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240 results on '"Christie, Amanda L."'

1. Targeting TRIP13 in favorable histology Wilms tumor with nuclear export inhibitors synergizes with doxorubicin

Author

Mittal, Karuna, Cooper, Garrett W., Lee, Benjamin P., Su, Yongdong, Skinner, Katie T., Shim, Jenny, Jonus, Hunter C., Kim, Won Jun, Doshi, Mihir, Almanza, Diego, Kynnap, Bryan D., Christie, Amanda L., Yang, Xiaoping, Cowley, Glenn S., Leeper, Brittaney A., Morton, Christopher L., Dwivedi, Bhakti, Lawrence, Taylor, Rupji, Manali, Keskula, Paula, Meyer, Stephanie, Clinton, Catherine M., Bhasin, Manoj, Crompton, Brian D., Tseng, Yuen-Yi, Boehm, Jesse S., Ligon, Keith L., Root, David E., Murphy, Andrew J., Weinstock, David M., Gokhale, Prafulla C., Spangle, Jennifer M., Rivera, Miguel N., Mullen, Elizabeth A., Stegmaier, Kimberly, Goldsmith, Kelly C., Hahn, William C., and Hong, Andrew L.

Published
2024
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2. PDX-MI: Minimal Information for Patient-Derived Tumor Xenograft Models

Author

Meehan, Terrence F, Conte, Nathalie, Goldstein, Theodore, Inghirami, Giorgio, Murakami, Mark A, Brabetz, Sebastian, Gu, Zhiping, Wiser, Jeffrey A, Dunn, Patrick, Begley, Dale A, Krupke, Debra M, Bertotti, Andrea, Bruna, Alejandra, Brush, Matthew H, Byrne, Annette T, Caldas, Carlos, Christie, Amanda L, Clark, Dominic A, Dowst, Heidi, Dry, Jonathan R, Doroshow, James H, Duchamp, Olivier, Evrard, Yvonne A, Ferretti, Stephane, Frese, Kristopher K, Goodwin, Neal C, Greenawalt, Danielle, Haendel, Melissa A, Hermans, Els, Houghton, Peter J, Jonkers, Jos, Kemper, Kristel, Khor, Tin O, Lewis, Michael T, Lloyd, KC Kent, Mason, Jeremy, Medico, Enzo, Neuhauser, Steven B, Olson, James M, Peeper, Daniel S, Rueda, Oscar M, Seong, Je Kyung, Trusolino, Livio, Vinolo, Emilie, Wechsler-Reya, Robert J, Weinstock, David M, Welm, Alana, Weroha, S John, Amant, Frédéric, Pfister, Stefan M, Kool, Marcel, Parkinson, Helen, Butte, Atul J, and Bult, Carol J

Subjects
Biomedical and Clinical Sciences, Oncology and Carcinogenesis, Cancer, 2.6 Resources and infrastructure (aetiology), Good Health and Well Being, Animals, Databases as Topic, Disease Models, Animal, Humans, Mice, Neoplasms, Patients, Xenograft Model Antitumor Assays, Oncology & Carcinogenesis, Biochemistry and cell biology, Oncology and carcinogenesis
Abstract

Patient-derived tumor xenograft (PDX) mouse models have emerged as an important oncology research platform to study tumor evolution, mechanisms of drug response and resistance, and tailoring chemotherapeutic approaches for individual patients. The lack of robust standards for reporting on PDX models has hampered the ability of researchers to find relevant PDX models and associated data. Here we present the PDX models minimal information standard (PDX-MI) for reporting on the generation, quality assurance, and use of PDX models. PDX-MI defines the minimal information for describing the clinical attributes of a patient's tumor, the processes of implantation and passaging of tumors in a host mouse strain, quality assurance methods, and the use of PDX models in cancer research. Adherence to PDX-MI standards will facilitate accurate search results for oncology models and their associated data across distributed repository databases and promote reproducibility in research studies using these models. Cancer Res; 77(21); e62-66. ©2017 AACR.

Published
2017

3. 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

6. 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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7. 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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8. HSP90 inhibition overcomes ibrutinib resistance in mantle cell lymphoma

Author

Jacobson, Caron, Kopp, Nadja, Layer, Jacob V., Redd, Robert A., Tschuri, Sebastian, Haebe, Sarah, van Bodegom, Diederik, Bird, Liat, Christie, Amanda L., Christodoulou, Alexandra, Saur, Amy, Tivey, Trevor, Zapf, Stefanie, Bararia, Deepak, Zimber-Strobl, Ursula, Rodig, Scott J., Weigert, Oliver, and Weinstock, David M.

