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1,127 results on '"Aster, Jon"'

1. Integrative cytogenetic and molecular studies unmask “chromosomal mimicry” in hematologic malignancies

Author

Zhao, Melissa, Ryall, Scott, Brody, Samuel J., Harris, Amyah C., Cabral, Kristin, Brownstein, Catherine, Kim, Jaeseung C., Smith, Adam C., Dal Cin, Paola, Narayan, Rupa, Sikkink, Kristin, Schmitt, Anthony, Hobbs, Gabriela S., Fathi, Amir T., Griffin, Gabriel K., Sait, Sheila N. J., Iafrate, Anthony J., Aster, Jon C., Graubert, Timothy A., Nardi, Valentina, and Dubuc, Adrian M.

Published
2025
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3. B Cell-Restricted Depletion of Dnmt3a Activates Notch Signaling and Causes Chronic Lymphocytic Leukemia

Author

Yin, Shanye, Biran, Anat, Kretzmer, Helene, Ten Hacken, Elisa, Parvin, Salma, Lucas, Fabienne, Uduman, Mohamed, Gutierrez, Catherine, Dangle, Nathan J, Billington, Leah, Regis, Fara, Rassenti, Laura Z, Mohammad, Arman W, Zheng, Mei, Witten, Elizabeth, Kipps, Thomas J, Aster, Jon C, Gnirke, Andreas, Neuberg, Donna S, Letai, Anthony G, Wang, Lili, Carrasco, Ruben D, Meissner, Alexander, and Wu, Catherine J

Subjects
Rare Diseases, Hematology, Lymphoma, Genetics, Cancer, Aetiology, 2.1 Biological and endogenous factors, Cardiorespiratory Medicine and Haematology, Clinical Sciences, Paediatrics and Reproductive Medicine, Immunology
Abstract

Abstract Previous studies have revealed a critical role of methylation deregulation in the onset and progression of chronic lymphocytic leukemia (CLL). In mammalian cells, DNA methylation is dynamically established by the DNA methyltransferase 3 (DNMT3) family of de novo methyltransferases DNMT3A. Although mutations of DNMT3A are rarely observed in CLL, our RNA-sequencing (RNA-seq) analysis of 107 human CLLs show that low DNMT3A expression is associated with more aggressive disease, and supports a driving role of DNMT3A loss in CLL. To test this hypothesis, we generated a conditional knock-out mouse model with B cell-restricted deletion of Dnmt3a. Homozygous Dnmt3a depletion in B cells resulted in the development of CD5+ B cell leukemia mimicking human CLL with 100% penetrance at a median age of onset of 5.3 months, and heterozygous Dnmt3a depletion yielded a disease penetrance of 89% with a median onset at 18.5 months, confirming its role as a haplo-insufficient tumor suppressor. Given the known role of Dnmt3a as a de novo methyltransferase, we first evaluated the impact of Dnmt3a depletion on global DNA methylation in non-leukemic CD5+ B cells isolated from the peritoneal cavity by cell sorting (i.e. B1a cells) using reduced representation bisulfite sequencing (RRBS). We identified a set of differentially methylated regions (DMRs) (difference>0.2), mostly hypomethylated, in Dnmt3afl/fl versus WT B1a cells (473 hypomethylated, 19 hypermethylated). Genes with dysregulated methylation were highly enriched in pathways involved in immune response (e.g., Interferon-α signaling, JAK/STAT3 signaling) and proliferation (Wnt Signaling and Notch signaling). Given the prominent hypomethylation changes observed in Dnmt3a depleted B1a cells, we investigated whether these would lead to altered gene transcript expression. Using RNA-seq, we detected 460 downregulated and 168 upregulated genes in the Dnmt3afl/fl B1a cells compared to WT B1a cells (FDR2). Consistent with the methylation data, differentially expressed genes were likewise enriched for JAK/STAT3 signaling, Wnt Signaling and Notch signaling, supporting a direct influence of dysregulated methylation on downstream signaling cascades. We investigated the changes in methylomes of the CLL cells arising from the Dnmt3afl/fl animals. Compared to WT B1a cells, Dnmt3afl/fl CLL cells generated 1335 hypomethylated and 2369 hypermethylated DMRs in. Focusing on genes that were hypomethylated in CLL compared to WT B1a cells, we found that these were highly enriched for several oncogenic signaling pathways including Notch signaling and Wnt Signaling, consistent with the pre-leukemia findings. RNA-seq analysis identified more upregulated (n=2801) than downregulated (n=1244) genes in CLL cells compared to WT B1a cells (FDR2), supporting a role of Dnmt3a depletion in transcriptional activation. We observed a general upregulation of Notch signaling genes and the downstream Notch targets, implicating Notch activation in this CLL mouse model. Of note, we showed Dnmt3a-depleted CLL cells to be highly sensitive to Notch inhibitor DAPT both in vitro and in a transplantable mouse model. Consistently, primary human CLL cells with low DNMT3A expression were more sensitive to DAPT than those with higher DNMT3A expression (P=0.005, Spearman correlation), despite similar sensitivity to ibrutinib and venetoclax. Together, our results have confirmed the causal role of Dnmt3a downregulation in CLL generation. We provide evidence in support of the interaction between Dnmt3a-dependent methylation changes and hyperactivation of Notch signaling in transcriptional reprogramming and transformation of B1a cells into CLL. Furthermore, we demonstrate differential sensitivity of DNMT3A high and low expressing primary CLLs to Notch inhibition, indicative of consistent dependencies of human and murine CLLs. Thus, the Dnmt3a models provides a unique opportunity for the study of non-mutational Notch activation, and a useful platform for the study of Notch-signaling targeted therapeutics. Disclosures Kipps: Abbott Laboratories: Consultancy, Research Funding; Celgene Corporation: Consultancy, Honoraria, Research Funding; Pharmacyclics LLC, an Abbvie Company: Consultancy, Honoraria, Other: Travel, Accommodations, Expenses, Research Funding, Speakers Bureau; Genentech, Inc.: Honoraria, Research Funding, Speakers Bureau; Gilead Sciences, Inc.: Honoraria, Research Funding; GlaxoSmithKline: Research Funding; MedImmune Inc: Research Funding; Moores Cancer Center: Current Employment; Oncternal Therapeutics, Inc.: Current holder of stock options in a privately-held company, Other: Stock or other ownership, Patents & Royalties: Cirmtuzumab was developed by Thomas J. Kipps in the Thomas J. Kipps laboratory and licensed by the University of California to Oncternal Therapeutics, Inc., which provided stock options and research funding to the Thomas J. Kipps laboratory., Research Funding; AbbVie: Consultancy, Honoraria, Other, Speakers Bureau; DAVAOncology: Consultancy, Honoraria, Other; DAVA Pharmaceuticals: Speakers Bureau; Bionest Partner: Other; Celgene: Consultancy, Honoraria, Other, Research Funding; Genetech: Honoraria, Other; Genentech-Roche: Consultancy; Gilead Sciences: Consultancy, Honoraria, Other, Speakers Bureau; Janssen: Consultancy, Honoraria, Other, Research Funding, Speakers Bureau; Roche: Honoraria, Other; MD Anderson Cancer Center: Research Funding; Velos: Research Funding; CRIM: Research Funding; Indy Hematology Review: Other; TG Therapeutics: Other; Verstem: Other, Speakers Bureau; University of California, San Diego: Current Employment; Pharmacyclics/AbbVie: Honoraria, Research Funding; Breast Cancer Research Foundation: Research Funding; SCOR - The Leukemia and Lymphoma Society: Research Funding; National Cancer Institute/NIH: Honoraria, Research Funding; Genentech/Roche: Honoraria; European Research Initiative on CLL (ERIC): Honoraria. Neuberg: Madrigal Pharmaceuticals: Other: Stock ownership; Pharmacyclics: Research Funding. Letai: Flash Therapeutics: Other: equity holding member of the scientific advisory board; Dialectic Therapeutics: Other: equity holding member of the scientific advisory board; Zentalis Pharmaceuticals: Other: equity holding member of the scientific advisory board. Wu: BioNTech: Current equity holder in publicly-traded company; Pharmacyclics: Research Funding.

