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1,135 results on '"Weinstock, David M"'

2. 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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4. PD-1 instructs a tumor-suppressive metabolic program that restricts glycolysis and restrains AP-1 activity in T cell lymphoma

Author

Wartewig, Tim, Daniels, Jay, Schulz, Miriam, Hameister, Erik, Joshi, Abhinav, Park, Joonhee, Morrish, Emma, Venkatasubramani, Anuroop V., Cernilogar, Filippo M., van Heijster, Frits H. A., Hundshammer, Christian, Schneider, Heike, Konstantinidis, Filippos, Gabler, Judith V., Klement, Christine, Kurniawan, Henry, Law, Calvin, Lee, Yujin, Choi, Sara, Guitart, Joan, Forne, Ignasi, Giustinani, Jérôme, Müschen, Markus, Jain, Salvia, Weinstock, David M., Rad, Roland, Ortonne, Nicolas, Schilling, Franz, Schotta, Gunnar, Imhof, Axel, Brenner, Dirk, Choi, Jaehyuk, and Ruland, Jürgen

Published
2023
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5. Geographic EBV variants confound disease-specific variant interpretation and predict variable immune therapy responses

Author

Briercheck, Edward L., Ravishankar, Shashidhar, Ahmed, Elshafa Hassan, Carías Alvarado, César Camilo, Barrios Menéndez, Juan Carlos, Silva, Oscar, Solórzano-Ortiz, Elizabeth, Siliézar Tala, Marcos Mauricio, Stevenson, Philip, Xu, Yuexin, Wohns, Anthony Wilder, Enriquez-Vera, Daniel, Barrionuevo, Carlos, Yu, Shan-Chi, Freud, Aharon G., Oakes, Christopher, Weigel, Christoph, Weinstock, David M., Klimaszewski, Haley L., Ngankeu, Apollinaire, Mutalima, Nora, Samayoa-Reyes, Gabriela, Newton, Robert, Rochford, Rosemary, Valvert, Fabiola, Natkunam, Yasodha, Shustov, Andrei, Baiocchi, Robert A., and Warren, Edus H.

Published
2024
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6. Sex-Biased ZRSR2 Mutations in Myeloid Malignancies Impair Plasmacytoid Dendritic Cell Activation and Apoptosis

Author

Togami, Katsuhiro, Chung, Sun Sook, Madan, Vikas, Booth, Christopher AG, Kenyon, Christopher M, Cabal-Hierro, Lucia, Taylor, Justin, Kim, Sunhee S, Griffin, Gabriel K, Ghandi, Mahmoud, Li, Jia, Li, Yvonne Y, Angelot-Delettre, Fanny, Biichle, Sabeha, Seiler, Michael, Buonamici, Silvia, Lovitch, Scott B, Louissaint, Abner, Morgan, Elizabeth A, Jardin, Fabrice, Piccaluga, Pier Paolo, Weinstock, David M, Hammerman, Peter S, Yang, Henry, Konopleva, Marina, Pemmaraju, Naveen, Garnache-Ottou, Francine, Abdel-Wahab, Omar, Koeffler, H Phillip, and Lane, Andrew A

Subjects
Rare Diseases, Clinical Research, Cancer, Hematology, Genetics, Aetiology, 2.1 Biological and endogenous factors, Inflammatory and immune system, Apoptosis, Dendritic Cells, Female, Gender Identity, Humans, Male, Mutation, Myeloproliferative Disorders, Ribonucleoproteins, Oncology and Carcinogenesis
Abstract

Blastic plasmacytoid dendritic cell neoplasm (BPDCN) is an aggressive leukemia of plasmacytoid dendritic cells (pDC). BPDCN occurs at least three times more frequently in men than in women, but the reasons for this sex bias are unknown. Here, studying genomics of primary BPDCN and modeling disease-associated mutations, we link acquired alterations in RNA splicing to abnormal pDC development and inflammatory response through Toll-like receptors. Loss-of-function mutations in ZRSR2, an X chromosome gene encoding a splicing factor, are enriched in BPDCN, and nearly all mutations occur in males. ZRSR2 mutation impairs pDC activation and apoptosis after inflammatory stimuli, associated with intron retention and inability to upregulate the transcription factor IRF7. In vivo, BPDCN-associated mutations promote pDC expansion and signatures of decreased activation. These data support a model in which male-biased mutations in hematopoietic progenitors alter pDC function and confer protection from apoptosis, which may impair immunity and predispose to leukemic transformation. SIGNIFICANCE: Sex bias in cancer is well recognized, but the underlying mechanisms are incompletely defined. We connect X chromosome mutations in ZRSR2 to an extremely male-predominant leukemia. Aberrant RNA splicing induced by ZRSR2 mutation impairs dendritic cell inflammatory signaling, interferon production, and apoptosis, revealing a sex- and lineage-related tumor suppressor pathway.This article is highlighted in the In This Issue feature, p. 275.