Published
2016
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9. 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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10. Supplementary Table 5 from Mechanisms of Lymphoma Clearance Induced by High-Dose Alkylating Agents

Author

Lossos, Chen, primary, Liu, Yunpeng, primary, Kolb, Kellie E., primary, Christie, Amanda L., primary, Van Scoyk, Alexandria, primary, Prakadan, Sanjay M., primary, Shigemori, Kay, primary, Stevenson, Kristen E., primary, Morrow, Sara, primary, Plana, Olivia D., primary, Fraser, Cameron, primary, Jones, Kristen L., primary, Liu, Huiyun, primary, Pallasch, Christian P., primary, Modiste, Rebecca, primary, Nguyen, Quang-De, primary, Craig, Jeffrey W., primary, Morgan, Elizabeth A., primary, Vega, Francisco, primary, Aster, Jon C., primary, Sarosiek, Kristopher A., primary, Shalek, Alex K., primary, Hemann, Michael T., primary, and Weinstock, David M., primary

Published
2023
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11. Supplementary Table 4 from Mechanisms of Lymphoma Clearance Induced by High-Dose Alkylating Agents

Author

Lossos, Chen, primary, Liu, Yunpeng, primary, Kolb, Kellie E., primary, Christie, Amanda L., primary, Van Scoyk, Alexandria, primary, Prakadan, Sanjay M., primary, Shigemori, Kay, primary, Stevenson, Kristen E., primary, Morrow, Sara, primary, Plana, Olivia D., primary, Fraser, Cameron, primary, Jones, Kristen L., primary, Liu, Huiyun, primary, Pallasch, Christian P., primary, Modiste, Rebecca, primary, Nguyen, Quang-De, primary, Craig, Jeffrey W., primary, Morgan, Elizabeth A., primary, Vega, Francisco, primary, Aster, Jon C., primary, Sarosiek, Kristopher A., primary, Shalek, Alex K., primary, Hemann, Michael T., primary, and Weinstock, David M., primary

Published
2023
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12. Supplementary Table 2 from Mechanisms of Lymphoma Clearance Induced by High-Dose Alkylating Agents

Author

Lossos, Chen, primary, Liu, Yunpeng, primary, Kolb, Kellie E., primary, Christie, Amanda L., primary, Van Scoyk, Alexandria, primary, Prakadan, Sanjay M., primary, Shigemori, Kay, primary, Stevenson, Kristen E., primary, Morrow, Sara, primary, Plana, Olivia D., primary, Fraser, Cameron, primary, Jones, Kristen L., primary, Liu, Huiyun, primary, Pallasch, Christian P., primary, Modiste, Rebecca, primary, Nguyen, Quang-De, primary, Craig, Jeffrey W., primary, Morgan, Elizabeth A., primary, Vega, Francisco, primary, Aster, Jon C., primary, Sarosiek, Kristopher A., primary, Shalek, Alex K., primary, Hemann, Michael T., primary, and Weinstock, David M., primary

Published
2023
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13. Data from Mechanisms of Lymphoma Clearance Induced by High-Dose Alkylating Agents

Author

Lossos, Chen, primary, Liu, Yunpeng, primary, Kolb, Kellie E., primary, Christie, Amanda L., primary, Van Scoyk, Alexandria, primary, Prakadan, Sanjay M., primary, Shigemori, Kay, primary, Stevenson, Kristen E., primary, Morrow, Sara, primary, Plana, Olivia D., primary, Fraser, Cameron, primary, Jones, Kristen L., primary, Liu, Huiyun, primary, Pallasch, Christian P., primary, Modiste, Rebecca, primary, Nguyen, Quang-De, primary, Craig, Jeffrey W., primary, Morgan, Elizabeth A., primary, Vega, Francisco, primary, Aster, Jon C., primary, Sarosiek, Kristopher A., primary, Shalek, Alex K., primary, Hemann, Michael T., primary, and Weinstock, David M., primary

Published
2023
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14. Supplementary Table 6 from Mechanisms of Lymphoma Clearance Induced by High-Dose Alkylating Agents

Author

Lossos, Chen, primary, Liu, Yunpeng, primary, Kolb, Kellie E., primary, Christie, Amanda L., primary, Van Scoyk, Alexandria, primary, Prakadan, Sanjay M., primary, Shigemori, Kay, primary, Stevenson, Kristen E., primary, Morrow, Sara, primary, Plana, Olivia D., primary, Fraser, Cameron, primary, Jones, Kristen L., primary, Liu, Huiyun, primary, Pallasch, Christian P., primary, Modiste, Rebecca, primary, Nguyen, Quang-De, primary, Craig, Jeffrey W., primary, Morgan, Elizabeth A., primary, Vega, Francisco, primary, Aster, Jon C., primary, Sarosiek, Kristopher A., primary, Shalek, Alex K., primary, Hemann, Michael T., primary, and Weinstock, David M., primary

Published
2023
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15. Supplementary Table 3 from Mechanisms of Lymphoma Clearance Induced by High-Dose Alkylating Agents

Author

Lossos, Chen, primary, Liu, Yunpeng, primary, Kolb, Kellie E., primary, Christie, Amanda L., primary, Van Scoyk, Alexandria, primary, Prakadan, Sanjay M., primary, Shigemori, Kay, primary, Stevenson, Kristen E., primary, Morrow, Sara, primary, Plana, Olivia D., primary, Fraser, Cameron, primary, Jones, Kristen L., primary, Liu, Huiyun, primary, Pallasch, Christian P., primary, Modiste, Rebecca, primary, Nguyen, Quang-De, primary, Craig, Jeffrey W., primary, Morgan, Elizabeth A., primary, Vega, Francisco, primary, Aster, Jon C., primary, Sarosiek, Kristopher A., primary, Shalek, Alex K., primary, Hemann, Michael T., primary, and Weinstock, David M., primary