Published
2021

4. Loss of glucocorticoid receptor expression mediates in vivo dexamethasone resistance in T-cell acute lymphoblastic leukemia

Author

Wandler, Anica M, Huang, Benjamin J, Craig, Jeffrey W, Hayes, Kathryn, Yan, Hannah, Meyer, Lauren K, Scacchetti, Alessandro, Monsalve, Gabriela, Dail, Monique, Li, Qing, Wong, Jasmine C, Weinberg, Olga, Hasserjian, Robert P, Kogan, Scott C, Jonsson, Philip, Yamamoto, Keith, Sampath, Deepak, Nakitandwe, Joy, Downing, James R, Zhang, Jinghui, Aster, Jon C, Taylor, Barry S, and Shannon, Kevin

Subjects
Medical Microbiology, Biomedical and Clinical Sciences, Rare Diseases, Childhood Leukemia, Pediatric, Pediatric Cancer, Orphan Drug, Genetics, Cancer, Hematology, 2.1 Biological and endogenous factors, Animals, Dexamethasone, Drug Resistance, Neoplasm, Humans, Indazoles, Male, Mice, Mice, Inbred C57BL, Mutation, Precursor T-Cell Lymphoblastic Leukemia-Lymphoma, Receptors, Glucocorticoid, Recurrence, Sulfonamides, Clinical Sciences, Oncology and Carcinogenesis, Immunology, Cardiovascular medicine and haematology, Clinical sciences, Oncology and carcinogenesis
Abstract

Despite decades of clinical use, mechanisms of glucocorticoid resistance are poorly understood. We treated primary murine T lineage acute lymphoblastic leukemias (T-ALLs) with the glucocorticoid dexamethasone (DEX) alone and in combination with the pan-PI3 kinase inhibitor GDC-0941 and observed a robust response to DEX that was modestly enhanced by GDC-0941. Continuous in vivo treatment invariably resulted in outgrowth of drug-resistant clones, ~30% of which showed markedly reduced glucocorticoid receptor (GR) protein expression. A similar proportion of relapsed human T-ALLs also exhibited low GR protein levels. De novo or preexisting mutations in the gene encoding GR (Nr3c1) occurred in relapsed clones derived from multiple independent parental leukemias. CRISPR/Cas9 gene editing confirmed that loss of GR expression confers DEX resistance. Exposing drug-sensitive T-ALLs to DEX in vivo altered transcript levels of multiple genes, and this response was attenuated in relapsed T-ALLs. These data implicate reduced GR protein expression as a frequent cause of glucocorticoid resistance in T-ALL.

Published
2020

7. Pharmacological disruption of the Notch transcription factor complex

Author

Lehal, Rajwinder, Zaric, Jelena, Vigolo, Michele, Urech, Charlotte, Frismantas, Viktoras, Zangger, Nadine, Cao, Linlin, Berger, Adeline, Chicote, Irene, Loubéry, Sylvain, Choi, Sung Hee, Koch, Ute, Blacklow, Stephen C., Palmer, Hector G., Bornhauser, Beat, González-Gaitán, Marcos, Arsenijevic, Yvan, Zoete, Vincent, Aster, Jon C., Bourquin, Jean-Pierre, and Radtke, Freddy

Published
2020

8. AL101, a gamma-secretase inhibitor, has potent antitumor activity against adenoid cystic carcinoma with activated NOTCH signaling

Author

Ferrarotto, Renata, Mishra, Vasudha, Herz, Elad, Yaacov, Adar, Solomon, Oz, Rauch, Rami, Mondshine, Adi, Motin, Maria, Leibovich-Rivkin, Tal, Davis, Matti, Kaye, Joel, Weber, Christopher R., Shen, Le, Pearson, Alexander T., Rosenberg, Ari J., Chen, Xiangying, Singh, Alka, Aster, Jon C., Agrawal, Nishant, and Izumchenko, Evgeny

Published
2022
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9. Single-cell RNA-seq reveals developmental plasticity with coexisting oncogenic states and immune evasion programs in ETP-ALL

Author

Anand, Praveen, Guillaumet-Adkins, Amy, Dimitrova, Valeriya, Yun, Huiyoung, Drier, Yotam, Sotudeh, Noori, Rogers, Anna, Ouseph, Madhu M., Nair, Monica, Potdar, Sayalee, Isenhart, Randi, Kloeber, Jake A., Vijaykumar, Tushara, Niu, Leili, Vincent, Tiffaney, Guo, Guangwu, Frede, Julia, Harris, Marian H., Place, Andrew E., Silverman, Lewis B., Teachey, David T., Lane, Andrew A., DeAngelo, Daniel J., Aster, Jon C., Bernstein, Bradley E., Lohr, Jens G., and Knoechel, Birgit

Published
2021
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12. The Human Tumor Atlas Network: Charting Tumor Transitions across Space and Time at Single-Cell Resolution

