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1. BRD9 determines the cell fate of hematopoietic stem cells by regulating chromatin state

Author

Xiao, Muran, Kondo, Shinji, Nomura, Masaki, Kato, Shinichiro, Nishimura, Koutarou, Zang, Weijia, Zhang, Yifan, Akashi, Tomohiro, Viny, Aaron, Shigehiro, Tsukasa, Ikawa, Tomokatsu, Yamazaki, Hiromi, Fukumoto, Miki, Tanaka, Atsushi, Hayashi, Yasutaka, Koike, Yui, Aoyama, Yumi, Ito, Hiromi, Nishikawa, Hiroyoshi, Kitamura, Toshio, Kanai, Akinori, Yokoyama, Akihiko, Fujiwara, Tohru, Goyama, Susumu, Noguchi, Hideki, Lee, Stanley C., Toyoda, Atsushi, Hinohara, Kunihiko, Abdel-Wahab, Omar, and Inoue, Daichi

Published
2023
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2. Verification of prognostic expression biomarkers is improved by examining enriched leukemic blasts rather than mononuclear cells from acute myeloid leukemia patients

Author

Pogosova-Agadjanyan, Era L., Hua, Xing, Othus, Megan, Appelbaum, Frederick R., Chauncey, Thomas R., Erba, Harry P., Fitzgibbon, Matthew P., Jenkins, Isaac C., Fang, Min, Lee, Stanley C., Moseley, Anna, Naru, Jasmine, Radich, Jerald P., Smith, Jenny L., Willborg, Brooke E., Willman, Cheryl L., Wu, Feinan, Meshinchi, Soheil, and Stirewalt, Derek L.

Published
2023
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3. An Open-Source, Vender Agnostic Hardware and Software Pipeline for Integration of Artificial Intelligence in Radiology Workflow.

Author

Sohn, Jae Ho, Chillakuru, Yeshwant Reddy, Lee, Stanley, Lee, Amie Y, Kelil, Tatiana, Hess, Christopher Paul, Seo, Youngho, Vu, Thienkhai, and Joe, Bonnie N

Subjects
Humans, Radiology, Systems Integration, Artificial Intelligence, Software, Radiology Information Systems, Workflow, Artificial intelligence, Informatics, Machine learning, PACS, Quality improvement, Bioengineering, Biomedical Imaging, Networking and Information Technology R&D (NITRD), Clinical Sciences, Nuclear Medicine & Medical Imaging
Abstract

Although machine learning (ML) has made significant improvements in radiology, few algorithms have been integrated into clinical radiology workflow. Complex radiology IT environments and Picture Archiving and Communication System (PACS) pose unique challenges in creating a practical ML schema. However, clinical integration and testing are critical to ensuring the safety and accuracy of ML algorithms. This study aims to propose, develop, and demonstrate a simple, efficient, and understandable hardware and software system for integrating ML models into the standard radiology workflow and PACS that can serve as a framework for testing ML algorithms. A Digital Imaging and Communications in Medicine/Graphics Processing Unit (DICOM/GPU) server and software pipeline was established at a metropolitan county hospital intranet to demonstrate clinical integration of ML algorithms in radiology. A clinical ML integration schema, agnostic to the hospital IT system and specific ML models/frameworks, was implemented and tested with a breast density classification algorithm and prospectively evaluated for time delays using 100 digital 2D mammograms. An open-source clinical ML integration schema was successfully implemented and demonstrated. This schema allows for simple uploading of custom ML models. With the proposed setup, the ML pipeline took an average of 26.52 s per second to process a batch of 100 studies. The most significant processing time delays were noted in model load and study stability times. The code is made available at " http://bit.ly/2Z121hX ". We demonstrated the feasibility to deploy and utilize ML models in radiology without disrupting existing radiology workflow.

Published
2020

4. Aberrant EVI1 splicing contributes to EVI1-rearranged leukemia

Author

Tanaka, Atsushi, Nakano, Taizo A., Nomura, Masaki, Yamazaki, Hiromi, Bewersdorf, Jan P., Mulet-Lazaro, Roger, Hogg, Simon, Liu, Bo, Penson, Alex, Yokoyama, Akihiko, Zang, Weijia, Havermans, Marije, Koizumi, Miho, Hayashi, Yasutaka, Cho, Hana, Kanai, Akinori, Lee, Stanley C., Xiao, Muran, Koike, Yui, Zhang, Yifan, Fukumoto, Miki, Aoyama, Yumi, Konuma, Tsuyoshi, Kunimoto, Hiroyoshi, Inaba, Toshiya, Nakajima, Hideaki, Honda, Hiroaki, Kawamoto, Hiroshi, Delwel, Ruud, Abdel-Wahab, Omar, and Inoue, Daichi