Published
2023
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16. Supplementary Table 7 from Mechanisms of Lymphoma Clearance Induced by High-Dose Alkylating Agents

Author

Lossos, Chen, primary, Liu, Yunpeng, primary, Kolb, Kellie E., primary, Christie, Amanda L., primary, Van Scoyk, Alexandria, primary, Prakadan, Sanjay M., primary, Shigemori, Kay, primary, Stevenson, Kristen E., primary, Morrow, Sara, primary, Plana, Olivia D., primary, Fraser, Cameron, primary, Jones, Kristen L., primary, Liu, Huiyun, primary, Pallasch, Christian P., primary, Modiste, Rebecca, primary, Nguyen, Quang-De, primary, Craig, Jeffrey W., primary, Morgan, Elizabeth A., primary, Vega, Francisco, primary, Aster, Jon C., primary, Sarosiek, Kristopher A., primary, Shalek, Alex K., primary, Hemann, Michael T., primary, and Weinstock, David M., primary

Published
2023
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17. Supplementary Table 1 from Mechanisms of Lymphoma Clearance Induced by High-Dose Alkylating Agents

Author

Lossos, Chen, primary, Liu, Yunpeng, primary, Kolb, Kellie E., primary, Christie, Amanda L., primary, Van Scoyk, Alexandria, primary, Prakadan, Sanjay M., primary, Shigemori, Kay, primary, Stevenson, Kristen E., primary, Morrow, Sara, primary, Plana, Olivia D., primary, Fraser, Cameron, primary, Jones, Kristen L., primary, Liu, Huiyun, primary, Pallasch, Christian P., primary, Modiste, Rebecca, primary, Nguyen, Quang-De, primary, Craig, Jeffrey W., primary, Morgan, Elizabeth A., primary, Vega, Francisco, primary, Aster, Jon C., primary, Sarosiek, Kristopher A., primary, Shalek, Alex K., primary, Hemann, Michael T., primary, and Weinstock, David M., primary

Published
2023
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18. Supplementary Figures and Methods from Mechanisms of Lymphoma Clearance Induced by High-Dose Alkylating Agents

Author

Lossos, Chen, primary, Liu, Yunpeng, primary, Kolb, Kellie E., primary, Christie, Amanda L., primary, Van Scoyk, Alexandria, primary, Prakadan, Sanjay M., primary, Shigemori, Kay, primary, Stevenson, Kristen E., primary, Morrow, Sara, primary, Plana, Olivia D., primary, Fraser, Cameron, primary, Jones, Kristen L., primary, Liu, Huiyun, primary, Pallasch, Christian P., primary, Modiste, Rebecca, primary, Nguyen, Quang-De, primary, Craig, Jeffrey W., primary, Morgan, Elizabeth A., primary, Vega, Francisco, primary, Aster, Jon C., primary, Sarosiek, Kristopher A., primary, Shalek, Alex K., primary, Hemann, Michael T., primary, and Weinstock, David M., primary

Published
2023
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19. Data from PDX-MI: Minimal Information for Patient-Derived Tumor Xenograft Models

Author

Meehan, Terrence F., primary, Conte, Nathalie, primary, Goldstein, Theodore, primary, Inghirami, Giorgio, primary, Murakami, Mark A., primary, Brabetz, Sebastian, primary, Gu, Zhiping, primary, Wiser, Jeffrey A., primary, Dunn, Patrick, primary, Begley, Dale A., primary, Krupke, Debra M., primary, Bertotti, Andrea, primary, Bruna, Alejandra, primary, Brush, Matthew H., primary, Byrne, Annette T., primary, Caldas, Carlos, primary, Christie, Amanda L., primary, Clark, Dominic A., primary, Dowst, Heidi, primary, Dry, Jonathan R., primary, Doroshow, James H., primary, Duchamp, Olivier, primary, Evrard, Yvonne A., primary, Ferretti, Stephane, primary, Frese, Kristopher K., primary, Goodwin, Neal C., primary, Greenawalt, Danielle, primary, Haendel, Melissa A., primary, Hermans, Els, primary, Houghton, Peter J., primary, Jonkers, Jos, primary, Kemper, Kristel, primary, Khor, Tin O., primary, Lewis, Michael T., primary, Lloyd, K.C. Kent, primary, Mason, Jeremy, primary, Medico, Enzo, primary, Neuhauser, Steven B., primary, Olson, James M., primary, Peeper, Daniel S., primary, Rueda, Oscar M., primary, Seong, Je Kyung, primary, Trusolino, Livio, primary, Vinolo, Emilie, primary, Wechsler-Reya, Robert J., primary, Weinstock, David M., primary, Welm, Alana, primary, Weroha, S. John, primary, Amant, Frédéric, primary, Pfister, Stefan M., primary, Kool, Marcel, primary, Parkinson, Helen, primary, Butte, Atul J., primary, and Bult, Carol J., primary

Published
2023
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20. S1 from PDX-MI: Minimal Information for Patient-Derived Tumor Xenograft Models