Published
2022

7. IFITM3 functions as a PIP3 scaffold to amplify PI3K signalling in B cells

Author

Lee, Jaewoong, Robinson, Mark E, Ma, Ning, Artadji, Dewan, Ahmed, Mohamed A, Xiao, Gang, Sadras, Teresa, Deb, Gauri, Winchester, Janet, Cosgun, Kadriye Nehir, Geng, Huimin, Chan, Lai N, Kume, Kohei, Miettinen, Teemu P, Zhang, Ye, Nix, Matthew A, Klemm, Lars, Chen, Chun Wei, Chen, Jianjun, Khairnar, Vishal, Wiita, Arun P, Thomas-Tikhonenko, Andrei, Farzan, Michael, Jung, Jae U, Weinstock, David M, Manalis, Scott R, Diamond, Michael S, Vaidehi, Nagarajan, and Müschen, Markus

Subjects
Biochemistry and Cell Biology, Biomedical and Clinical Sciences, Oncology and Carcinogenesis, Biological Sciences, Hematology, Cancer, Lymphoma, Rare Diseases, 2.1 Biological and endogenous factors, Aetiology, Animals, Antigens, CD19, B-Lymphocytes, Cell Transformation, Neoplastic, Female, Germinal Center, Humans, Integrins, Membrane Microdomains, Membrane Proteins, Mice, Mice, Inbred C57BL, Mice, Inbred NOD, Models, Molecular, Phosphatidylinositol 3-Kinases, Phosphatidylinositol Phosphates, Phosphorylation, RNA-Binding Proteins, Receptors, Antigen, B-Cell, Signal Transduction, General Science & Technology
Abstract

Interferon-induced transmembrane protein 3 (IFITM3) has previously been identified as an endosomal protein that blocks viral infection1-3. Here we studied clinical cohorts of patients with B cell leukaemia and lymphoma, and identified IFITM3 as a strong predictor of poor outcome. In normal resting B cells, IFITM3 was minimally expressed and mainly localized in endosomes. However, engagement of the B cell receptor (BCR) induced both expression of IFITM3 and phosphorylation of this protein at Tyr20, which resulted in the accumulation of IFITM3 at the cell surface. In B cell leukaemia, oncogenic kinases phosphorylate IFITM3 at Tyr20, which causes constitutive localization of this protein at the plasma membrane. In a mouse model, Ifitm3-/- naive B cells developed in normal numbers; however, the formation of germinal centres and the production of antigen-specific antibodies were compromised. Oncogenes that induce the development of leukaemia and lymphoma did not transform Ifitm3-/- B cells. Conversely, the phosphomimetic IFITM3(Y20E) mutant induced oncogenic PI3K signalling and initiated the transformation of premalignant B cells. Mechanistic experiments revealed that IFITM3 functions as a PIP3 scaffold and central amplifier of PI3K signalling. The amplification of PI3K signals depends on IFITM3 using two lysine residues (Lys83 and Lys104) in its conserved intracellular loop as a scaffold for the accumulation of PIP3. In Ifitm3-/- B cells, lipid rafts were depleted of PIP3, which resulted in the defective expression of over 60 lipid-raft-associated surface receptors, and impaired BCR signalling and cellular adhesion. We conclude that the phosphorylation of IFITM3 that occurs after B cells encounter antigen induces a dynamic switch from antiviral effector functions in endosomes to a PI3K amplification loop at the cell surface. IFITM3-dependent amplification of PI3K signalling, which in part acts downstream of the BCR, is critical for the rapid expansion of B cells with high affinity to antigen. In addition, multiple oncogenes depend on IFITM3 to assemble PIP3-dependent signalling complexes and amplify PI3K signalling for malignant transformation.

Published
2020

8. New scaffolds for type II JAK2 inhibitors overcome the acquired G993A resistance mutation

Author

Arwood, Matthew L., Liu, Yao, Harkins, Shannon K., Weinstock, David M., Yang, Lei, Stevenson, Kristen E., Plana, Olivia D., Dong, Jingyun, Cirka, Haley, Jones, Kristen L., Virtanen, Anniina T., Gupta, Dikshat G., Ceas, Amanda, Lawney, Brian, Yoda, Akinori, Leahy, Catharine, Hao, Mingfeng, He, Zhixiang, Choi, Hwan Geun, Wang, Yaning, Silvennoinen, Olli, Hubbard, Stevan R., Zhang, Tinghu, Gray, Nathanael S., and Li, Loretta S.

Published
2023
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9. Signalling input from divergent pathways subverts B cell transformation

Author

Chan, Lai N, Murakami, Mark A, Robinson, Mark E, Caeser, Rebecca, Sadras, Teresa, Lee, Jaewoong, Cosgun, Kadriye Nehir, Kume, Kohei, Khairnar, Vishal, Xiao, Gang, Ahmed, Mohamed A, Aghania, Eamon, Deb, Gauri, Hurtz, Christian, Shojaee, Seyedmehdi, Hong, Chao, Pölönen, Petri, Nix, Matthew A, Chen, Zhengshan, Chen, Chun Wei, Chen, Jianjun, Vogt, Andreas, Heinäniemi, Merja, Lohi, Olli, Wiita, Arun P, Izraeli, Shai, Geng, Huimin, Weinstock, David M, and Müschen, Markus

Subjects
Genetics, Cancer, 2.1 Biological and endogenous factors, Aetiology, Animals, B-Lymphocytes, Cell Line, Tumor, Cell Transformation, Neoplastic, Enzyme Activation, Extracellular Signal-Regulated MAP Kinases, Female, Humans, Leukemia, B-Cell, Mice, Protein Tyrosine Phosphatase, Non-Receptor Type 6, Proto-Oncogene Proteins c-bcl-6, Proto-Oncogene Proteins c-myc, STAT5 Transcription Factor, Signal Transduction, General Science & Technology
Abstract