Published
2022
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5. Table S2 from R-Loop Accumulation in Spliceosome Mutant Leukemias Confers Sensitivity to PARP1 Inhibition by Triggering Transcription–Replication Conflicts

Author

Liu, Zhiyan Silvia, primary, Sinha, Sayantani, primary, Bannister, Maxwell, primary, Song, Axia, primary, Arriaga-Gomez, Erica, primary, McKeeken, Alexander J., primary, Bonner, Elizabeth A., primary, Hanson, Benjamin K., primary, Sarchi, Martina, primary, Takashima, Kouhei, primary, Zong, Dawei, primary, Corral, Victor M., primary, Nguyen, Evan, primary, Yoo, Jennifer, primary, Chiraphapphaiboon, Wannasiri, primary, Leibson, Cassandra, primary, McMahon, Matthew C., primary, Rai, Sumit, primary, Swisher, Elizabeth M., primary, Sachs, Zohar, primary, Chatla, Srinivas, primary, Stirewalt, Derek L., primary, Deeg, H. Joachim, primary, Skorski, Tomasz, primary, Papapetrou, Eirini P., primary, Walter, Matthew J., primary, Graubert, Timothy A., primary, Doulatov, Sergei, primary, Lee, Stanley C., primary, and Nguyen, Hai Dang, primary

Published
2024
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6. Figure S1-S8 from R-Loop Accumulation in Spliceosome Mutant Leukemias Confers Sensitivity to PARP1 Inhibition by Triggering Transcription–Replication Conflicts

Author

Liu, Zhiyan Silvia, primary, Sinha, Sayantani, primary, Bannister, Maxwell, primary, Song, Axia, primary, Arriaga-Gomez, Erica, primary, McKeeken, Alexander J., primary, Bonner, Elizabeth A., primary, Hanson, Benjamin K., primary, Sarchi, Martina, primary, Takashima, Kouhei, primary, Zong, Dawei, primary, Corral, Victor M., primary, Nguyen, Evan, primary, Yoo, Jennifer, primary, Chiraphapphaiboon, Wannasiri, primary, Leibson, Cassandra, primary, McMahon, Matthew C., primary, Rai, Sumit, primary, Swisher, Elizabeth M., primary, Sachs, Zohar, primary, Chatla, Srinivas, primary, Stirewalt, Derek L., primary, Deeg, H. Joachim, primary, Skorski, Tomasz, primary, Papapetrou, Eirini P., primary, Walter, Matthew J., primary, Graubert, Timothy A., primary, Doulatov, Sergei, primary, Lee, Stanley C., primary, and Nguyen, Hai Dang, primary

Published
2024
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7. Robust hyperparameter estimation protects against hypervariable genes and improves power to detect differential expression

Author

Phipson, Belinda, Lee, Stanley, Majewski, Ian J., Alexander, Warren S., and Smyth, Gordon K.

Subjects
Statistics - Applications, Quantitative Biology - Genomics, 62F35 (primary), 62P10 (secondary)
Abstract

One of the most common analysis tasks in genomic research is to identify genes that are differentially expressed (DE) between experimental conditions. Empirical Bayes (EB) statistical tests using moderated genewise variances have been very effective for this purpose, especially when the number of biological replicate samples is small. The EB procedures can however be heavily influenced by a small number of genes with very large or very small variances. This article improves the differential expression tests by robustifying the hyperparameter estimation procedure. The robust procedure has the effect of decreasing the informativeness of the prior distribution for outlier genes while increasing its informativeness for other genes. This effect has the double benefit of reducing the chance that hypervariable genes will be spuriously identified as DE while increasing statistical power for the main body of genes. The robust EB algorithm is fast and numerically stable. The procedure allows exact small-sample null distributions for the test statistics and reduces exactly to the original EB procedure when no outlier genes are present. Simulations show that the robustified tests have similar performance to the original tests in the absence of outlier genes but have greater power and robustness when outliers are present. The article includes case studies for which the robust method correctly identifies and downweights genes associated with hidden covariates and detects more genes likely to be scientifically relevant to the experimental conditions. The new procedure is implemented in the limma software package freely available from the Bioconductor repository., Comment: 23 pages, 4 figures

Published
2016
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8. R-loop accumulation in spliceosome mutant leukemias confers sensitivity to PARP1 inhibition by triggering transcription-replication conflicts