Author

Meehan, Terrence F., primary, Conte, Nathalie, primary, Goldstein, Theodore, primary, Inghirami, Giorgio, primary, Murakami, Mark A., primary, Brabetz, Sebastian, primary, Gu, Zhiping, primary, Wiser, Jeffrey A., primary, Dunn, Patrick, primary, Begley, Dale A., primary, Krupke, Debra M., primary, Bertotti, Andrea, primary, Bruna, Alejandra, primary, Brush, Matthew H., primary, Byrne, Annette T., primary, Caldas, Carlos, primary, Christie, Amanda L., primary, Clark, Dominic A., primary, Dowst, Heidi, primary, Dry, Jonathan R., primary, Doroshow, James H., primary, Duchamp, Olivier, primary, Evrard, Yvonne A., primary, Ferretti, Stephane, primary, Frese, Kristopher K., primary, Goodwin, Neal C., primary, Greenawalt, Danielle, primary, Haendel, Melissa A., primary, Hermans, Els, primary, Houghton, Peter J., primary, Jonkers, Jos, primary, Kemper, Kristel, primary, Khor, Tin O., primary, Lewis, Michael T., primary, Lloyd, K.C. Kent, primary, Mason, Jeremy, primary, Medico, Enzo, primary, Neuhauser, Steven B., primary, Olson, James M., primary, Peeper, Daniel S., primary, Rueda, Oscar M., primary, Seong, Je Kyung, primary, Trusolino, Livio, primary, Vinolo, Emilie, primary, Wechsler-Reya, Robert J., primary, Weinstock, David M., primary, Welm, Alana, primary, Weroha, S. John, primary, Amant, Frédéric, primary, Pfister, Stefan M., primary, Kool, Marcel, primary, Parkinson, Helen, primary, Butte, Atul J., primary, and Bult, Carol J., primary

Published
2023
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21. Supplementary Tables 1 - 3 from High-Throughput Tyrosine Kinase Activity Profiling Identifies FAK as a Candidate Therapeutic Target in Ewing Sarcoma

Author

Crompton, Brian D., primary, Carlton, Anne L., primary, Thorner, Aaron R., primary, Christie, Amanda L., primary, Du, Jinyan, primary, Calicchio, Monica L., primary, Rivera, Miguel N., primary, Fleming, Mark D., primary, Kohl, Nancy E., primary, Kung, Andrew L., primary, and Stegmaier, Kimberly, primary

Published
2023
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22. Supplementary Figures 1 - 5 from High-Throughput Tyrosine Kinase Activity Profiling Identifies FAK as a Candidate Therapeutic Target in Ewing Sarcoma

Author

Crompton, Brian D., primary, Carlton, Anne L., primary, Thorner, Aaron R., primary, Christie, Amanda L., primary, Du, Jinyan, primary, Calicchio, Monica L., primary, Rivera, Miguel N., primary, Fleming, Mark D., primary, Kohl, Nancy E., primary, Kung, Andrew L., primary, and Stegmaier, Kimberly, primary

Published
2023
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24. Supplementary Figure Legend from High-Throughput Tyrosine Kinase Activity Profiling Identifies FAK as a Candidate Therapeutic Target in Ewing Sarcoma

Author

Crompton, Brian D., primary, Carlton, Anne L., primary, Thorner, Aaron R., primary, Christie, Amanda L., primary, Du, Jinyan, primary, Calicchio, Monica L., primary, Rivera, Miguel N., primary, Fleming, Mark D., primary, Kohl, Nancy E., primary, Kung, Andrew L., primary, and Stegmaier, Kimberly, primary

Published
2023
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25. Activity of the Type II JAK2 Inhibitor CHZ868 in B Cell Acute Lymphoblastic Leukemia

Author

Wu, Shuo-Chieh, Li, Loretta S., Kopp, Nadja, Montero, Joan, Chapuy, Bjoern, Yoda, Akinori, Christie, Amanda L., Liu, Huiyun, Christodoulou, Alexandra, van Bodegom, Diederik, van der Zwet, Jordy, Layer, Jacob V., Tivey, Trevor, Lane, Andrew A., Ryan, Jeremy A., Ng, Samuel Y., DeAngelo, Daniel J., Stone, Richard M., Steensma, David, Wadleigh, Martha, Harris, Marian, Mandon, Emeline, Ebel, Nicolas, Andraos, Rita, Romanet, Vincent, Dölemeyer, Arno, Sterker, Dario, Zender, Michael, Rodig, Scott J., Murakami, Masato, Hofmann, Francesco, Kuo, Frank, Eck, Michael J., Silverman, Lewis B., Sallan, Stephen E., Letai, Anthony, Baffert, Fabienne, Vangrevelinghe, Eric, Radimerski, Thomas, Gaul, Christoph, and Weinstock, David M.

Published
2015
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28. 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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29. Mediator kinase inhibition further activates super-enhancer-associated genes in AML

Author

Pelish, Henry E., Liau, Brian B., Nitulescu, Ioana I., Tangpeerachaikul, Anupong, Poss, Zachary C., Silva, Diogo H. Da, Caruso, Brittany T., Arefolov, Alexander, Fadeyi, Olugbeminiyi, Christie, Amanda L., Du, Karrie, Banka, Deepti, Schneider, Elisabeth V., Jestel, Anja, Zou, Ge, Si, Chong, Ebmeier, Christopher C., Bronson, Roderick T., Krivtsov, Andrei V., Myers, Andrew G., Kohl, Nancy E., Kung, Andrew L., Armstrong, Scott A., Lemieux, Madeleine E., Taatjes, Dylan J., and Shair, Matthew D.