Malignant transformation of cells typically involves several genetic lesions, whose combined activity gives rise to cancer1. Here we analyse 1,148 patient-derived B-cell leukaemia (B-ALL) samples, and find that individual mutations do not promote leukaemogenesis unless they converge on one single oncogenic pathway that is characteristic of the differentiation stage of transformed B cells. Mutations that are not aligned with this central oncogenic driver activate divergent pathways and subvert transformation. Oncogenic lesions in B-ALL frequently mimic signalling through cytokine receptors at the pro-B-cell stage (via activation of the signal-transduction protein STAT5)2-4 or pre-B-cell receptors in more mature cells (via activation of the protein kinase ERK)5-8. STAT5- and ERK-activating lesions are found frequently, but occur together in only around 3% of cases (P = 2.2 × 10-16). Single-cell mutation and phospho-protein analyses reveal the segregation of oncogenic STAT5 and ERK activation to competing clones. STAT5 and ERK engage opposing biochemical and transcriptional programs that are orchestrated by the transcription factors MYC and BCL6, respectively. Genetic reactivation of the divergent (suppressed) pathway comes at the expense of the principal oncogenic driver and reverses transformation. Conversely, deletion of divergent pathway components accelerates leukaemogenesis. Thus, persistence of divergent signalling pathways represents a powerful barrier to transformation, while convergence on one principal driver defines a central event in leukaemia initiation. Pharmacological reactivation of suppressed divergent circuits synergizes strongly with inhibition of the principal oncogenic driver. Hence, reactivation of divergent pathways can be leveraged as a previously unrecognized strategy to enhance treatment responses.

Published
2020

10. Mutation and cell state compatibility is required and targetable in Ph+ acute lymphoblastic leukemia minimal residual disease

Author

Winter, Peter S., primary, Ramseier, Michelle L., additional, Navia, Andrew W., additional, Saksena, Sachit, additional, Strouf, Haley, additional, Senhaji, Nezha, additional, DenAdel, Alan, additional, Mirza, Mahnoor, additional, An, Hyun Hwan, additional, Bilal, Laura, additional, Dennis, Peter, additional, Leahy, Catharine S., additional, Shigemori, Kay, additional, Galvez-Reyes, Jennyfer, additional, Zhang, Ye, additional, Powers, Foster, additional, Mulugeta, Nolawit, additional, Gupta, Alejandro J., additional, Calistri, Nicholas, additional, Van Scoyk, Alex, additional, Jones, Kristen, additional, Liu, Huiyun, additional, Stevenson, Kristen E., additional, Ren, Siyang, additional, Luskin, Marlise R., additional, Couturier, Charles P., additional, Amini, Ava P., additional, Raghavan, Srivatsan, additional, Kimmerling, Robert J., additional, Stevens, Mark M., additional, Crawford, Lorin, additional, Weinstock, David M., additional, Manalis, Scott R., additional, Shalek, Alex K., additional, and Murakami, Mark A., additional

Published
2024
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11. Correction: Chimeric Antigen Receptor T Cells Targeting CD79b Show Efficacy in Lymphoma with or without Cotargeting CD19

Author

Ormhøj, Maria, primary, Scarfò, Irene, additional, Cabral, Maria L., additional, Bailey, Stefanie R., additional, Lorrey, Selena J., additional, Bouffard, Amanda A., additional, Castano, Ana P., additional, Larson, Rebecca C., additional, Riley, Lauren S., additional, Schmidts, Andrea, additional, Choi, Bryan D., additional, Andersen, Rikke S., additional, Cédile, Oriane, additional, Nyvold, Charlotte G., additional, Christensen, Jacob H., additional, Gjerstorff, Morten F., additional, Ditzel, Henrik J., additional, Weinstock, David M., additional, Barington, Torben, additional, Frigault, Matthew J., additional, and Maus, Marcela V., additional

Published
2024
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12. Figure S11 from Acquired Multidrug Resistance in AML Is Caused by Low Apoptotic Priming in Relapsed Myeloblasts

Author

Olesinski, Elyse A., primary, Bhatia, Karanpreet Singh, primary, Wang, Chuqi, primary, Pioso, Marissa S., primary, Lin, Xiao Xian, primary, Mamdouh, Ahmed M., primary, Ng, Shu Xuan, primary, Sandhu, Vedant, primary, Jasdanwala, Shaista Shabbir, primary, Yilma, Binyam, primary, Bohl, Stephan, primary, Ryan, Jeremy A., primary, Malani, Disha, primary, Luskin, Marlise R., primary, Kallioniemi, Olli, primary, Porkka, Kimmo, primary, Adamia, Sophia, primary, Chng, Wee Joo, primary, Osato, Motomi, primary, Weinstock, David M., primary, Garcia, Jacqueline S., primary, Letai, Anthony, primary, and Bhatt, Shruti, primary

Published
2024
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13. Data from Acquired Multidrug Resistance in AML Is Caused by Low Apoptotic Priming in Relapsed Myeloblasts

Author

Olesinski, Elyse A., primary, Bhatia, Karanpreet Singh, primary, Wang, Chuqi, primary, Pioso, Marissa S., primary, Lin, Xiao Xian, primary, Mamdouh, Ahmed M., primary, Ng, Shu Xuan, primary, Sandhu, Vedant, primary, Jasdanwala, Shaista Shabbir, primary, Yilma, Binyam, primary, Bohl, Stephan, primary, Ryan, Jeremy A., primary, Malani, Disha, primary, Luskin, Marlise R., primary, Kallioniemi, Olli, primary, Porkka, Kimmo, primary, Adamia, Sophia, primary, Chng, Wee Joo, primary, Osato, Motomi, primary, Weinstock, David M., primary, Garcia, Jacqueline S., primary, Letai, Anthony, primary, and Bhatt, Shruti, primary

Published
2024
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15. Next-generation characterization of the Cancer Cell Line Encyclopedia