Author

Liu, Zhiyan Silvia, primary, Sinha, Sayantani, additional, Bannister, Maxwell, additional, Song, Axia, additional, Arriaga-Gomez, Erica, additional, McKeeken, Alexander J., additional, Bonner, Elizabeth A., additional, Hanson, Benjamin K., additional, Sarchi, Martina, additional, Takashima, Kouhei, additional, Zong, Dawei, additional, Corral, Victor M., additional, Nguyen, Evan, additional, Yoo, Jennifer, additional, Chiraphapphaiboon, Wannasiri, additional, Leibson, Cassandra, additional, McMahon, Matthew C., additional, Rai, Sumit, additional, Swisher, Elizabeth M., additional, Sachs, Zohar, additional, Chatla, Srinivas, additional, Stirewalt, Derek L., additional, Deeg, H. Joachim, additional, Skorski, Tomasz, additional, Papapetrou, Eirini P., additional, Walter, Matthew J., additional, Graubert, Timothy A., additional, Doulatov, Sergei, additional, Lee, Stanley C., additional, and Nguyen, Hai Dang, additional

Published
2023
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10. Menin inhibitor MI-3454 induces remission in MLL1-rearranged and NPM1-mutated models of leukemia

Author

Klossowski, Szymon, Miao, Hongzhi, Kempinska, Katarzyna, Wu, Tao, Purohit, Trupta, Kim, EunGi, Linhares, Brian M., Chen, Dong, Jih, Gloria, Perkey, Eric, Huang, Huang, He, Miao, Wen, Bo, Wang, Yi, Yu, Ke, Lee, Stanley Chun-Wei, Danet-Desnoyers, Gwenn, Trotman, Winifred, Kandarpa, Malathi, Cotton, Anitria, Abdel-Wahab, Omar, Lei, Hongwei, Dou, Yali, Guzman, Monica, Peterson, Luke, Gruber, Tanja, Choi, Sarah, Sun, Duxin, Ren, Pingda, Li, Lian-Sheng, Liu, Yi, Burrows, Francis, Maillard, Ivan, Cierpicki, Tomasz, and Grembecka, Jolanta

Subjects
Protein-protein interactions -- Genetic aspects -- Analysis -- Models, Genes, Time, Acute leukemia, Health care industry, University of Michigan
Abstract

The protein-protein interaction between menin and mixed lineage leukemia 1 (MLL1) plays a critical role in acute leukemias with translocations of the MLL1 gene or with mutations in the nucleophosmin 1 (NPM1) gene. As a step toward clinical translation of menin-MLL1 inhibitors, we report development of MI-3454, a highly potent and orally bioavailable inhibitor of the menin-MLL1 interaction. MI-3454 profoundly inhibited proliferation and induced differentiation in acute leukemia cells and primary patient samples with MLL1 translocations or NPM1 mutations. When applied as a single agent, MI-3454 induced complete remission or regression of leukemia in mouse models of MLLI-rearranged or NPMI-mutated leukemia, including patient-derived xenograft models, through downregulation of key genes involved in leukemogenesis. We also identified MEIS1 as a potential pharmacodynamic biomarker of treatment response with MI-3454 in leukemia, and demonstrated that this compound is well tolerated and did not impair normal hematopoiesis in mice. Overall, this study demonstrates, for the first time to our knowledge, profound activity of the menin-MLL1 inhibitor as a single agent in clinically relevant PDX models of leukemia. These data provide a strong rationale for clinical translation of MI-3454 or its analogs for leukemia patients with MLL1 rearrangements or NPM1 mutations., Introduction The development of acute leukemia is associated with heterogeneous genetic and epigenetic alterations (1, 2), making it difficult to identify new effective therapies for leukemia patients. Despite these challenges, [...]

Published
2020
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12. DNA methylation disruption reshapes the hematopoietic differentiation landscape

Author

Izzo, Franco, Lee, Stanley C., Poran, Asaf, Chaligne, Ronan, Gaiti, Federico, Gross, Baptiste, Murali, Rekha R., Deochand, Sunil D., Ang, Chelston, Jones, Philippa Wyndham, Nam, Anna S., Kim, Kyu-Tae, Kothen-Hill, Steven, Schulman, Rafael C., Ki, Michelle, Lhoumaud, Priscillia, Skok, Jane A., Viny, Aaron D., Levine, Ross L., Kenigsberg, Ephraim, Abdel-Wahab, Omar, and Landau, Dan A.