Subjects
Enzymes -- Regulation, Phosphotransferases -- Properties, Environmental issues, Science and technology, Zoology and wildlife conservation
Abstract

Super-enhancers (SEs), which are composed of large clusters of enhancers densely loaded with the Mediator complex, transcription factors and chromatin regulators, drive high expression of genes implicated in cell identity [...]

Published
2015

31. Targeting TRIP13 in Wilms Tumor with Nuclear Export Inhibitors

Author

Mittal, Karuna, primary, Lee, Benjamin P., additional, Cooper, Garrett W., additional, Shim, Jenny, additional, Jonus, Hunter C., additional, Kim, Won Jun, additional, Doshi, Mihir, additional, Almanza, Diego, additional, Kynnap, Bryan D., additional, Christie, Amanda L., additional, Yang, Xiaoping, additional, Cowley, Glenn S., additional, Leeper, Brittaney A., additional, Morton, Christopher L., additional, Dwivedi, Bhakti, additional, Lawrence, Taylor, additional, Rupji, Manali, additional, Keskula, Paula, additional, Meyer, Stephanie, additional, Clinton, Catherine M., additional, Bhasin, Manoj, additional, Crompton, Brian D., additional, Tseng, Yuen-Yi, additional, Boehm, Jesse S., additional, Ligon, Keith L., additional, Root, David E., additional, Murphy, Andrew J., additional, Weinstock, David M., additional, Gokhale, Prafulla C., additional, Spangle, Jennifer M., additional, Rivera, Miguel N., additional, Mullen, Elizabeth A., additional, Stegmaier, Kimberly, additional, Goldsmith, Kelly C., additional, Hahn, William C., additional, and Hong, Andrew L., additional

Published
2022
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32. Mutations in G protein β subunits promote transformation and kinase inhibitor resistance

Author

Yoda, Akinori, Adelmant, Guillaume, Tamburini, Jerome, Chapuy, Bjoern, Shindoh, Nobuaki, Yoda, Yuka, Weigert, Oliver, Kopp, Nadja, Wu, Shuo-Chieh, Kim, Sunhee S., Liu, Huiyun, Tivey, Trevor, Christie, Amanda L., Elpek, Kutlu G., Card, Joseph, Gritsman, Kira, Gotlib, Jason, Deininger, Michael W., Makishima, Hideki, Turley, Shannon J., Javidi-Sharifi, Nathalie, Maciejewski, Jaroslaw P., Jaiswal, Siddhartha, Ebert, Benjamin L., Rodig, Scott J., Tyner, Jeffrey W., Marto, Jarrod A., Weinstock, David M., and Lane, Andrew A.

Subjects
Gene mutations -- Physiological aspects -- Research, Tumors -- Risk factors -- Genetic aspects -- Research, G proteins -- Physiological aspects -- Genetic aspects -- Research, Biological sciences, Health
Abstract

Activating mutations in genes encoding G protein α (Gα) subunits occur in 4-5% of all human cancers (1), but oncogenic alterations in Gβ subunits have not been defined. Here we demonstrate that recurrent mutations in the Gβ proteins GNB1 and GNB2 confer cytokine-independent growth and activate canonical G protein signaling. Multiple mutations in GNB1 affect the protein interface that binds Gα subunits as well as downstream effectors and disrupt Gα interactions with the Gβg dimer. Different mutations in Gβ proteins clustered partly on the basis of lineage; for example, all 11 GNB1 K57 mutations were in myeloid neoplasms, and seven of eight GNB1 I80 mutations were in B cell neoplasms. Expression of patient-derived GNB1 variants in Cdkn2a-deficient mouse bone marrow followed by transplantation resulted in either myeloid or B cell malignancies. In vivo treatment with the dual PI3K-mTOR inhibitor BEZ235 suppressed GNB1-induced signaling and markedly increased survival. In several human tumors, mutations in the gene encoding GNB1 co-occurred with oncogenic kinase alterations, including the BCR-ABL fusion protein, the V617F substitution in JAK2 and the V600K substitution in BRAF. Coexpression of patient-derived GNB1 variants with these mutant kinases resulted in inhibitor resistance in each context. Thus, GNB1 and GNB2 alterations confer transformed and resistance phenotypes across a range of human tumors and may be targetable with inhibitors of G protein signaling., Numerous somatic mutations are present in less than 5% of cases across multiple tumor types. To extensively catalog mutations in these 'long-tail' genes (2) will require sequencing thousands of additional [...]