Author

Aberle, Denise, Achilefu, Samuel I., Ademuyiwa, Foluso O., Adey, Andrew C., Aft, Rebecca L., Agarwal, Rachana, Aguilar, Ruben A., Alikarami, Fatemeh, Allaj, Viola, Amos, Christopher, Anders, Robert A., Angelo, Michael R., Anton, Kristen, Ashenberg, Orr, Aster, Jon C., Babur, Ozgun, Bahmani, Amir, Balsubramani, Akshay, Barrett, David, Beane, Jennifer, Bender, Diane E., Bernt, Kathrin, Berry, Lynne, Betts, Courtney B., Bletz, Julie, Blise, Katie, Boire, Adrienne, Boland, Genevieve, Borowsky, Alexander, Bosse, Kristopher, Bott, Matthew, Boyden, Ed, Brooks, James, Bueno, Raphael, Burlingame, Erik A., Cai, Qiuyin, Campbell, Joshua, Caravan, Wagma, Cerami, Ethan, Chaib, Hassan, Chan, Joseph M., Chang, Young Hwan, Chatterjee, Deyali, Chaudhary, Ojasvi, Chen, Alyce A., Chen, Bob, Chen, Changya, Chen, Chia-hui, Chen, Feng, Chen, Yu-An, Chheda, Milan G., Chin, Koei, Chiu, Roxanne, Chu, Shih-Kai, Chuaqui, Rodrigo, Chun, Jaeyoung, Cisneros, Luis, Coffey, Robert J., Colditz, Graham A., Cole, Kristina, Collins, Natalie, Contrepois, Kevin, Coussens, Lisa M., Creason, Allison L., Crichton, Daniel, Curtis, Christina, Davidsen, Tanja, Davies, Sherri R., de Bruijn, Ino, Dellostritto, Laura, De Marzo, Angelo, Demir, Emek, DeNardo, David G., Diep, Dinh, Ding, Li, Diskin, Sharon, Doan, Xengie, Drewes, Julia, Dubinett, Stephen, Dyer, Michael, Egger, Jacklynn, Eng, Jennifer, Engelhardt, Barbara, Erwin, Graham, Esplin, Edward D., Esserman, Laura, Felmeister, Alex, Feiler, Heidi S., Fields, Ryan C., Fisher, Stephen, Flaherty, Keith, Flournoy, Jennifer, Ford, James M., Fortunato, Angelo, Frangieh, Allison, Frye, Jennifer L., Fulton, Robert S., Galipeau, Danielle, Gan, Siting, Gao, Jianjiong, Gao, Long, Gao, Peng, Gao, Vianne R., Geiger, Tim, George, Ajit, Getz, Gad, Ghosh, Sharmistha, Giannakis, Marios, Gibbs, David L., Gillanders, William E., Goecks, Jeremy, Goedegebuure, Simon P., Gould, Alanna, Gowers, Kate, Gray, Joe W., Greenleaf, William, Gresham, Jeremy, Guerriero, Jennifer L., Guha, Tuhin K., Guimaraes, Alexander R., Guinney, Justin, Gutman, David, Hacohen, Nir, Hanlon, Sean, Hansen, Casey R., Harismendy, Olivier, Harris, Kathleen A., Hata, Aaron, Hayashi, Akimasa, Heiser, Cody, Helvie, Karla, Herndon, John M., Hirst, Gilliam, Hodi, Frank, Hollmann, Travis, Horning, Aaron, Hsieh, James J., Hughes, Shannon, Huh, Won Jae, Hunger, Stephen, Hwang, Shelley E., Iacobuzio-Donahue, Christine A., Ijaz, Heba, Izar, Benjamin, Jacobson, Connor A., Janes, Samuel, Jané-Valbuena, Judit, Jayasinghe, Reyka G., Jiang, Lihua, Johnson, Brett E., Johnson, Bruce, Ju, Tao, Kadara, Humam, Kaestner, Klaus, Kagan, Jacob, Kalinke, Lukas, Keith, Robert, Khan, Aziz, Kibbe, Warren, Kim, Albert H., Kim, Erika, Kim, Junhyong, Kolodzie, Annette, Kopytra, Mateusz, Kotler, Eran, Krueger, Robert, Krysan, Kostyantyn, Kundaje, Anshul, Ladabaum, Uri, Lake, Blue B., Lam, Huy, Laquindanum, Rozelle, Lau, Ken S., Laughney, Ashley M., Lee, Hayan, Lenburg, Marc, Leonard, Carina, Leshchiner, Ignaty, Levy, Rochelle, Li, Jerry, Lian, Christine G., Lim, Kian-Huat, Lin, Jia-Ren, Lin, Yiyun, Liu, Qi, Liu, Ruiyang, Lively, Tracy, Longabaugh, William J.R., Longacre, Teri, Ma, Cynthia X., Macedonia, Mary Catherine, Madison, Tyler, Maher, Christopher A., Maitra, Anirban, Makinen, Netta, Makowski, Danika, Maley, Carlo, Maliga, Zoltan, Mallo, Diego, Maris, John, Markham, Nick, Marks, Jeffrey, Martinez, Daniel, Mashl, Robert J., Masilionais, Ignas, Mason, Jennifer, Massagué, Joan, Massion, Pierre, Mattar, Marissa, Mazurchuk, Richard, Mazutis, Linas, Mazzilli, Sarah A., McKinley, Eliot T., McMichael, Joshua F., Merrick, Daniel, Meyerson, Matthew, Miessner, Julia R., Mills, Gordon B., Mills, Meredith, Mondal, Suman B., Mori, Motomi, Mori, Yuriko, Moses, Elizabeth, Mosse, Yael, Muhlich, Jeremy L., Murphy, George F., Navin, Nicholas E., Nawy, Tal, Nederlof, Michel, Ness, Reid, Nevins, Stephanie, Nikolov, Milen, Nirmal, Ajit Johnson, Nolan, Garry, Novikov, Edward, Oberdoerffer, Philipp, O’Connell, Brendan, Offin, Michael, Oh, Stephen T., Olson, Anastasiya, Ooms, Alex, Ossandon, Miguel, Owzar, Kouros, Parmar, Swapnil, Patel, Tasleema, Patti, Gary J., Pe’er, Dana, Pe'er, Itsik, Peng, Tao, Persson, Daniel, Petty, Marvin, Pfister, Hanspeter, Polyak, Kornelia, Pourfarhangi, Kamyar, Puram, Sidharth V., Qiu, Qi, Quintanal-Villalonga, Álvaro, Raj, Arjun, Ramirez-Solano, Marisol, Rashid, Rumana, Reeb, Ashley N., Regev, Aviv, Reid, Mary, Resnick, Adam, Reynolds, Sheila M., Riesterer, Jessica L., Rodig, Scott, Roland, Joseph T., Rosenfield, Sonia, Rotem, Asaf, Roy, Sudipta, Rozenblatt-Rosen, Orit, Rudin, Charles M., Ryser, Marc D., Santagata, Sandro, Santi-Vicini, Maria, Sato, Kazuhito, Schapiro, Denis, Schrag, Deborah, Schultz, Nikolaus, Sears, Cynthia L., Sears, Rosalie C., Sen, Subrata, Sen, Triparna, Shalek, Alex, Sheng, Jeff, Sheng, Quanhu, Shoghi, Kooresh I., Shrubsole, Martha J., Shyr, Yu, Sibley, Alexander B., Siex, Kiara, Simmons, Alan J., Singer, Dinah S., Sivagnanam, Shamilene, Slyper, Michal, Snyder, Michael P., Sokolov, Artem, Song, Sheng-Kwei, Sorger, Peter K., Southard-Smith, Austin, Spira, Avrum, Srivastava, Sudhir, Stein, Janet, Storm, Phillip, Stover, Elizabeth, Strand, Siri H., Su, Timothy, Sudar, Damir, Sullivan, Ryan, Surrey, Lea, Suvà, Mario, Tan, Kai, Terekhanova, Nadezhda V., Ternes, Luke, Thammavong, Lisa, Thibault, Guillaume, Thomas, George V., Thorsson, Vésteinn, Todres, Ellen, Tran, Linh, Tyler, Madison, Uzun, Yasin, Vachani, Anil, Van Allen, Eliezer, Vandekar, Simon, Veis, Deborah J., Vigneau, Sébastien, Vossough, Arastoo, Waanders, Angela, Wagle, Nikhil, Wang, Liang-Bo, Wendl, Michael C., West, Robert, Williams, Elizabeth H., Wu, Chi-yun, Wu, Hao, Wu, Hung-Yi, Wyczalkowski, Matthew A., Xie, Yubin, Yang, Xiaolu, Yapp, Clarence, Yu, Wenbao, Yuan, Yinyin, Zhang, Dadong, Zhang, Kun, Zhang, Mianlei, Zhang, Nancy, Zhang, Yantian, Zhao, Yanyan, Zhou, Daniel Cui, Zhou, Zilu, Zhu, Houxiang, Zhu, Qin, Zhu, Xiangzhu, Zhu, Yuankun, Zhuang, Xiaowei, Hupalowska, Anna, Rood, Jennifer E., Hanlon, Sean E., Hughes, Shannon K., Hwang, E. Shelley, Johnson, Bruce E., Shalek, Alex K., Spira, Avrum E., and West, Robert B.