Published
2020
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16. Coordinated alterations in RNA splicing and epigenetic regulation drive leukaemogenesis

Author

Yoshimi, Akihide, Lin, Kuan-Ting, Wiseman, Daniel H., Rahman, Mohammad Alinoor, Pastore, Alessandro, Wang, Bo, and Lee, Stanley Chun-Wei

Subjects
Leukemia -- Development and progression -- Genetic aspects, RNA splicing -- Methods, Epigenetic inheritance -- Control, Environmental issues, Science and technology, Zoology and wildlife conservation
Abstract

Transcription and pre-mRNA splicing are key steps in the control of gene expression and mutations in genes regulating each of these processes are common in leukaemia.sup.1,2. Despite the frequent overlap of mutations affecting epigenetic regulation and splicing in leukaemia, how these processes influence one another to promote leukaemogenesis is not understood and, to our knowledge, there is no functional evidence that mutations in RNA splicing factors initiate leukaemia. Here, through analyses of transcriptomes from 982 patients with acute myeloid leukaemia, we identified frequent overlap of mutations in IDH2 and SRSF2 that together promote leukaemogenesis through coordinated effects on the epigenome and RNA splicing. Whereas mutations in either IDH2 or SRSF2 imparted distinct splicing changes, co-expression of mutant IDH2 altered the splicing effects of mutant SRSF2 and resulted in more profound splicing changes than either mutation alone. Consistent with this, co-expression of mutant IDH2 and SRSF2 resulted in lethal myelodysplasia with proliferative features in vivo and enhanced self-renewal in a manner not observed with either mutation alone. IDH2 and SRSF2 double-mutant cells exhibited aberrant splicing and reduced expression of INTS3, a member of the integrator complex.sup.3, concordant with increased stalling of RNA polymerase II (RNAPII). Aberrant INTS3 splicing contributed to leukaemogenesis in concert with mutant IDH2 and was dependent on mutant SRSF2 binding to cis elements in INTS3 mRNA and increased DNA methylation of INTS3. These data identify a pathogenic crosstalk between altered epigenetic state and splicing in a subset of leukaemias, provide functional evidence that mutations in splicing factors drive myeloid malignancy development, and identify spliceosomal changes as a mediator of IDH2-mutant leukaemogenesis. Analyses of transcriptomes from patients with acute myeloid leukaemia identified frequently co-occurring mutations of IDH2 and SRSF2, which functional analyses showed to have distinct and coordinated leukaemogenic effects on the epigenome and RNA splicing., Author(s): Akihide Yoshimi [sup.1] , Kuan-Ting Lin [sup.2] , Daniel H. Wiseman [sup.3] [sup.4] , Mohammad Alinoor Rahman [sup.2] , Alessandro Pastore [sup.1] , Bo Wang [sup.1] , Stanley Chun-Wei [...]

Published
2019
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17. Spliceosomal disruption of the non-canonical BAF complex in cancer

Author

Inoue, Daichi, Chew, Guo-Liang, Liu, Bo, Michel, Brittany C., Pangallo, Joseph, D’Avino, Andrew R., Hitchman, Tyler, North, Khrystyna, Lee, Stanley Chun-Wei, Bitner, Lillian, Block, Ariele, Moore, Amanda R., Yoshimi, Akihide, Escobar-Hoyos, Luisa, Cho, Hana, Penson, Alex, Lu, Sydney X., Taylor, Justin, Chen, Yu, Kadoch, Cigall, Abdel-Wahab, Omar, and Bradley, Robert K.

Published
2019
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19. Robust patient-derived xenografts of MDS/MPN overlap syndromes capture the unique characteristics of CMML and JMML

Author

Yoshimi, Akihide, Balasis, Maria E., Vedder, Alexis, Feldman, Kira, Ma, Yan, Zhang, Hailing, Lee, Stanley Chun-Wei, Letson, Christopher, Niyongere, Sandrine, Lu, Sydney X., Ball, Markus, Taylor, Justin, Zhang, Qing, Zhao, Yulong, Youssef, Salma, Chung, Young Rock, Zhang, Xiao Jing, Durham, Benjamin H., Yang, Wendy, List, Alan F., Loh, Mignon L., Klimek, Virginia, Berger, Michael F., Stieglitz, Elliot, Padron, Eric, and Abdel-Wahab, Omar

Published
2017
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20. H3B-8800, an orally available small-molecule splicing modulator, induces lethality in spliceosome-mutant cancers

Author

Seiler, Michael, Yoshimi, Akihide, Darman, Rachel, Chan, Betty, Keaney, Gregg, Thomas, Michael, Agrawal, Anant A, Caleb, Benjamin, Csibi, Alfredo, Sean, Eckley, Fekkes, Peter, Karr, Craig, Klimek, Virginia, Lai, George, Lee, Linda, Kumar, Pavan, Lee, Stanley Chun-Wei, Liu, Xiang, Mackenzie, Crystal, Meeske, Carol, Mizui, Yoshiharu, Padron, Eric, Park, Eunice, Pazolli, Ermira, Peng, Shouyong, Prajapati, Sudeep, Taylor, Justin, Teng, Teng, Wang, John, Warmuth, Markus, Yao, Huilan, Yu, Lihua, Zhu, Ping, Abdel-Wahab, Omar, Smith, Peter G, and Buonamici, Silvia