Published
2015

33. regulates cellular apoptosis by targeting MCL1 for ubiquitylation and destruction

Author

Inuzuka, Hiroyuki, Shaik, Shavali, Onoyama, Ichiro, Gao, Daming, Tseng, Alan, Maser, Richard S., Zhai, Bo, Wan, Lixin, Gutierrez, Alejandro, Lau, Alan W., Xiao, Yonghong, Christie, Amanda L., Aster, Jon, Settleman, Jeffrey, Gygi, Steven P., Kung, Andrew L., Look, Thomas, Nakayama, Keiichi I., DePinho, Ronald A., and Wei, Wenyi

Subjects
Ubiquitin -- Genetic aspects, Proteins -- Genetic aspects, Apoptosis -- Management -- Genetic aspects, Company business management, Environmental issues, Science and technology, Zoology and wildlife conservation
Abstract

The effective use of targeted therapy is highly dependent on the identification of responder patient populations. Loss of FBW7, which encodes a tumour-suppressor protein, is frequently found in various types of human cancer, including breast cancer, colon cancer (1) and T-cell acute lymphoblastic leukaemia (T-ALL) (2). In line with these genomic data, engineered deletion of Fbw7 in mouse T cells results in T-ALL (3-5), validating FBW7 as a T-ALL tumour suppressor. Determining the precise molecular mechanisms by which FBW7 exerts antitumour activity is an area of intensive investigation. These mechanisms are thought to relate in part to FBW7-mediated destruction of key proteins relevant to cancer, including Jun (6), Myc (7), cyclin E (8) and notch 1 (ref. 9), all of which have oncoprotein activity and are overexpressed in various human cancers, including leukaemia. In addition to accelerating cell growth (10), overexpression of Jun, Myc or notch 1 can also induce programmed cell death (11). Thus, considerable uncertainty surrounds how FBW7-deficient cells evade cell death in the setting of upregulated Jun, Mbc and/or notch 1. Here we show that the E3 ubiquitin ligase [SCF.sup.FBW7] (a SKP1-cullin-1-F-box complex that contains FBW7 as the F-box protein) governs cellular apoptosis by targeting MCL1, a pro-survival BCL2 family member, for ubiquitylation and destruction in a manner that depends on phosphorylation by glycogen synthase kinase 3. Human T-ALL cell lines showed a close relationship between FBW7 loss and MCL1 overexpression. Correspondingly, T-ALL cell lines with defective FBW7 are particularly sensitive to the multi-kinase inhibitor sorafenib but resistant to the BCL2 antagonist ABT-737. On the genetic level, FBW7 reconstitution or MCL1 depletion restores sensitivity to ABT-737, establishing MCL1 as a therapeutically relevant bypass survival mechanism that enables FBW7-deficient cells to evade apoptosis. Therefore, our work provides insight into the molecular mechanism of direct tumour suppression by FBW7 and has implications for the targeted treatment of patients with FBW7-deficient T-ALL., MCL1 is frequently overexpressed in various leukaemias through mechanisms that are not fully understood (12). MCL1 is distinct from other BCL2 family members in its extremely unstable nature (13), which [...]

Published
2011
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34. Abstract 2957: A novel circulating tumor DNA (ctDNA) assay enables monitoring of disease progression and treatment response in disseminated preclinical hematologic cancer models

Author

Christie, Amanda L., primary, Labrousse, Paul, additional, Andersen, Courtney L., additional, Roderick, Justine E., additional, Gordon, Jacob, additional, Lawson, Deborah, additional, Hughes, Denise, additional, Maratea, Kimberly, additional, Stetson, Daniel, additional, Willis, Brandon, additional, Bloecher, Andrew, additional, Reimer, Corinne, additional, and Dougherty, Brian, additional

Published
2021
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35. Mechanisms of lymphoma clearance induced by high-dose alkylating agents

Author

Koch Institute for Integrative Cancer Research at MIT, Massachusetts Institute of Technology. Institute for Medical Engineering & Science, Massachusetts Institute of Technology. Department of Chemistry, Ragon Institute of MGH, MIT and Harvard, Lossos, Chen, Liu, Yunpeng, Kolb, Kellie E, Christie, Amanda L, van Scoyk, Alexandria, Prakadan, Sanjay M, Shigemori, Kay, Stevenson, Kristen E, Morrow, Sara, Plana, Olivia D, Fraser, Cameron, Jones, Kristen L, Liu, Huiyun, Pallasch, Christian P, Modiste, Rebecca, Nguyen, Quang-De, Craig, Jeffrey W, Morgan, Elizabeth A, Vega, Francisco, Aster, Jon C, Sarosiek, Kristopher A, Shalek, Alex K, Hemann, Michael T, Weinstock, David M, Koch Institute for Integrative Cancer Research at MIT, Massachusetts Institute of Technology. Institute for Medical Engineering & Science, Massachusetts Institute of Technology. Department of Chemistry, Ragon Institute of MGH, MIT and Harvard, Lossos, Chen, Liu, Yunpeng, Kolb, Kellie E, Christie, Amanda L, van Scoyk, Alexandria, Prakadan, Sanjay M, Shigemori, Kay, Stevenson, Kristen E, Morrow, Sara, Plana, Olivia D, Fraser, Cameron, Jones, Kristen L, Liu, Huiyun, Pallasch, Christian P, Modiste, Rebecca, Nguyen, Quang-De, Craig, Jeffrey W, Morgan, Elizabeth A, Vega, Francisco, Aster, Jon C, Sarosiek, Kristopher A, Shalek, Alex K, Hemann, Michael T, and Weinstock, David M