Author

Ghandi, Mahmoud, Huang, Franklin W, Jané-Valbuena, Judit, Kryukov, Gregory V, Lo, Christopher C, McDonald, E Robert, Barretina, Jordi, Gelfand, Ellen T, Bielski, Craig M, Li, Haoxin, Hu, Kevin, Andreev-Drakhlin, Alexander Y, Kim, Jaegil, Hess, Julian M, Haas, Brian J, Aguet, François, Weir, Barbara A, Rothberg, Michael V, Paolella, Brenton R, Lawrence, Michael S, Akbani, Rehan, Lu, Yiling, Tiv, Hong L, Gokhale, Prafulla C, de Weck, Antoine, Mansour, Ali Amin, Oh, Coyin, Shih, Juliann, Hadi, Kevin, Rosen, Yanay, Bistline, Jonathan, Venkatesan, Kavitha, Reddy, Anupama, Sonkin, Dmitriy, Liu, Manway, Lehar, Joseph, Korn, Joshua M, Porter, Dale A, Jones, Michael D, Golji, Javad, Caponigro, Giordano, Taylor, Jordan E, Dunning, Caitlin M, Creech, Amanda L, Warren, Allison C, McFarland, James M, Zamanighomi, Mahdi, Kauffmann, Audrey, Stransky, Nicolas, Imielinski, Marcin, Maruvka, Yosef E, Cherniack, Andrew D, Tsherniak, Aviad, Vazquez, Francisca, Jaffe, Jacob D, Lane, Andrew A, Weinstock, David M, Johannessen, Cory M, Morrissey, Michael P, Stegmeier, Frank, Schlegel, Robert, Hahn, William C, Getz, Gad, Mills, Gordon B, Boehm, Jesse S, Golub, Todd R, Garraway, Levi A, and Sellers, William R

Subjects
Genetics, Human Genome, Lung, Cancer, Biotechnology, Lung Cancer, Aetiology, 2.1 Biological and endogenous factors, Good Health and Well Being, Antineoplastic Agents, Biomarkers, Tumor, Cell Line, Tumor, DNA Methylation, Drug Resistance, Neoplasm, Ethnicity, Gene Editing, Histones, Humans, MicroRNAs, Molecular Targeted Therapy, Neoplasms, Protein Array Analysis, RNA Splicing, General Science & Technology
Abstract

Large panels of comprehensively characterized human cancer models, including the Cancer Cell Line Encyclopedia (CCLE), have provided a rigorous framework with which to study genetic variants, candidate targets, and small-molecule and biological therapeutics and to identify new marker-driven cancer dependencies. To improve our understanding of the molecular features that contribute to cancer phenotypes, including drug responses, here we have expanded the characterizations of cancer cell lines to include genetic, RNA splicing, DNA methylation, histone H3 modification, microRNA expression and reverse-phase protein array data for 1,072 cell lines from individuals of various lineages and ethnicities. Integration of these data with functional characterizations such as drug-sensitivity, short hairpin RNA knockdown and CRISPR-Cas9 knockout data reveals potential targets for cancer drugs and associated biomarkers. Together, this dataset and an accompanying public data portal provide a resource for the acceleration of cancer research using model cancer cell lines.

Published
2019

16. Fanconi-BRCA pathway mutations in childhood T-cell acute lymphoblastic leukemia

Author

Pouliot, Gayle P, Degar, James, Hinze, Laura, Kochupurakkal, Bose, Vo, Chau D, Burns, Melissa A, Moreau, Lisa, Ganesa, Chirag, Roderick, Justine, Peirs, Sofie, Menten, Bjorn, Loh, Mignon L, Hunger, Stephen P, Silverman, Lewis B, Harris, Marian H, Stevenson, Kristen E, Weinstock, David M, Weng, Andrew P, Van Vlierberghe, Pieter, D’Andrea, Alan D, and Gutierrez, Alejandro

Subjects
Biological Sciences, Biomedical and Clinical Sciences, Genetics, Oncology and Carcinogenesis, Hematology, Pediatric Cancer, Orphan Drug, Pediatric, Childhood Leukemia, Pediatric Research Initiative, Cancer, Rare Diseases, Human Genome, Aetiology, 2.1 Biological and endogenous factors, Animals, BRCA2 Protein, Cell Line, Tumor, Child, Fanconi Anemia Complementation Group D2 Protein, Genes, BRCA1, Genes, BRCA2, Haploinsufficiency, Heterografts, Humans, Jurkat Cells, Male, Mice, Mice, Inbred NOD, Mutagenesis, Site-Directed, Mutation, Precursor T-Cell Lymphoblastic Leukemia-Lymphoma, Radiation Tolerance, Sequence Analysis, DNA, Sequence Analysis, RNA, Ultraviolet Rays, General Science & Technology
Abstract

BRCA2 (also known as FANCD1) is a core component of the Fanconi pathway and suppresses transformation of immature T-cells in mice. However, the contribution of Fanconi-BRCA pathway deficiency to human T-cell acute lymphoblastic leukemia (T-ALL) remains undefined. We identified point mutations in 9 (23%) of 40 human T-ALL cases analyzed, with variant allele fractions consistent with heterozygous mutations early in tumor evolution. Two of these mutations were present in remission bone marrow specimens, suggesting germline alterations. BRCA2 was the most commonly mutated gene. The identified Fanconi-BRCA mutations encode hypomorphic or null alleles, as evidenced by their inability to fully rescue Fanconi-deficient cells from chromosome breakage, cytotoxicity and/or G2/M arrest upon treatment with DNA cross-linking agents. Disabling the tumor suppressor activity of the Fanconi-BRCA pathway is generally thought to require biallelic gene mutations. However, all mutations identified were monoallelic, and most cases appeared to retain expression of the wild-type allele. Using isogenic T-ALL cells, we found that BRCA2 haploinsufficiency induces selective hypersensitivity to ATR inhibition, in vitro and in vivo. These findings implicate Fanconi-BRCA pathway haploinsufficiency in the molecular pathogenesis of T-ALL, and provide a therapeutic rationale for inhibition of ATR or other druggable effectors of homologous recombination.