Subjects
RNA splicing -- Health aspects, Gene mutation -- Health aspects, Carcinogenesis -- Genetic aspects, Biological sciences, Health
Abstract

Author(s): Michael Seiler [1]; Akihide Yoshimi [2]; Rachel Darman [1]; Betty Chan [1]; Gregg Keaney [1]; Michael Thomas [1]; Anant A Agrawal [1]; Benjamin Caleb [1]; Alfredo Csibi [1]; Eckley [...]

Published
2018
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22. Examining the impact of age on the prognostic value of ELN-2017 and ELN-2022 acute myeloid leukemia risk stratifications: a report from the SWOG Cancer Research Network

Author

Termini, Christina M., primary, Moseley, Anna, additional, Othus, Megan, additional, Appelbaum, Frederick R., additional, Chauncey, Thomas R., additional, Erba, Harry P., additional, Fang, Min, additional, Lee, Stanley C., additional, Naru, Jasmine, additional, Pogosova-Agadjanyan, Era L., additional, Radich, Jerald P., additional, Willman, Cheryl L., additional, Wu, Feinan, additional, Meshinchi, Soheil, additional, and Stirewalt, Derek L., additional

Published
2023
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23. Abstract 6183: PARP inhibitors preferentially sensitize splicing factor mutant myeloid neoplasms

Author

Nguyen, Dang Hai, primary, Sinha, Sayantani, additional, Liu, Zhiyan Silvia, additional, Bannister, Maxwell Henry, additional, Arriaga-Gomez, Erica, additional, Song, Axia, additional, Zong, Dawei, additional, Sarchi, Martina, additional, Corral, Victor, additional, Chiraphapphaiboon, Wannasiri, additional, Yoo, Jennifer, additional, McMahon, Matthew, additional, Leibson, Cassandra, additional, Stirewalt, Derek L., additional, Deeg, H Joachim, additional, Rai, Sumit, additional, Walter, Matthew, additional, Graubert, Timothy A., additional, Doulatov, Sergei, additional, and Lee, Stanley C., additional

Published
2023
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24. Data from Diverse and Targetable Kinase Alterations Drive Histiocytic Neoplasms

Author

Diamond, Eli L., primary, Durham, Benjamin H., primary, Haroche, Julien, primary, Yao, Zhan, primary, Ma, Jing, primary, Parikh, Sameer A., primary, Wang, Zhaoming, primary, Choi, John, primary, Kim, Eunhee, primary, Cohen-Aubart, Fleur, primary, Lee, Stanley Chun-Wei, primary, Gao, Yijun, primary, Micol, Jean-Baptiste, primary, Campbell, Patrick, primary, Walsh, Michael P., primary, Sylvester, Brooke, primary, Dolgalev, Igor, primary, Aminova, Olga, primary, Heguy, Adriana, primary, Zappile, Paul, primary, Nakitandwe, Joy, primary, Ganzel, Chezi, primary, Dalton, James D., primary, Ellison, David W., primary, Estrada-Veras, Juvianee, primary, Lacouture, Mario, primary, Gahl, William A., primary, Stephens, Philip J., primary, Miller, Vincent A., primary, Ross, Jeffrey S., primary, Ali, Siraj M., primary, Briggs, Samuel R., primary, Fasan, Omotayo, primary, Block, Jared, primary, Héritier, Sebastien, primary, Donadieu, Jean, primary, Solit, David B., primary, Hyman, David M., primary, Baselga, José, primary, Janku, Filip, primary, Taylor, Barry S., primary, Park, Christopher Y., primary, Amoura, Zahir, primary, Dogan, Ahmet, primary, Emile, Jean-Francois, primary, Rosen, Neal, primary, Gruber, Tanja A., primary, and Abdel-Wahab, Omar, primary

Published
2023
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25. Table S5 from Altered Nuclear Export Signal Recognition as a Driver of Oncogenesis