Abstract

© 2019 American Association for Cancer Research. The extraordinary activity of high-dose cyclophosphamide against some high-grade lymphomas was described nearly 60 years ago. Here we address mechanisms that mediate cyclophosphamide activity in bona fide human double-hit lymphoma. We show that antibody resistance within the bone marrow (BM) is not present upon early engraftment but develops during lymphoma progression. This resistance required a high tumor:macrophage ratio, was recapitulated in spleen by partial macrophage depletion, and was overcome by multiple, high-dose alkylating agents. Cyclophosphamide induced endoplasmic reticulum (ER) stress in BM-resident lymphoma cells in vivo that resulted in ATF4-mediated paracrine secretion of VEGFA, massive macrophage infiltration, and clearance of alemtuzumab-opsonized cells. BM macrophages isolated after cyclophosphamide treatment had increased phagocytic capacity that was reversed by VEGFA blockade or SYK inhibition. Single-cell RNA sequencing of these macrophages identified a “super-phagocytic” subset that expressed CD36/FCGR4. Together, these findings define a novel mechanism through which high-dose alkylating agents promote macrophage-dependent lymphoma clearance. SIGNIFICANCE: mAbs are effective against only a small subset of cancers. Herein, we recapitulate compartment-specific antibody resistance and define an ER stress–dependent mechanism induced by high-dose alkylating agents that promotes phagocytosis of opsonized tumor cells. This approach induces synergistic effects with mAbs and merits testing across additional tumor types.

Published
2021

38. Selective inhibition of BET bromodomains

Author

Filippakopoulos, Panagis, Qi, Jun, Picaud, Sarah, Shen, Yao, Smith, William B., Fedorov, Oleg, Morse, Elizabeth M., Keates, Tracey, Hickman, Tyler T., Felletar, Ildiko, Philpott, Martin, Munro, Shonagh, McKeown, Michael R., Wang, Yuchuan, Christie, Amanda L., West, Nathan, Cameron, Michael J., Schwartz, Brian, Heightman, Tom D., La Thangue, Nicholas, French, Christopher A., Wiest, Olaf, Kung, Andrew L., Knapp, Stefan, and Bradner, James E.

Published
2010
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40. Identification of Novel Combination Therapies Active in BCL2 Inhibitor-Resistant Patient-Derived AML Models

Author

Andersen, Courtney L, primary, Christie, Amanda L, additional, Rosen, Alan, additional, Maratea, Kim, additional, Hattersley, Maureen, additional, Travers, Jon, additional, Cidado, Justin, additional, Pulukuri, Sai, additional, Saeh, Jamal, additional, Clark, Edwin, additional, Reimer, Corinne, additional, and Mettetal, Jerome, additional

Published
2019
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41. Mechanisms of Lymphoma Clearance Induced by High-Dose Alkylating Agents

Author

Lossos, Chen, primary, Liu, Yunpeng, additional, Kolb, Kellie E., additional, Christie, Amanda L., additional, Van Scoyk, Alexandria, additional, Prakadan, Sanjay M., additional, Shigemori, Kay, additional, Stevenson, Kristen E., additional, Morrow, Sara, additional, Plana, Olivia D., additional, Fraser, Cameron, additional, Jones, Kristen L., additional, Liu, Huiyun, additional, Pallasch, Christian P., additional, Modiste, Rebecca, additional, Nguyen, Quang-De, additional, Craig, Jeffrey W., additional, Morgan, Elizabeth A., additional, Vega, Francisco, additional, Aster, Jon C., additional, Sarosiek, Kristopher A., additional, Shalek, Alex K., additional, Hemann, Michael T., additional, and Weinstock, David M., additional

Published
2019
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42. Mechanisms of Lymphoma Clearance Induced by High-Dose Alkylating Agents

Author

Lossos, Chen, Liu, Yunpeng, Kolb, Kellie E., Christie, Amanda L., Van Scoyk, Alexandria, Prakadan, Sanjay M., Shigemori, Kay, Stevenson, Kristen E., Morrow, Sara, Plana, Olivia D., Fraser, Cameron, Jones, Kristen L., Liu, Huiyun, Pallasch, Christian P., Modiste, Rebecca, Craig, Jeffrey W., Morgan, Elizabeth A., Vega, Francisco, Aster, Jon C., Sarosiek, Kristopher A., Shalek, Alex K., Hemann, Michael T., Weinstock, David M., Lossos, Chen, Liu, Yunpeng, Kolb, Kellie E., Christie, Amanda L., Van Scoyk, Alexandria, Prakadan, Sanjay M., Shigemori, Kay, Stevenson, Kristen E., Morrow, Sara, Plana, Olivia D., Fraser, Cameron, Jones, Kristen L., Liu, Huiyun, Pallasch, Christian P., Modiste, Rebecca, Craig, Jeffrey W., Morgan, Elizabeth A., Vega, Francisco, Aster, Jon C., Sarosiek, Kristopher A., Shalek, Alex K., Hemann, Michael T., and Weinstock, David M.