Published
2020
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14. Transcriptomic Characterization of SF3B1 Mutation Reveals Its Pleiotropic Effects in Chronic Lymphocytic Leukemia

Author

Wang, Lili, Brooks, Angela N, Fan, Jean, Wan, Youzhong, Gambe, Rutendo, Li, Shuqiang, Hergert, Sarah, Yin, Shanye, Freeman, Samuel S, Levin, Joshua Z, Fan, Lin, Seiler, Michael, Buonamici, Silvia, Smith, Peter G, Chau, Kevin F, Cibulskis, Carrie L, Zhang, Wandi, Rassenti, Laura Z, Ghia, Emanuela M, Kipps, Thomas J, Fernandes, Stacey, Bloch, Donald B, Kotliar, Dylan, Landau, Dan A, Shukla, Sachet A, Aster, Jon C, Reed, Robin, DeLuca, David S, Brown, Jennifer R, Neuberg, Donna, Getz, Gad, Livak, Kenneth J, Meyerson, Matthew M, Kharchenko, Peter V, and Wu, Catherine J

Subjects
Biological Sciences, Biomedical and Clinical Sciences, Oncology and Carcinogenesis, Clinical Research, Hematology, Lymphatic Research, Human Genome, Genetics, Rare Diseases, Cancer, Lymphoma, 2.1 Biological and endogenous factors, Alternative Splicing, Cell Line, Tumor, Dishevelled Proteins, Gene Expression Profiling, Gene Expression Regulation, Neoplastic, Humans, Leukemia, Lymphocytic, Chronic, B-Cell, Mutation, Phosphoproteins, RNA Splicing Factors, Receptors, Notch, Signal Transduction, CLL, Notch signaling, RNA sequencing, SF3B1, alternative splicing, Neurosciences, Oncology & Carcinogenesis, Biochemistry and cell biology, Oncology and carcinogenesis
Abstract

Mutations in SF3B1, which encodes a spliceosome component, are associated with poor outcome in chronic lymphocytic leukemia (CLL), but how these contribute to CLL progression remains poorly understood. We undertook a transcriptomic characterization of primary human CLL cells to identify transcripts and pathways affected by SF3B1 mutation. Splicing alterations, identified in the analysis of bulk cells, were confirmed in single SF3B1-mutated CLL cells and also found in cell lines ectopically expressing mutant SF3B1. SF3B1 mutation was found to dysregulate multiple cellular functions including DNA damage response, telomere maintenance, and Notch signaling (mediated through KLF8 upregulation, increased TERC and TERT expression, or altered splicing of DVL2 transcript, respectively). SF3B1 mutation leads to diverse changes in CLL-related pathways.