Author

Taylor, Justin, primary, Sendino, Maria, primary, Gorelick, Alexander N., primary, Pastore, Alessandro, primary, Chang, Matthew T., primary, Penson, Alexander V., primary, Gavrila, Elena I., primary, Stewart, Connor, primary, Melnik, Ella M., primary, Herrejon Chavez, Florisela, primary, Bitner, Lillian, primary, Yoshimi, Akihide, primary, Lee, Stanley Chun-Wei, primary, Inoue, Daichi, primary, Liu, Bo, primary, Zhang, Xiao J., primary, Mato, Anthony R., primary, Dogan, Ahmet, primary, Kharas, Michael G., primary, Chen, Yuhong, primary, Wang, Demin, primary, Soni, Rajesh K., primary, Hendrickson, Ronald C., primary, Prieto, Gorka, primary, Rodriguez, Jose A., primary, Taylor, Barry S., primary, and Abdel-Wahab, Omar, primary

Published
2023
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26. Data from Altered Nuclear Export Signal Recognition as a Driver of Oncogenesis

Author

Taylor, Justin, primary, Sendino, Maria, primary, Gorelick, Alexander N., primary, Pastore, Alessandro, primary, Chang, Matthew T., primary, Penson, Alexander V., primary, Gavrila, Elena I., primary, Stewart, Connor, primary, Melnik, Ella M., primary, Herrejon Chavez, Florisela, primary, Bitner, Lillian, primary, Yoshimi, Akihide, primary, Lee, Stanley Chun-Wei, primary, Inoue, Daichi, primary, Liu, Bo, primary, Zhang, Xiao J., primary, Mato, Anthony R., primary, Dogan, Ahmet, primary, Kharas, Michael G., primary, Chen, Yuhong, primary, Wang, Demin, primary, Soni, Rajesh K., primary, Hendrickson, Ronald C., primary, Prieto, Gorka, primary, Rodriguez, Jose A., primary, Taylor, Barry S., primary, and Abdel-Wahab, Omar, primary

Published
2023
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27. Supplementary Figures from Altered Nuclear Export Signal Recognition as a Driver of Oncogenesis

Author

Taylor, Justin, primary, Sendino, Maria, primary, Gorelick, Alexander N., primary, Pastore, Alessandro, primary, Chang, Matthew T., primary, Penson, Alexander V., primary, Gavrila, Elena I., primary, Stewart, Connor, primary, Melnik, Ella M., primary, Herrejon Chavez, Florisela, primary, Bitner, Lillian, primary, Yoshimi, Akihide, primary, Lee, Stanley Chun-Wei, primary, Inoue, Daichi, primary, Liu, Bo, primary, Zhang, Xiao J., primary, Mato, Anthony R., primary, Dogan, Ahmet, primary, Kharas, Michael G., primary, Chen, Yuhong, primary, Wang, Demin, primary, Soni, Rajesh K., primary, Hendrickson, Ronald C., primary, Prieto, Gorka, primary, Rodriguez, Jose A., primary, Taylor, Barry S., primary, and Abdel-Wahab, Omar, primary

Published
2023
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28. Data from Mutations in the RNA Splicing Factor SF3B1 Promote Tumorigenesis through MYC Stabilization

Author

Liu, Zhaoqi, primary, Yoshimi, Akihide, primary, Wang, Jiguang, primary, Cho, Hana, primary, Chun-Wei Lee, Stanley, primary, Ki, Michelle, primary, Bitner, Lillian, primary, Chu, Timothy, primary, Shah, Harshal, primary, Liu, Bo, primary, Mato, Anthony R., primary, Ruvolo, Peter, primary, Fabbri, Giulia, primary, Pasqualucci, Laura, primary, Abdel-Wahab, Omar, primary, and Rabadan, Raul, primary

Published
2023
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29. Supplementary Data from Mutations in the RNA Splicing Factor SF3B1 Promote Tumorigenesis through MYC Stabilization

Author

Liu, Zhaoqi, primary, Yoshimi, Akihide, primary, Wang, Jiguang, primary, Cho, Hana, primary, Chun-Wei Lee, Stanley, primary, Ki, Michelle, primary, Bitner, Lillian, primary, Chu, Timothy, primary, Shah, Harshal, primary, Liu, Bo, primary, Mato, Anthony R., primary, Ruvolo, Peter, primary, Fabbri, Giulia, primary, Pasqualucci, Laura, primary, Abdel-Wahab, Omar, primary, and Rabadan, Raul, primary

Published
2023
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30. Supplementary Methods from Altered Nuclear Export Signal Recognition as a Driver of Oncogenesis

