Yung, primary, Yang, Henry, primary, and Koeffler, H. Phillip, primary

Published
2023
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46. Supplementary Fig 2 from Mutational Landscape of Pediatric Acute Lymphoblastic Leukemia

Author

Ding, Ling-Wen, primary, Sun, Qiao-Yang, primary, Tan, Kar-Tong, primary, Chien, Wenwen, primary, Thippeswamy, Anand Mayakonda, primary, Eng Juh Yeoh, Allen, primary, Kawamata, Norihiko, primary, Nagata, Yasunobu, primary, Xiao, Jin-Fen, primary, Loh, Xin-Yi, primary, Lin, De-Chen, primary, Garg, Manoj, primary, Jiang, Yan-Yi, primary, Xu, Liang, primary, Lim, Su-Lin, primary, Liu, Li-Zhen, primary, Madan, Vikas, primary, Sanada, Masashi, primary, Fernández, Lucia Torres, primary, Preethi, Hema, primary, Lill, Michael, primary, Kantarjian, Hagop M., primary, Kornblau, Steven M., primary, Miyano, Satoru, primary, Liang, Der-Cherng, primary, Ogawa, Seishi, primary, Shih, Lee-Yung, primary, Yang, Henry, primary, and Koeffler, H. Phillip, primary

Published
2023
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47. Supplementary Fig 5 from Mutational Landscape of Pediatric Acute Lymphoblastic Leukemia

Author

Ding, Ling-Wen, primary, Sun, Qiao-Yang, primary, Tan, Kar-Tong, primary, Chien, Wenwen, primary, Thippeswamy, Anand Mayakonda, primary, Eng Juh Yeoh, Allen, primary, Kawamata, Norihiko, primary, Nagata, Yasunobu, primary, Xiao, Jin-Fen, primary, Loh, Xin-Yi, primary, Lin, De-Chen, primary, Garg, Manoj, primary, Jiang, Yan-Yi, primary, Xu, Liang, primary, Lim, Su-Lin, primary, Liu, Li-Zhen, primary, Madan, Vikas, primary, Sanada, Masashi, primary, Fernández, Lucia Torres, primary, Preethi, Hema, primary, Lill, Michael, primary, Kantarjian, Hagop M., primary, Kornblau, Steven M., primary, Miyano, Satoru, primary, Liang, Der-Cherng, primary, Ogawa, Seishi, primary, Shih, Lee-Yung, primary, Yang, Henry, primary, and Koeffler, H. Phillip, primary

Published
2023
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48. Supplementary Tables from Mutational Landscape of Pediatric Acute Lymphoblastic Leukemia

Author

Ding, Ling-Wen, primary, Sun, Qiao-Yang, primary, Tan, Kar-Tong, primary, Chien, Wenwen, primary, Thippeswamy, Anand Mayakonda, primary, Eng Juh Yeoh, Allen, primary, Kawamata, Norihiko, primary, Nagata, Yasunobu, primary, Xiao, Jin-Fen, primary, Loh, Xin-Yi, primary, Lin, De-Chen, primary, Garg, Manoj, primary, Jiang, Yan-Yi, primary, Xu, Liang, primary, Lim, Su-Lin, primary, Liu, Li-Zhen, primary, Madan, Vikas, primary, Sanada, Masashi, primary, Fernández, Lucia Torres, primary, Preethi, Hema, primary, Lill, Michael, primary, Kantarjian, Hagop M., primary, Kornblau, Steven M., primary, Miyano, Satoru, primary, Liang, Der-Cherng, primary, Ogawa, Seishi, primary, Shih, Lee-Yung, primary, Yang, Henry, primary, and Koeffler, H. Phillip, primary

Published
2023
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49. Comparison of Clinical and Molecular Features Between Patients With Essential Thrombocythemia and Early/Prefibrotic Primary Myelofibrosis Presenting With Thrombocytosis in Taiwan

Author

Kuo, Ming-Chung, primary, Chuang, Wen-Yu, additional, Chang, Hung, additional, Lin, Tung-Huei, additional, Wu, Jin-Hou, additional, Lin, Tung-Liang, additional, Ou, Che-Wei, additional, Hung, Yu-Shin, additional, Huang, Ting-Yu, additional, Huang, Ying-Jung, additional, Wang, Po-Nan, additional, and Shih, Lee-Yung, additional

Published
2023
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50. Author Correction: Implications of TP53 allelic state for genome stability, clinical presentation and outcomes in myelodysplastic syndromes

Author

Bernard, Elsa, Nannya, Yasuhito, Hasserjian, Robert P., Devlin, Sean M., Tuechler, Heinz, Medina-Martinez, Juan S., Yoshizato, Tetsuichi, Shiozawa, Yusuke, Saiki, Ryunosuke, Malcovati, Luca, Levine, Max F., Arango, Juan E., Zhou, Yangyu, Solé, Francesc, Cargo, Catherine A., Haase, Detlef, Creignou, Maria, Germing, Ulrich, Zhang, Yanming, Gundem, Gunes, Sarian, Araxe, van de Loosdrecht, Arjan A., Jädersten, Martin, Tobiasson, Magnus, Kosmider, Olivier, Follo, Matilde Y., Thol, Felicitas, Pinheiro, Ronald F., Santini, Valeria, Kotsianidis, Ioannis, Boultwood, Jacqueline, Santos, Fabio P. S., Schanz, Julie, Kasahara, Senji, Ishikawa, Takayuki, Tsurumi, Hisashi, Takaori-Kondo, Akifumi, Kiguchi, Toru, Polprasert, Chantana, Bennett, John M., Klimek, Virginia M., Savona, Michael R., Belickova, Monika, Ganster, Christina, Palomo, Laura, Sanz, Guillermo, Ades, Lionel, Della Porta, Matteo Giovanni, Elias, Harold K., Smith, Alexandra G., Werner, Yesenia, Patel, Minal, Viale, Agnès, Vanness, Katelynd, Neuberg, Donna S., Stevenson, Kristen E., Menghrajani, Kamal, Bolton, Kelly L., Fenaux, Pierre, Pellagatti, Andrea, Platzbecker, Uwe, Heuser, Michael, Valent, Peter, Chiba, Shigeru, Miyazaki, Yasushi, Finelli, Carlo, Voso, Maria Teresa, Shih, Lee-Yung, Fontenay, Michaela, Jansen, Joop H., Cervera, José, Atsuta, Yoshiko, Gattermann, Norbert, Ebert, Benjamin L., Bejar, Rafael, Greenberg, Peter L., Cazzola, Mario, Hellström-Lindberg, Eva, Ogawa, Seishi, and Papaemmanuil, Elli

Published
2021
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