Published
2016

15. The Public Repository of Xenografts Enables Discovery and Randomized Phase II-like Trials in Mice

Author

Townsend, Elizabeth C, Murakami, Mark A, Christodoulou, Alexandra, Christie, Amanda L, Köster, Johannes, DeSouza, Tiffany A, Morgan, Elizabeth A, Kallgren, Scott P, Liu, Huiyun, Wu, Shuo-Chieh, Plana, Olivia, Montero, Joan, Stevenson, Kristen E, Rao, Prakash, Vadhi, Raga, Andreeff, Michael, Armand, Philippe, Ballen, Karen K, Barzaghi-Rinaudo, Patrizia, Cahill, Sarah, Clark, Rachael A, Cooke, Vesselina G, Davids, Matthew S, DeAngelo, Daniel J, Dorfman, David M, Eaton, Hilary, Ebert, Benjamin L, Etchin, Julia, Firestone, Brant, Fisher, David C, Freedman, Arnold S, Galinsky, Ilene A, Gao, Hui, Garcia, Jacqueline S, Garnache-Ottou, Francine, Graubert, Timothy A, Gutierrez, Alejandro, Halilovic, Ensar, Harris, Marian H, Herbert, Zachary T, Horwitz, Steven M, Inghirami, Giorgio, Intlekofer, Andrew M, Ito, Moriko, Izraeli, Shai, Jacobsen, Eric D, Jacobson, Caron A, Jeay, Sébastien, Jeremias, Irmela, Kelliher, Michelle A, Koch, Raphael, Konopleva, Marina, Kopp, Nadja, Kornblau, Steven M, Kung, Andrew L, Kupper, Thomas S, LeBoeuf, Nicole R, LaCasce, Ann S, Lees, Emma, Li, Loretta S, Look, A Thomas, Murakami, Masato, Muschen, Markus, Neuberg, Donna, Ng, Samuel Y, Odejide, Oreofe O, Orkin, Stuart H, Paquette, Rachel R, Place, Andrew E, Roderick, Justine E, Ryan, Jeremy A, Sallan, Stephen E, Shoji, Brent, Silverman, Lewis B, Soiffer, Robert J, Steensma, David P, Stegmaier, Kimberly, Stone, Richard M, Tamburini, Jerome, Thorner, Aaron R, van Hummelen, Paul, Wadleigh, Martha, Wiesmann, Marion, Weng, Andrew P, Wuerthner, Jens U, Williams, David A, Wollison, Bruce M, Lane, Andrew A, Letai, Anthony, Bertagnolli, Monica M, Ritz, Jerome, Brown, Myles, Long, Henry, Aster, Jon C, Shipp, Margaret A, Griffin, James D, and Weinstock, David M

Subjects
Biomedical and Clinical Sciences, Oncology and Carcinogenesis, Biotechnology, Clinical Trials and Supportive Activities, Orphan Drug, Clinical Research, Hematology, Cancer, Rare Diseases, 5.1 Pharmaceuticals, Development of treatments and therapeutic interventions, Good Health and Well Being, Animals, Antineoplastic Agents, Biomarkers, Tumor, Cell Lineage, Female, Gene Expression Profiling, Genes, p53, Heterografts, Humans, Internet, Isoquinolines, Leukemia, Leukemia, Experimental, Lymphoma, Male, Mice, Mice, Inbred NOD, Molecular Targeted Therapy, Neoplasm Proteins, Neoplasm Transplantation, Phenotype, Piperazines, Precursor B-Cell Lymphoblastic Leukemia-Lymphoma, Proteome, Proto-Oncogene Proteins c-mdm2, Random Allocation, Randomized Controlled Trials as Topic, Research Design, Tissue Banks, Transcriptome, Xenograft Model Antitumor Assays, Neurosciences, Oncology & Carcinogenesis, Biochemistry and cell biology, Oncology and carcinogenesis
Abstract

More than 90% of drugs with preclinical activity fail in human trials, largely due to insufficient efficacy. We hypothesized that adequately powered trials of patient-derived xenografts (PDX) in mice could efficiently define therapeutic activity across heterogeneous tumors. To address this hypothesis, we established a large, publicly available repository of well-characterized leukemia and lymphoma PDXs that undergo orthotopic engraftment, called the Public Repository of Xenografts (PRoXe). PRoXe includes all de-identified information relevant to the primary specimens and the PDXs derived from them. Using this repository, we demonstrate that large studies of acute leukemia PDXs that mimic human randomized clinical trials can characterize drug efficacy and generate transcriptional, functional, and proteomic biomarkers in both treatment-naive and relapsed/refractory disease.

Published
2016

19. Single-Cell RNA-Seq Reveals AML Hierarchies Relevant to Disease Progression and Immunity

Author

van Galen, Peter, Hovestadt, Volker, Wadsworth II, Marc H., Hughes, Travis K., Griffin, Gabriel K., Battaglia, Sofia, Verga, Julia A., Stephansky, Jason, Pastika, Timothy J., Lombardi Story, Jennifer, Pinkus, Geraldine S., Pozdnyakova, Olga, Galinsky, Ilene, Stone, Richard M., Graubert, Timothy A., Shalek, Alex K., Aster, Jon C., Lane, Andrew A., and Bernstein, Bradley E.

Published
2019
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20. Loss of oncogenic Notch1 with resistance to a PI3K inhibitor in T-cell leukaemia

Author

Dail, Monique, Wong, Jason, Lawrence, Jessica, O’Connor, Daniel, Nakitandwe, Joy, Chen, Shann-Ching, Xu, Jin, Lee, Leslie B, Akagi, Keiko, Li, Qing, Aster, Jon C, Pear, Warren S, Downing, James R, Sampath, Deepak, and Shannon, Kevin

Subjects
Pediatric, Cancer, Rare Diseases, Pediatric Cancer, Childhood Leukemia, Hematology, 5.1 Pharmaceuticals, Development of treatments and therapeutic interventions, Animals, Benzamides, Clone Cells, Diphenylamine, Down-Regulation, Drug Resistance, Neoplasm, Drug Synergism, Genes, ras, Indazoles, Male, Mice, Mice, Inbred C57BL, Mitogen-Activated Protein Kinase Kinases, Phosphoinositide-3 Kinase Inhibitors, Precursor T-Cell Lymphoblastic Leukemia-Lymphoma, Protein Kinase Inhibitors, Protein Structure, Tertiary, Proto-Oncogene Proteins c-akt, Receptor, Notch1, Signal Transduction, Sulfonamides, General Science & Technology
Abstract

Mutations that deregulate Notch1 and Ras/phosphoinositide 3 kinase (PI3K)/Akt signalling are prevalent in T-cell acute lymphoblastic leukaemia (T-ALL), and often coexist. Here we show that the PI3K inhibitor GDC-0941 is active against primary T-ALLs from wild-type and Kras(G12D) mice, and addition of the MEK inhibitor PD0325901 increases its efficacy. Mice invariably relapsed after treatment with drug-resistant clones, most of which unexpectedly had reduced levels of activated Notch1 protein, downregulated many Notch1 target genes, and exhibited cross-resistance to γ-secretase inhibitors. Multiple resistant primary T-ALLs that emerged in vivo did not contain somatic Notch1 mutations present in the parental leukaemia. Importantly, resistant clones upregulated PI3K signalling. Consistent with these data, inhibiting Notch1 activated the PI3K pathway, providing a likely mechanism for selection against oncogenic Notch1 signalling. These studies validate PI3K as a therapeutic target in T-ALL and raise the unexpected possibility that dual inhibition of PI3K and Notch1 signalling could promote drug resistance in T-ALL.