Author

Taylor, Justin, primary, Sendino, Maria, primary, Gorelick, Alexander N., primary, Pastore, Alessandro, primary, Chang, Matthew T., primary, Penson, Alexander V., primary, Gavrila, Elena I., primary, Stewart, Connor, primary, Melnik, Ella M., primary, Herrejon Chavez, Florisela, primary, Bitner, Lillian, primary, Yoshimi, Akihide, primary, Lee, Stanley Chun-Wei, primary, Inoue, Daichi, primary, Liu, Bo, primary, Zhang, Xiao J., primary, Mato, Anthony R., primary, Dogan, Ahmet, primary, Kharas, Michael G., primary, Chen, Yuhong, primary, Wang, Demin, primary, Soni, Rajesh K., primary, Hendrickson, Ronald C., primary, Prieto, Gorka, primary, Rodriguez, Jose A., primary, Taylor, Barry S., primary, and Abdel-Wahab, Omar, primary

Published
2023
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31. Supplementary Methods, Figures 1 - 5, Tables 1 - 5 from Diverse and Targetable Kinase Alterations Drive Histiocytic Neoplasms

Author

Diamond, Eli L., primary, Durham, Benjamin H., primary, Haroche, Julien, primary, Yao, Zhan, primary, Ma, Jing, primary, Parikh, Sameer A., primary, Wang, Zhaoming, primary, Choi, John, primary, Kim, Eunhee, primary, Cohen-Aubart, Fleur, primary, Lee, Stanley Chun-Wei, primary, Gao, Yijun, primary, Micol, Jean-Baptiste, primary, Campbell, Patrick, primary, Walsh, Michael P., primary, Sylvester, Brooke, primary, Dolgalev, Igor, primary, Aminova, Olga, primary, Heguy, Adriana, primary, Zappile, Paul, primary, Nakitandwe, Joy, primary, Ganzel, Chezi, primary, Dalton, James D., primary, Ellison, David W., primary, Estrada-Veras, Juvianee, primary, Lacouture, Mario, primary, Gahl, William A., primary, Stephens, Philip J., primary, Miller, Vincent A., primary, Ross, Jeffrey S., primary, Ali, Siraj M., primary, Briggs, Samuel R., primary, Fasan, Omotayo, primary, Block, Jared, primary, Héritier, Sebastien, primary, Donadieu, Jean, primary, Solit, David B., primary, Hyman, David M., primary, Baselga, José, primary, Janku, Filip, primary, Taylor, Barry S., primary, Park, Christopher Y., primary, Amoura, Zahir, primary, Dogan, Ahmet, primary, Emile, Jean-Francois, primary, Rosen, Neal, primary, Gruber, Tanja A., primary, and Abdel-Wahab, Omar, primary

Published
2023
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32. Supplementary Table Captions from Altered Nuclear Export Signal Recognition as a Driver of Oncogenesis

Author

Taylor, Justin, primary, Sendino, Maria, primary, Gorelick, Alexander N., primary, Pastore, Alessandro, primary, Chang, Matthew T., primary, Penson, Alexander V., primary, Gavrila, Elena I., primary, Stewart, Connor, primary, Melnik, Ella M., primary, Herrejon Chavez, Florisela, primary, Bitner, Lillian, primary, Yoshimi, Akihide, primary, Lee, Stanley Chun-Wei, primary, Inoue, Daichi, primary, Liu, Bo, primary, Zhang, Xiao J., primary, Mato, Anthony R., primary, Dogan, Ahmet, primary, Kharas, Michael G., primary, Chen, Yuhong, primary, Wang, Demin, primary, Soni, Rajesh K., primary, Hendrickson, Ronald C., primary, Prieto, Gorka, primary, Rodriguez, Jose A., primary, Taylor, Barry S., primary, and Abdel-Wahab, Omar, primary

Published
2023
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33. Data from Epigenetic Regulator Smchd1 Functions as a Tumor Suppressor

Author

Leong, Huei San, primary, Chen, Kelan, primary, Hu, Yifang, primary, Lee, Stanley, primary, Corbin, Jason, primary, Pakusch, Miha, primary, Murphy, James M., primary, Majewski, Ian J., primary, Smyth, Gordon K., primary, Alexander, Warren S., primary, Hilton, Douglas J., primary, and Blewitt, Marnie E., primary

Published
2023
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39. Therapeutic Targeting of Spliceosome Mutant Myeloid Neoplasms Via PARP1 Inhibition

Author

Sinha, Sayantani, primary, Liu, Zhiyan Silvia, additional, Bannister, Maxwell, additional, Arriaga-Gomez, Erica, additional, Song, Axia, additional, Zong, Dawei, additional, Sarchi, Martina, additional, Bonner, Elizabeth, additional, Corral, Victor, additional, Leibson, Cassandra, additional, Chiraphapphaiboon, Wannasiri, additional, Stirewalt, Derek, additional, Deeg, Joachim, additional, Rai, Sumit, additional, Walter, Matthew J, additional, Graubert, Timothy A., additional, Doulatov, Sergei, additional, Nguyen, Dang Hai, additional, and Lee, Stanley Chun-Wei, additional