Published
2019

17. Overcoming IMiD resistance in T-cell lymphomas through potent degradation of ZFP91 and IKZF1

Author

Wu, Wenchao, Nelson, Geoffrey M., Koch, Raphael, Donovan, Katherine A., Nowak, Radosław P., Heavican-Foral, Tayla B., Nirmal, Ajit J., Liu, Huiyun, Yang, Lei, Duffy, Jessica, Powers, Foster, Stevenson, Kristen E., Jones, Marcus Kenneth, Ng, Samuel Y., Wu, Gongwei, Jain, Salvia, Xu, Ran, Amaka, Sam, Trevisani, Christopher, Donaldson, Nicholas L., Hagner, Patrick R., de Leval, Laurence, Gaulard, Philippe, Iqbal, Javeed, Thakurta, Anjan, Fischer, Eric S., Adelman, Karen, and Weinstock, David M.

Published
2022
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19. B-Cell-Specific Diversion of Glucose Carbon Utilization Reveals a Unique Vulnerability in B Cell Malignancies

Author

Xiao, Gang, Chan, Lai N, Klemm, Lars, Braas, Daniel, Chen, Zhengshan, Geng, Huimin, Zhang, Qiuyi Chen, Aghajanirefah, Ali, Cosgun, Kadriye Nehir, Sadras, Teresa, Lee, Jaewoong, Mirzapoiazova, Tamara, Salgia, Ravi, Ernst, Thomas, Hochhaus, Andreas, Jumaa, Hassan, Jiang, Xiaoyan, Weinstock, David M, Graeber, Thomas G, and Müschen, Markus

Subjects
Cancer, Aetiology, 2.1 Biological and endogenous factors, Animals, B-Lymphocytes, Carbon, Cell Line, Tumor, Cell Survival, Glucose, Glucosephosphate Dehydrogenase, Glycolysis, Humans, Ikaros Transcription Factor, Mice, Mice, Inbred C57BL, Mice, Inbred NOD, Oxidative Stress, PAX5 Transcription Factor, Pentose Phosphate Pathway, Precursor Cell Lymphoblastic Leukemia-Lymphoma, Protein Phosphatase 2, Proto-Oncogene Proteins c-bcl-2, Transcription, Genetic, B cell malignancies, G6PD, PP2A, glucose metabolism, lineage-specific vulnerability, redox homeostasis, transcriptional repression, Biological Sciences, Medical and Health Sciences, Developmental Biology
Abstract

B cell activation during normal immune responses and oncogenic transformation impose increased metabolic demands on B cells and their ability to retain redox homeostasis. While the serine/threonine-protein phosphatase 2A (PP2A) was identified as a tumor suppressor in multiple types of cancer, our genetic studies revealed an essential role of PP2A in B cell tumors. Thereby, PP2A redirects glucose carbon utilization from glycolysis to the pentose phosphate pathway (PPP) to salvage oxidative stress. This unique vulnerability reflects constitutively low PPP activity in B cells and transcriptional repression of G6PD and other key PPP enzymes by the B cell transcription factors PAX5 and IKZF1. Reflecting B-cell-specific transcriptional PPP-repression, glucose carbon utilization in B cells is heavily skewed in favor of glycolysis resulting in lack of PPP-dependent antioxidant protection. These findings reveal a gatekeeper function of the PPP in a broad range of B cell malignancies that can be efficiently targeted by small molecule inhibition of PP2A and G6PD.

Published
2018

20. Inhibition of mTORC1/C2 signaling improves anti-leukemia efficacy of JAK/STAT blockade in CRLF2 rearranged and/or JAK driven Philadelphia chromosome–like acute B-cell lymphoblastic leukemia

Author

Zhang, Qi, Shi, Ce, Han, Lina, Jain, Nitin, Roberts, Kathryn G, Ma, Helen, Cai, Tianyu, Cavazos, Antonio, Tabe, Yoko, Jacamo, Rodrigo O, Mu, Hong, Zhao, Yang, Wang, Jing, Wu, Shuo-Chieh, Cao, Fenglin, Zeng, Zhihong, Zhou, Jin, Mi, Yingchang, Jabbour, Elias J, Levine, Ross, Tasian, Sarah K, Mullighan, Charles G, Weinstock, David M, Fruman, David A, and Konopleva, Marina

Subjects
Childhood Leukemia, Cancer, Pediatric, Rare Diseases, Hematology, Pediatric Cancer, Development of treatments and therapeutic interventions, 5.1 Pharmaceuticals, JAK, Ph-like ALL, mTOR, Oncology and Carcinogenesis
Abstract