Published
2014

24. Activity of the PI3K-δ,γ inhibitor duvelisib in a phase 1 trial and preclinical models of T-cell lymphoma

Author

Horwitz, Steven M., Koch, Raphael, Porcu, Pierluigi, Oki, Yasuhiro, Moskowitz, Alison, Perez, Megan, Myskowski, Patricia, Officer, Adam, Jaffe, Jacob D., Morrow, Sara N., Allen, Kerstin, Douglas, Mark, Stern, Howard, Sweeney, Jennifer, Kelly, Patrick, Kelly, Virginia, Aster, Jon C., Weaver, David, Foss, Francine M., and Weinstock, David M.

Published
2018
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25. DNA methyltransferase inhibition overcomes diphthamide pathway deficiencies underlying CD123-targeted treatment resistance

Author

Togami, Katsuhiro, Pastika, Timothy, Stephansky, Jason, Ghandi, Mahmoud, Christie, Amanda L., Jones, Kristen L., Johnson, Carl A., Lindsay, Ross W., Brooks, Christopher L., Letai, Anthony, Craig, Jeffrey W., Pozdnyakova, Olga, Weinstock, David M., Montero, Joan, Aster, Jon C., Johannessen, Cory M., and Lane, Andrew A.

Subjects
Thermo Fisher Scientific Inc., Interleukins, Blinatumomab, Methylation, Transferases, DNA, Dendritic cells, Inotuzumab ozogamicin, Scientific equipment industry, Tagraxofusp, Acute myelocytic leukemia, Cancer, Myeloid leukemia, Tumors, Genomes, Enzymes, Diphtheria, Health care industry
Abstract

The interleukin-3 receptor [alpha] subunit, CD123, is expressed in many hematologic malignancies including acute myeloid leukemia (AML) and blastic plasmacytoid dendritic cell neoplasm (BPDCN). Tagraxofusp (SL-401) is a CD123-targeted therapy consisting of interleukin-3 fused to a truncated diphtheria toxin payload. Factors influencing response to tagraxofusp other than CD123 expression are largely unknown. We interrogated tagraxofusp resistance in patients and experimental models and found that it was not associated with CD123 loss. Rather, resistant AML and BPDCN cells frequently acquired deficiencies in the diphthamide synthesis pathway, impairing tagraxofusp's ability to ADP- ribosylate cellular targets. Expression of DPH1, encoding a diphthamide pathway enzyme, was reduced by DNA CpG methylation in resistant cells. Treatment with the DNA methyltransferase inhibitor azacitidine restored DPH1 expression and tagraxofusp sensitivity. We also developed a drug-dependent ADP-ribosylation assay in primary cells that correlated with tagraxofusp activity and may represent an additional novel biomarker. As predicted by these results and our observation that resistance also increased mitochondrial apoptotic priming, we found that the combination of tagraxofusp and azacitidine was effective in patient-derived xenografts treated in vivo. These data have important implications for clinical use of tagraxofusp and led to a phase 1 study combining tagraxofusp and azacitidine in myeloid malignancies., Introduction CD123, or the interleukin-3 (IL-3) receptor (IL-3R) [alpha] chain, is a cell-surface marker associated with a variety of hematologic malignancies and is often enriched on tumor cells compared with [...]

Published
2019
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26. Vulnerabilities in mIDH2 AML confer sensitivity to APL-like targeted combination therapy

Author

Mugoni, Vera, Panella, Riccardo, Cheloni, Giulia, Chen, Ming, Pozdnyakova, Olga, Stroopinsky, Dina, Guarnerio, Jlenia, Monteleone, Emanuele, Lee, Jonathan David, Mendez, Lourdes, Menon, Archita Venugopal, Aster, Jon Christopher, Lane, Andrew A., Stone, Richard Maury, Galinsky, Ilene, Zamora, José Cervera, Lo-Coco, Francesco, Bhasin, Manoj Kumar, Avigan, David, Longo, Letizia, Clohessy, John Gerard, and Pandolfi, Pier Paolo

Published
2019
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27. A Zebrafish bmyb Mutation Causes Genome Instability and Increased Cancer Susceptibility

Author

Shepard, Jennifer L., Amatruda, James F., Stern, Howard M., Subramanian, Aravind, Finkelstein, David, Ziai, James, Finley, K. Rose, Pfaff, Kathleen L., Hersey, Candace, Zhou, Yi, Barut, Bruce, Freedman, Matthew, Lee, Charles, Spitsbergen, Jan, Neuberg, Donna, Weber, Gerhard, Golub, Todd R., Glickman, Jonathan N., Kutok, Jeffery L., Aster, Jon C., Zon, Leonard I., and Kunkel, Louis M.

Published
2005

28. Abstract PR015: Tumor-specific immunity generated by a personalized neoantigen vaccination incorporating locally delivered ipilimumab in renal cell carcinoma

Author

Braun, David A., primary, Keskin, Derin B., additional, Shukla, Sachet A., additional, McGregor, Bradley A., additional, Schindler, Nicholas R., additional, Blass, Eryn, additional, Klaeger, Susan, additional, Pomerance, Lucas, additional, Sarkizova, Siranush, additional, Li, Shuqiang, additional, Southard, Jackson, additional, Moranzoni, Giorgia, additional, Pedersen, Christina B., additional, Liu, Yiwen, additional, Chang, Steven L., additional, Hirsch, Michelle S., additional, LeBoeuf, Nicole R., additional, Mossanen, Matthew, additional, Chea, Vipheaviny, additional, Carulli, Isabel, additional, Olive, Oriol, additional, Mehndiratta, Ambica, additional, Greenslade, Haley, additional, Oliveira, Giacomo, additional, Iorgulescu, J. Bryan, additional, Signoretti, Sabina, additional, Aster, Jon C., additional, Elagina, Liudmila, additional, Leshchiner, Ignaty, additional, Getz, Gad, additional, Harden, Maegan, additional, Gabriel, Stacey, additional, Olsen, Lars R., additional, Neuberg, Donna S., additional, Fritsch, Edward F., additional, Hacohen, Nir, additional, Livak, Kenneth J., additional, Carr, Steven, additional, Ott, Patrick A., additional, Wu, Catherine J., additional, and Choueiri, Toni K., additional

Published
2023
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29. Abstract A013: Tumor-specific immunity generated by a personalized neoantigen vaccination incorporating locally delivered ipilimumab in renal cell carcinoma