Published
2022
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41. A non‐canonical function of Ezh2 preserves immune homeostasis

Author

Vasanthakumar, Ajithkumar, Xu, Dakang, Lun, Aaron TL, Kueh, Andrew J, van Gisbergen, Klaas PJM, Iannarella, Nadia, Li, Xiaofang, Yu, Liang, Wang, Die, Williams, Bryan RG, Lee, Stanley CW, Majewski, Ian J, Godfrey, Dale I, Smyth, Gordon K, Alexander, Warren S, Herold, Marco J, Kallies, Axel, Nutt, Stephen L, and Allan, Rhys S

Published
2017
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43. Therapeutic targeting of splicing in cancer

Author

Lee, Stanley Chun-Wei and Abdel-Wahab, Omar

Subjects
Cancer treatment -- Innovations, Protein-protein interactions -- Health aspects, RNA splicing -- Health aspects, Molecular targeted therapy -- Methods, Biological sciences, Health
Abstract

Recent studies have highlighted that splicing patterns are frequently altered in cancer and that mutations in genes encoding spliceosomal proteins, as well as mutations affecting the splicing of key cancer-associated genes, are enriched in cancer. In parallel, there is also accumulating evidence that several molecular subtypes of cancer are highly dependent on splicing function for cell survival. These findings have resulted in a growing interest in targeting splicing catalysis, splicing regulatory proteins, and/or specific key altered splicing events in the treatment of cancer. Here we present strategies that exist and that are in development to target altered dependency on the spliceosome, as well as aberrant splicing, in cancer. These include drugs to target global splicing in cancer subtypes that are preferentially dependent on wild-type splicing for survival, methods to alter post-translational modifications of splicing-regulating proteins, and strategies to modulate pathologic splicing events and protein-RNA interactions in cancer., Author(s): Stanley Chun-Wei Lee [1]; Omar Abdel-Wahab (corresponding author) [1, 2] The majority of genes in the human genome consists of multiple exons interspersed with introns that undergo splicing to [...]

Published
2016
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44. Modulation of splicing catalysis for therapeutic targeting of leukemia with mutations in genes encoding spliceosomal proteins

Author

Lee, Stanley Chun-Wei, Dvinge, Heidi, Kim, Eunhee, Cho, Hana, Micol, Jean-Baptiste, Chung, Young Rock, Durham, Benjamin H, Yoshimi, Akihide, Kim, Young Joon, Thomas, Michael, Lobry, Camille, Chen, Chun-Wei, Pastore, Alessandro, Taylor, Justin, Wang, Xujun, Krivtsov, Andrei, Armstrong, Scott A, Palacino, James, Buonamici, Silvia, Smith, Peter G, Bradley, Robert K, and Abdel-Wahab, Omar

Subjects
Catalysis -- Health aspects -- Research, Gene mutation -- Research, Leukemia -- Genetic aspects -- Risk factors -- Care and treatment, Biological sciences, Health
Abstract

Author(s): Stanley Chun-Wei Lee [1]; Heidi Dvinge [2, 3]; Eunhee Kim [1]; Hana Cho [1]; Jean-Baptiste Micol [1]; Young Rock Chung [1]; Benjamin H Durham [1]; Akihide Yoshimi [1]; Young [...]

Published
2016
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48. The mutational landscape of paroxysmal nocturnal hemoglobinuria revealed: new insights into clonal dominance

Author

Lee, Stanley Chun-Wei and Abdel-Wahab, Omar

Subjects
Gene mutations -- Identification and classification, Hemoglobinuria, Paroxysmal -- Genetic aspects -- Development and progression, Health care industry
Abstract

Paroxysmal nocturnal hemoglobinuria (PNH) is a disorder of hematopoietic stem cells that has largely been considered a monogenic disorder due to acquisition of mutations in the gene encoding PIGA, which is required for glycosylphosphatidylinositol (GPI) anchor biosynthesis. In this issue of the JCI, Shen et al. discovered that PNH is in fact a complex genetic disorder orchestrated by many genetic alterations in addition to PIGA mutations. Some of these mutations predate the acquisition of PIGA mutations, while others occur later. Surprisingly, this work indicates that PNH has a clonal evolution and architecture strikingly similar to that of other myeloid neoplasms, highlighting a potentially broader mechanism of disease pathogenesis in this disorder., Paroxysmal nocturnal hemoglobinuria: a monogenic disorder? Paroxysmal nocturnal hemoglobinuria (PNH) is an acquired clonal disorder that arises from hematopoietic stem cells (HSCs) and affects 1-2 people per million, with a [...]

Published
2014
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