Abstract

The extraordinary activity of high-dose cyclophosphamide against some high-grade lymphomas was described nearly 60 years ago. Here we address mechanisms that mediate cyclophosphamide activity in bona fide human double-hit lymphoma. We show that antibody resistance within the bone marrow (BM) is not present upon early engraftment but develops during lymphoma progression. This resistance required a high tumor:macrophage ratio, was recapitulated in spleen by partial macrophage depletion, and was overcome by multiple, high-dose alkylating agents. Cyclophosphamide induced endoplasmic reticulum (ER) stress in BM-resident lymphoma cells in vivo that resulted in ATF4-mediated paracrine secretion of VEGFA, massive macrophage infiltration, and clearance of alemtuzumab-opsonized cells. BM macrophages isolated after cyclophosphamide treatment had increased phagocytic capacity that was reversed by VEGFA blockade or SYK inhibition. Single-cell RNA sequencing of these macrophages identified a super-phagocytic subset that expressed CD36/FCGR4. Together, these findings define a novel mechanism through which high-dose alkylating agents promote macrophage-dependent lymphoma clearance. SIGNIFICANCE: mAbs are effective against only a small subset of cancers. Herein, we recapitulate compartment-specific antibody resistance and define an ER stress-dependent mechanism induced by high-dose alkylating agents that promotes phagocytosis of opsonized tumor cells. This approach induces synergistic effects with mAbs and merits testing across additional tumor types.

Published
2019

44. Alkylating Agent-Induced ER Stress Overcomes Microenvironmental Resistance to Lymphoma Therapy

Author

Lossos, Chen, primary, Kolb, Kellie E., additional, Christie, Amanda L., additional, Scoyk, Alexandria Van, additional, Prakadan, Sanjay, additional, Shigamori, Kay, additional, Stevenson, Kristen, additional, Morrow, Sara, additional, Plana, Olivia D., additional, Fraser, Cameron, additional, Liu, Huiyun, additional, Pallasch, Christian C., additional, Modiste, Rebecca, additional, Nguyen, Quang-De, additional, Craig, Jeffrey W., additional, Morgan, Elizabeth A., additional, Aster, Jon C., additional, Sarosiek, Kristopher A., additional, Shalek, Alex K., additional, Hemann, Michael T., additional, and Weinstock, David M., additional

Published
2018
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46. Characterization of midostaurin as a dual inhibitor of FLT3 and SYK and potentiation of FLT3 inhibition against FLT3-ITD-driven leukemia harboring activated SYK kinase

Author

Weisberg, Ellen L., primary, Puissant, Alexandre, additional, Stone, Richard, additional, Sattler, Martin, additional, Buhrlage, Sara J., additional, Yang, Jing, additional, Manley, Paul W., additional, Meng, Chengcheng, additional, Buonopane, Michael, additional, Daley, John F., additional, Lazo, Suzan, additional, Wright, Renee, additional, Weinstock, David M., additional, Christie, Amanda L., additional, Stegmaier, Kimberly, additional, and Griffin, James D., additional

Published
2017
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47. Notch-Regulated Enhancers in B-Cell Lymphoma Activate MYC and Potentiate B-Cell Receptor Signaling

Author

Ryan, Russell J.H., primary, Petrovic, Jelena, additional, Rausch, Dylan, additional, Lareau, Caleb, additional, Lee, Winston, additional, Donohue, Laura, additional, Christie, Amanda L., additional, Gillespie, Shawn, additional, Kluk, Michael J., additional, Nardi, Valentina, additional, Faryabi, Robert B., additional, Hochberg, Ephraim P., additional, Weinstock, David M., additional, Bernstein, Bradley E., additional, Aster, Jon C., additional, and Pear, Warren S., additional

Published
2016
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48. Inhibition of USP10 Induces Degradation of Oncogenic FLT3: A Novel Approach to Therapy of Leukemia

Author

Buhrlage, Sara, primary, Weisberg, Ellen, additional, Schauer, Nathan, additional, Yang, Jing, additional, Lamberto, Ilaria, additional, Doherty, Laura, additional, Nonami, Atsushi, additional, Christie, Amanda L., additional, Weinstock, David M., additional, Stone, Richard M., additional, Gray, Nathanael, additional, and Griffin, James D, additional

Published
2016
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50. T-Cell Lymphoma Patient-Derived Xenografts and Newly Developed Cell Lines Recapitulate Aspects of Disease Biology and Represent Novel Tools for Preclinical Drug Development

Author

Christie, Amanda L., primary, Ng, Samuel Y., additional, Koch, Raphael, additional, Christodoulou, Alexandra N., additional, DeSouza, Tiffany, additional, Murakami, Mark A., additional, Tseng, Moony, additional, Peng, Anson, additional, Molla, Vadim, additional, Jacobson, Caron A., additional, Shoji, Brent, additional, LeBoeuf, Nicole R., additional, Bertagnolli, Monica, additional, Armand, Philippe, additional, Pinkus, Geraldine S, additional, Boehm, Jesse, additional, Shipp, Margaret A., additional, Dorfman, David M., additional, Jacobsen, Eric D., additional, Fisher, David C., additional, Morgan, Elizabeth A., additional, Aster, Jon C., additional, and Weinstock, David M., additional

Published
2016
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