Author

Braun, David A., primary, Keskin, Derin B., additional, Shukla, Sachet A., additional, McGregor, Bradley A., additional, Schindler, Nicholas R., additional, Blass, Eryn, additional, Klaeger, Susan, additional, Pomerance, Lucas, additional, Sarkizova, Siranush, additional, Li, Shuqiang, additional, Southard, Jackson, additional, Moranzoni, Giorgia, additional, Pedersen, Christina B., additional, Liu, Yiwen, additional, Chang, Steven L., additional, Hirsch, Michelle S., additional, LeBoeuf, Nicole R., additional, Mossanen, Matthew, additional, Chea, Vipheaviny, additional, Carulli, Isabel, additional, Olive, Oriol, additional, Mehndiratta, Ambica, additional, Greenslade, Haley, additional, Oliveira, Giacomo, additional, Iorgulescu, J. Bryan, additional, Signoretti, Sabina, additional, Aster, Jon C., additional, Elagina, Liudmila, additional, Leshchiner, Ignaty, additional, Getz, Gad, additional, Harden, Maegan, additional, Gabriel, Stacey, additional, Olsen, Lars R., additional, Neuberg, Donna S., additional, Fritsch, Edward F., additional, Hacohen, Nir, additional, Livak, Kenneth J., additional, Carr, Steven, additional, Ott, Patrick A., additional, Wu, Catherine J., additional, and Choueiri, Toni K., additional

Published
2023
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30. P324: CELL PLASTICITY PREDETERMINES TREATMENT RESPONSE IN T-ALL

Author

Dimitrova, Valeriya, primary, Frede, Julia, additional, Montanaro, Anna, additional, Potdar, Sayalee, additional, Stuart, Hannah, additional, Sotoudeh, Noori, additional, Van Scoyk, Alexandria, additional, Bhatt, Shruti, additional, Letai, Anthony, additional, Aster, Jon, additional, Lohr, Jens, additional, and Knoechel, Birgit, additional

Published
2023
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31. Myc-Induced T Cell Leukemia in Transgenic Zebrafish

Author

Langenau, David M., Traver, David, Ferrando, Adolfo A., Kutok, Jeffery L., Aster, Jon C., Kanki, John P., Lin, Shuo, Prochownik, Ed, Trede, Nikolaus S., Zon, Leonard I., and Look, A. Thomas

Published
2003

32. A B Cell Regulome Links Notch to Downstream Oncogenic Pathways in Small B Cell Lymphomas

Author

Ryan, Russell J.H., Petrovic, Jelena, Rausch, Dylan M., Zhou, Yeqiao, Lareau, Caleb A., Kluk, Michael J., Christie, Amanda L., Lee, Winston Y., Tarjan, Daniel R., Guo, Bingqian, Donohue, Laura K.H., Gillespie, Shawn M., Nardi, Valentina, Hochberg, Ephraim P., Blacklow, Stephen C., Weinstock, David M., Faryabi, Robert B., Bernstein, Bradley E., Aster, Jon C., and Pear, Warren S.

Published
2017
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33. Adaptive Chromatin Remodeling Drives Glioblastoma Stem Cell Plasticity and Drug Tolerance

Author

Liau, Brian B., Sievers, Cem, Donohue, Laura K., Gillespie, Shawn M., Flavahan, William A., Miller, Tyler E., Venteicher, Andrew S., Hebert, Christine H., Carey, Christopher D., Rodig, Scott J., Shareef, Sarah J., Najm, Fadi J., van Galen, Peter, Wakimoto, Hiroaki, Cahill, Daniel P., Rich, Jeremy N., Aster, Jon C., Suvà, Mario L., Patel, Anoop P., and Bernstein, Bradley E.

Published
2017
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35. The Tel-Abl (ETV6-Abl) tyrosine kinase, product of complex (9;12) translocations in human leukemia, induces distinct myeloproliferative disease in mice.

Author

Million, Ryan P, Aster, Jon, Gilliland, D Gary, and Van Etten, Richard A

Subjects
Animals, Bone Marrow Cells: metabolism, pathology, Bone Marrow Transplantation, Chromosomes, Human, Pair 12, Chromosomes, Human, Pair 9, Female, Fusion Proteins, bcr-abl: adverse effects, genetics, Humans, Intestinal Diseases: etiology, mortality, Leukemia, Myelogenous, Chronic, BCR-ABL Positive: etiology, pathology, Mice, Mice, Inbred BALB C, Myeloproliferative Disorders: etiology, mortality, pathology, Neoplasm Transplantation: adverse effects, mortality, pathology, Oncogene Proteins, Fusion: adverse effects, genetics, Protein-Tyrosine Kinases: adverse effects, genetics, Survival Rate, Transduction, Genetic, Translocation, Genetic
Abstract

Several patients with clinical features of chronic myeloid leukemia (CML) have fusion of the TEL (ETV6) gene on 12p13 with ABL on 9q34 and express a chimeric Tel-Abl protein that contains the same portion of the Abl tyrosine kinase fused to Tel, an Ets family transcription factor, rather than Bcr. In a murine retroviral bone marrow transduction-transplantation model, a Tel (exon 1-5)-Abl fusion protein induced 2 distinct illnesses: a CML-like myeloproliferative disease very similar to that induced by Bcr-Abl but with increased latency and a novel syndrome characterized by small-bowel myeloid cell infiltration and necrosis, increased circulating endotoxin and tumor necrosis factor alpha levels, and fulminant hepatic and renal failure. Induction of both diseases required the Tel pointed homology oligomerization domain and Abl tyrosine kinase activity. Myeloid cells from mice with both diseases expressed Tel-Abl protein. CML-like disease induced by Tel-Abl and Bcr-Abl was polyclonal and originated from cells with multilineage (myeloid, erythroid, and B- and T-lymphoid) repopulating ability and the capacity to generate day-12 spleen colonies in secondary transplantations. In contrast to findings with Bcr-Abl, however, neither Tel-Abl-induced disease could be adoptively transferred to irradiated secondary recipient syngeneic mice. These results show that Tel-Abl has leukemogenic properties from distinct from those of Bcr-Abl and may act in a different bone marrow progenitor.

Published
2002

38. Diffuse large B-cell lymphoma patient-derived xenograft models capture the molecular and biological heterogeneity of the disease

Author

Chapuy, Bjoern, Cheng, Hongwei, Watahiki, Akira, Ducar, Matthew D., Tan, Yuxiang, Chen, Linfeng, Roemer, Margaretha G.M., Ouyang, Jing, Christie, Amanda L., Zhang, Liye, Gusenleitner, Daniel, Abo, Ryan P., Farinha, Pedro, von Bonin, Frederike, Thorner, Aaron R., Sun, Heather H., Gascoyne, Randy D., Pinkus, Geraldine S., van Hummelen, Paul, Wulf, Gerald G., Aster, Jon C., Weinstock, David M., Monti, Stefano, Rodig, Scott J., Wang, Yuzhuo, and Shipp, Margaret A.