Patients with cytokine receptor-like factor 2 rearranged (CRLF2-re) subgroup Philadelphia chromosome-like B-cell acute lymphoblastic leukemia (Ph-like B-ALL) have a high relapse rate and poor clinical outcomes. CRFL2-re Ph-like B-ALL is characterized by heightened activation of multiple signaling pathways, including the JAK/STAT and PI3K/AKT/mTOR pathways. We hypothesized that the combined inhibition by JAK2 and mTOR inhibitors would induce an additive antileukemia effect in CRLF2-re Ph-like B-ALL. In this study, we tested the antileukemia efficacy of the type I JAK inhibitor ruxolitinib and type II JAK inhibitor NVP-BBT594 (hereafter abbreviated BBT594) [1] alone and combined with allosteric mTOR inhibitor rapamycin and a second generation ATP-competitive mTOR kinase inhibitor AZD2014. We found that BBT594/AZD2014 combination produced robust anti-leukemic effects in Ph-like cell lines in vitro and in patient-derived xenograft (PDX) cells cultured ex vivo. JAK2/mTOR inhibition arrested the cell cycle and reduced cell survival to a greater extent in Ph-like B-ALL cells with CRLF2-re and JAK2 mutation. Synergistic cell killing was associated with the greater inhibition of JAK2 phosphorylation by BBT594 than by ruxolitinib and the greater inhibition of AKT and 4E-BP1 phosphorylation by AZD2014 than by rapamycin. In vivo, BBT594/AZD2014 co-treatment was most efficacious in reducing spleen size in three Ph-like PDX models, and markedly depleted bone marrow and spleen ALL cells in an ATF7IP-JAK2 fusion PDX. In summary, combined inhibition of JAK/STAT and mTOR pathways by next-generation inhibitors had promising antileukemia efficacy in preclinical models of CRFL2-re Ph-like B-ALL.

Published
2018

21. 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, 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

22. KLRG1 Cell Depletion as a Novel Therapeutic Strategy in Patients with Mature T-Cell Lymphoma Subtypes

Author

Assatova, Bimarzhan, primary, Willim, Robert, additional, Trevisani, Christopher, additional, Haskett, Garrett, additional, Kariya, Khyati Maulik, additional, Chopra, Kusha, additional, Park, Sung Rye, additional, Tolstorukov, Michael Yevgeniy, additional, McCabe, Sean M., additional, Duffy, Jessica, additional, Louissaint, Abner, additional, Huuhtanen, Jani, additional, Bhattacharya, Dipabarna, additional, Mustjoki, Satu, additional, Koh, Min Jung, additional, Powers, Foster, additional, Morgan, Elizabeth A., additional, Yang, Lei, additional, Pinckney, Brandy, additional, Cotton, Matthew J., additional, Crabbe, Andrew, additional, Ziemba, Jessica Beth, additional, Brain, Ian, additional, Heavican-Foral, Tayla B., additional, Iqbal, Javeed, additional, Nemec, Ronald, additional, Rider, Anna Baird, additional, Ford, Josie Germain, additional, Koh, Min Ji, additional, Scanlan, Nora, additional, Feith, David J., additional, Loughran, Thomas P., additional, Kim, Won Seog, additional, Choi, Jaehyuk, additional, Roels, Juliette, additional, Boehme, Lena, additional, Putteman, Tom, additional, Taghon, Tom, additional, Barnes, Jeffrey A., additional, Johnson, P. Connor, additional, Jacobsen, Eric D., additional, Greenberg, Steven A., additional, Weinstock, David M., additional, and Jain, Salvia, additional

Published
2024
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23. Combined epigenetic and metabolic treatments overcome differentiation blockade in acute myeloid leukemia

Author

Zee, Barry M., Poels, Kamrine E., Yao, Cong-Hui, Kawabata, Kimihito C., Wu, Gongwei, Duy, Cihangir, Jacobus, William D., Senior, Elizabeth, Endress, Jennifer E., Jambhekar, Ashwini, Lovitch, Scott B., Ma, Jiexian, Dhall, Abhinav, Harris, Isaac S., Blanco, M. Andres, Sykes, David B., Licht, Jonathan D., Weinstock, David M., Melnick, Ari, Haigis, Marcia C., Michor, Franziska, and Shi, Yang

Published
2021
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25. Genomic landscape of cutaneous follicular lymphomas reveals 2 subgroups with clinically predictive molecular features

Author

Zhou, Xiaolong Alan, Yang, Jingyi, Ringbloom, Kimberly G., Martinez-Escala, Maria Estela, Stevenson, Kristen E., Wenzel, Alexander T., Fantini, Damiano, Martin, Haley K., Moy, Andrea P., Morgan, Elizabeth A., Harkins, Shannon, Paxton, Christian N., Hong, Bo, Andersen, Erica F., Guitart, Joan, Weinstock, David M., Cerroni, Lorenzo, Choi, Jaehyuk, and Louissaint, Abner, Jr

Published
2021
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26. The promise of organ and tissue preservation to transform medicine

Author

Giwa, Sebastian, Lewis, Jedediah K, Alvarez, Luis, Langer, Robert, Roth, Alvin E, Church, George M, Markmann, James F, Sachs, David H, Chandraker, Anil, Wertheim, Jason A, Rothblatt, Martine, Boyden, Edward S, Eidbo, Elling, Lee, WP Andrew, Pomahac, Bohdan, Brandacher, Gerald, Weinstock, David M, Elliott, Gloria, Nelson, David, Acker, Jason P, Uygun, Korkut, Schmalz, Boris, Weegman, Brad P, Tocchio, Alessandro, Fahy, Greg M, Storey, Kenneth B, Rubinsky, Boris, Bischof, John, Elliott, Janet AW, Woodruff, Teresa K, Morris, G John, Demirci, Utkan, Brockbank, Kelvin GM, Woods, Erik J, Ben, Robert N, Baust, John G, Gao, Dayong, Fuller, Barry, Rabin, Yoed, Kravitz, David C, Taylor, Michael J, and Toner, Mehmet