Published
2016
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40. An immunogenic personal neoantigen vaccine for patients with melanoma

Author

Ott, Patrick A., Hu, Zhuting, Keskin, Derin B., Shukla, Sachet A., Sun, Jing, Bozym, David J., Zhang, Wandi, Luoma, Adrienne, Giobbie-Hurder, Anita, Peter, Lauren, Chen, Christina, Olive, Oriol, Carter, Todd A., Li, Shuqiang, Lieb, David J., Eisenhaure, Thomas, Gjini, Evisa, Stevens, Jonathan, Lane, William J., Javeri, Indu, Nellaiappan, Kaliappanadar, Salazar, Andres M., Daley, Heather, Seaman, Michael, Buchbinder, Elizabeth I., Yoon, Charles H., Harden, Maegan, Lennon, Niall, Gabriel, Stacey, Rodig, Scott J., Barouch, Dan H., Aster, Jon C., Getz, Gad, Wucherpfennig, Kai, Neuberg, Donna, Ritz, Jerome, Lander, Eric S., Fritsch, Edward F., Hacohen, Nir, and Wu, Catherine J.

Published
2017
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43. Cellular Plasticity As Mechanisms to Escape from NOTCH1-Inhibition in T-ALL

Author

Dimitrova, Valeriya, primary, Sotudeh, Noori, additional, Knoechel, Birgit, additional, Lohr, Jens G., additional, Montanaro, Anna, additional, Potdar, Sayalee V., additional, Frede, Julia, additional, Van Scoyk, Alexandria, additional, Bhatt, Shruti, additional, Anand, Praveen, additional, Aster, Jon C., additional, Weinstock, David M, additional, and Letai, Anthony G., additional

Published
2022
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44. A Novel Cryopreservation and Biobanking Strategy to Study Lymphoid Tissue Stromal Cells in Lymphoproliferative Disorders

Author

Brandstadter, Joshua D, primary, De Martin, Angelina, additional, Lϋetge, Mechthild, additional, Ferreira, Antonio, additional, Gaudette, Brian T., additional, Gonzalez, Michael, additional, Stanossek, Yves, additional, Camiolo, Edward, additional, Wertheim, Gerald, additional, Allman, David, additional, Fajgenbaum, David C, additional, Aster, Jon C., additional, Ludewig, Burkhard, additional, and Maillard, Ivan, additional

Published
2022
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45. Single-cell RNA sequencing identifies a paracrine interaction that may drive oncogenic notch signaling in human adenoid cystic carcinoma

Author

Parikh, Anuraag S., primary, Wizel, Avishai, additional, Davis, Daniel, additional, Lefranc-Torres, Armida, additional, Rodarte-Rascon, Alejandro I., additional, Miller, Lauren E., additional, Emerick, Kevin S., additional, Varvares, Mark A., additional, Deschler, Daniel G., additional, Faquin, William C., additional, Aster, Jon C., additional, Lin, Derrick T., additional, Bernstein, Bradley E., additional, Drier, Yotam, additional, and Puram, Sidharth V., additional

Published
2022
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47. SYK Is a Critical Regulator of FLT3 in Acute Myeloid Leukemia

Author

Puissant, Alexandre, Fenouille, Nina, Alexe, Gabriela, Pikman, Yana, Bassil, Christopher F., Mehta, Swapnil, Du, Jinyan, Kazi, Julhash U., Luciano, Frédéric, Rönnstrand, Lars, Kung, Andrew L., Aster, Jon C., Galinsky, Ilene, Stone, Richard M., DeAngelo, Daniel J., Hemann, Michael T., and Stegmaier, Kimberly

Published
2014
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48. Uremic Toxin Indoxyl Sulfate Promotes Proinflammatory Macrophage Activation Via the Interplay of OATP2B1 and Dll4-Notch Signaling: Potential Mechanism for Accelerated Atherogenesis in Chronic Kidney Disease

Author

Nakano, Toshiaki, Katsuki, Shunsuke, Chen, Mingxian, Decano, Julius L., Halu, Arda, Lee, Lang Ho, Pestana, Diego V. S., Kum, Angelo S. T., Kuromoto, Rodrigo K., Golden, Whitney S., Boff, Mario S., Guimaraes, Gabriel C., Higashi, Hideyuki, Kauffman, Kevin J., Maejima, Takashi, Suzuki, Takehiro, Iwata, Hiroshi, Barabási, Albert-László, Aster, Jon C., Anderson, Daniel G., Sharma, Amitabh, Singh, Sasha A., Aikawa, Elena, and Aikawa, Masanori

Published
2019
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49. Long-range enhancer activity determines Myc sensitivity to Notch inhibitors in T cell leukemia

Author

Yashiro-Ohtani, Yumi, Wang, Hongfang, Zang, Chongzhi, Arnett, Kelly L., Bailis, Will, Ho, Yugong, Knoechel, Birgit, Lanauze, Claudia, Louis, Lumena, Forsyth, Katherine S., Chen, Sujun, Chung, Yoonjie, Schug, Jonathan, Blobel, Gerd A., Liebhaber, Stephen A., Bernstein, Bradley E., Blacklow, Stephen C., Liu, Xiaole Shirley, Aster, Jon C., and Pear, Warren S.

Published
2014
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50. Targetable vulnerabilities in T- and NK-cell lymphomas identified through preclinical models

Author

Ng, Samuel Y., Yoshida, Noriaki, Christie, Amanda L., Ghandi, Mahmoud, Dharia, Neekesh V., Dempster, Joshua, Murakami, Mark, Shigemori, Kay, Morrow, Sara N., Van Scoyk, Alexandria, Cordero, Nicolas A., Stevenson, Kristen E., Puligandla, Maneka, Haas, Brian, Lo, Christopher, Meyers, Robin, Gao, Galen, Cherniack, Andrew, Louissaint, Jr, Abner, Nardi, Valentina, Thorner, Aaron R., Long, Henry, Qiu, Xintao, Morgan, Elizabeth A., Dorfman, David M., Fiore, Danilo, Jang, Julie, Epstein, Alan L., Dogan, Ahmet, Zhang, Yanming, Horwitz, Steven M., Jacobsen, Eric D., Santiago, Solimar, Ren, Jian-Guo, Guerlavais, Vincent, Annis, D. Allen, Aivado, Manuel, Saleh, Mansoor N., Mehta, Amitkumar, Tsherniak, Aviad, Root, David, Vazquez, Francisca, Hahn, William C., Inghirami, Giorgio, Aster, Jon C., Weinstock, David M., and Koch, Raphael

Published
2018
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