Subjects
Health Services and Systems, Biomedical and Clinical Sciences, Health Sciences, Cancer, Generic health relevance, Good Health and Well Being, Cryopreservation, Forecasting, Humans, Organ Culture Techniques, Organ Preservation, Organ Transplantation, Regenerative Medicine, Tissue Preservation
Abstract

The ability to replace organs and tissues on demand could save or improve millions of lives each year globally and create public health benefits on par with curing cancer. Unmet needs for organ and tissue preservation place enormous logistical limitations on transplantation, regenerative medicine, drug discovery, and a variety of rapidly advancing areas spanning biomedicine. A growing coalition of researchers, clinicians, advocacy organizations, academic institutions, and other stakeholders has assembled to address the unmet need for preservation advances, outlining remaining challenges and identifying areas of underinvestment and untapped opportunities. Meanwhile, recent discoveries provide proofs of principle for breakthroughs in a family of research areas surrounding biopreservation. These developments indicate that a new paradigm, integrating multiple existing preservation approaches and new technologies that have flourished in the past 10 years, could transform preservation research. Capitalizing on these opportunities will require engagement across many research areas and stakeholder groups. A coordinated effort is needed to expedite preservation advances that can transform several areas of medicine and medical science.

Published
2017

29. 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

30. Supplementary Data from Targeting Aggressive B-cell Lymphomas through Pharmacological Activation of the Mitochondrial Protease OMA1

Author

Schwarzer, Adrian, primary, Oliveira, Matheus, primary, Kleppa, Marc-Jens, primary, Slattery, Scott D., primary, Anantha, Andy, primary, Cooper, Alan, primary, Hannink, Mark, primary, Schambach, Axel, primary, Dörrie, Anneke, primary, Kotlyarov, Alexey, primary, Gaestel, Matthias, primary, Hembrough, Todd, primary, Levine, Jedd, primary, Luther, Michael, primary, Stocum, Michael, primary, Stiles, Linsey, primary, Weinstock, David M., primary, Liesa, Marc, primary, and Kostura, Matthew J., primary

Published
2023
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31. Supplementary Table S4 from Targeting Aggressive B-cell Lymphomas through Pharmacological Activation of the Mitochondrial Protease OMA1

Author

Schwarzer, Adrian, primary, Oliveira, Matheus, primary, Kleppa, Marc-Jens, primary, Slattery, Scott D., primary, Anantha, Andy, primary, Cooper, Alan, primary, Hannink, Mark, primary, Schambach, Axel, primary, Dörrie, Anneke, primary, Kotlyarov, Alexey, primary, Gaestel, Matthias, primary, Hembrough, Todd, primary, Levine, Jedd, primary, Luther, Michael, primary, Stocum, Michael, primary, Stiles, Linsey, primary, Weinstock, David M., primary, Liesa, Marc, primary, and Kostura, Matthew J., primary

Published
2023
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32. Data from Targeting Aggressive B-cell Lymphomas through Pharmacological Activation of the Mitochondrial Protease OMA1

Author

Schwarzer, Adrian, primary, Oliveira, Matheus, primary, Kleppa, Marc-Jens, primary, Slattery, Scott D., primary, Anantha, Andy, primary, Cooper, Alan, primary, Hannink, Mark, primary, Schambach, Axel, primary, Dörrie, Anneke, primary, Kotlyarov, Alexey, primary, Gaestel, Matthias, primary, Hembrough, Todd, primary, Levine, Jedd, primary, Luther, Michael, primary, Stocum, Michael, primary, Stiles, Linsey, primary, Weinstock, David M., primary, Liesa, Marc, primary, and Kostura, Matthew J., primary

Published
2023
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33. Supplementary Figures from Targeting Aggressive B-cell Lymphomas through Pharmacological Activation of the Mitochondrial Protease OMA1

Author

Schwarzer, Adrian, primary, Oliveira, Matheus, primary, Kleppa, Marc-Jens, primary, Slattery, Scott D., primary, Anantha, Andy, primary, Cooper, Alan, primary, Hannink, Mark, primary, Schambach, Axel, primary, Dörrie, Anneke, primary, Kotlyarov, Alexey, primary, Gaestel, Matthias, primary, Hembrough, Todd, primary, Levine, Jedd, primary, Luther, Michael, primary, Stocum, Michael, primary, Stiles, Linsey, primary, Weinstock, David M., primary, Liesa, Marc, primary, and Kostura, Matthew J., primary

Published
2023
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34. Parp3 promotes long-range end joining in murine cells

Author

Layer, Jacob V., Cleary, J. Patrick, Brown, Alexander J., Stevenson, Kristen E., Morrow, Sara N., Van Scoyk, Alexandria, Blasco, Rafael B., Karaca, Elif, Meng, Fei-Long, Frock, Richard L., Tivey, Trevor, Kim, Sunhee, Fuchs, Hailey, Chiarle, Roberto, Alt, Frederick W., Roberts, Steven A., Weinstock, David M., and Day, Tovah A.

Published
2018

36. 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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40. Duodenal-type and nodal follicular lymphomas differ by their immune microenvironment rather than their mutation profiles

Author

Hellmuth, Johannes C., Louissaint, Abner, Jr, Szczepanowski, Monika, Haebe, Sarah, Pastore, Alessandro, Alig, Stefan, Staiger, Annette M., Hartmann, Sylvia, Kridel, Robert, Ducar, Matthew D., Koch, Peter, Dreyling, Martin, Hansmann, Martin-Leo, Ott, German, Rosenwald, Andreas, Gascoyne, Randy D., Weinstock, David M., Hiddemann, Wolfgang, Klapper, Wolfram, and Weigert, Oliver

Published
2018
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42. TP63 fusions drive multicomplex enhancer rewiring, lymphomagenesis, and EZH2 dependence

Author

Wu, Gongwei, primary, Yoshida, Noriaki, additional, Liu, Jihe, additional, Zhang, Xiaoyang, additional, Xiong, Yuan, additional, Heavican-Foral, Tayla B., additional, Mandato, Elisa, additional, Liu, Huiyun, additional, Nelson, Geoffrey M., additional, Yang, Lu, additional, Chen, Renee, additional, Donovan, Katherine A., additional, Jones, Marcus K., additional, Roshal, Mikhail, additional, Zhang, Yanming, additional, Xu, Ran, additional, Nirmal, Ajit J., additional, Jain, Salvia, additional, Leahy, Catharine, additional, Jones, Kristen L., additional, Stevenson, Kristen E., additional, Galasso, Natasha, additional, Ganesan, Nivetha, additional, Chang, Tiffany, additional, Wu, Wen-Chao, additional, Louissaint, Abner, additional, Debaize, Lydie, additional, Yoon, Hojong, additional, Dal Cin, Paola, additional, Chan, Wing C., additional, Ho Sui, Shannan J., additional, Ng, Samuel Y., additional, Feldman, Andrew L., additional, Horwitz, Steven M., additional, Adelman, Karen, additional, Fischer, Eric S., additional, Chen, Chun-Wei, additional, Weinstock, David M., additional, and Brown, Myles, additional

Published
2023
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43. Leukemia circulation kinetics revealed through blood exchange method

Author

Miller, Alex B., primary, Langenbucher, Adam, additional, Rodriguez, Felicia H., additional, Lin, Lin, additional, Bray, Christina, additional, Duquette, Sarah, additional, Zhang, Ye, additional, Goulet, Dan, additional, Lane, Andrew A., additional, Weinstock, David M., additional, Hemann, Michael T., additional, and Manalis, Scott R., additional

Published
2023
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45. Targeting aggressive B-cell lymphomas through pharmacological activation of the mitochondrial protease OMA1

Author

Schwarzer, Adrian, primary, Oliveira, Matheus, additional, Kleppa, Marc-Jens, additional, Slattery, Scott D., additional, Anantha, Andy, additional, Cooper, Alan, additional, Hannink, Mark, additional, Schambach, Axel, additional, Doerrie, Anneke, additional, Kotylarov, Alexey, additional, Gaestel, Matthias, additional, Hembrough, Todd, additional, Levine, Jedd, additional, Luther, Michael, additional, Stocum, Michael, additional, Stiles, Linsey, additional, Weinstock, David M., additional, Liesa, Marc, additional, and Kostura, Matthew J., additional

Published
2023
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46. P1207: SERIAL SINGLE-CELL PROFILING OF MANTLE CELL LYMPHOMA REVEALS FUNCTIONAL AND MOLECULAR CORRELATES OF RESISTANCE TO BTK INHIBITOR-INCLUSIVE TRIPLET THERAPY

Author

Debaize, Lydie, primary, Zhang, Ye, additional, Ramseier, Michelle, additional, Zhang, Mingzeng, additional, Langenbucher, Adam, additional, Winter, Peter S., additional, Xu, Ran, additional, Senhaji, Nezha, additional, Redd, Robert A, additional, Aryee, Martin J., additional, Branch, Paul H., additional, Kim, Austin I., additional, Weinstock, David M., additional, Shalek, Alex, additional, Manalis, Scott R., additional, and Murakami, Mark A., additional

Published
2023
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48. Outcomes after Allogeneic Stem Cell Transplantation in Patients with Double-Hit and Double-Expressor Lymphoma

Author

Herrera, Alex F., Rodig, Scott J., Song, Joo Y., Kim, Young, Griffin, Gabriel K., Yang, Dongyun, Nikolaenko, Liana, Mei, Matthew, Bedell, Victoria, Dal Cin, Paola, Pak, Christine, Alyea, Edwin P., Budde, Lihua E., Chen, Robert, Chen, Yi-Bin, Chan, Wing C., Cutler, Corey S., Ho, Vincent T., Koreth, John, Krishnan, Amrita, Murata-Collins, Joyce L., Nikiforow, Sarah, Palmer, Joycelynne, Pihan, German A., Pillai, Raju, Popplewell, Leslie, Rosen, Steven T., Siddiqi, Tanya, Sohani, Aliyah R., Zain, Jasmine, Kwak, Larry W., Weisenburger, Dennis D., Weinstock, David M., Soiffer, Robert J., Antin, Joseph H., Forman, Stephen J., Nademanee, Auayporn P., and Armand, Philippe

Published
2018
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49. 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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50. Functional proteogenomics reveals biomarkers and therapeutic targets in lymphomas

Author

Rolland, Delphine C.M., Basrur, Venkatesha, Jeon, Yoon-Kyung, McNeil-Schwalm, Carla, Fermin, Damian, Conlon, Kevin P., Zhou, Yeqiao, Ng, Samuel Y., Tsou, Chih-Chiang, Brown, Noah A., Thomas, Dafydd G., Bailey, Nathanael G., Omenn, Gilbert S., Nesvizhskii, Alexey I., Root, David E., Weinstock, David M., Faryabi, Robert B., Lim, Megan S., and Elenitoba-Johnson, Kojo S. J.

Published
2017

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