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1,485 results on '"Leonard, Warren"'

2. LIM-domain-only 4 (LMO4) enhances CD8+ T-cell stemness and tumor rejection by boosting IL-21-STAT3 signaling

Author

Schelker, Roland C., Fioravanti, Jessica, Mastrogiovanni, Fabio, Baldwin, Jeremy G., Rana, Nisha, Li, Peng, Chen, Ping, Vadász, Timea, Spolski, Rosanne, Heuser-Loy, Christoph, Slavkovic-Lukic, Dragana, Noronha, Pedro, Damiano, Giuseppe, Raccosta, Laura, Maggioni, Daniela, Pullugula, Sree, Lin, Jian-Xin, Oh, Jangsuk, Grandinetti, Patrick, Lecce, Mario, Hesse, Leo, Kocks, Emilia, Martín-Santos, Azucena, Gebhard, Claudia, Telford, William G., Ji, Yun, Restifo, Nicholas P., Russo, Vincenzo, Rehli, Michael, Herr, Wolfgang, Leonard, Warren J., and Gattinoni, Luca

Published
2024
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3. Design of cell-type-specific hyperstable IL-4 mimetics via modular de novo scaffolds.

Author

Yang, Huilin, Ulge, Umut, Quijano-Rubio, Alfredo, Bernstein, Zachary, Maestas, David, Chun, Jung-Ho, Wang, Wentao, Lin, Jian-Xin, Jude, Kevin, Singh, Srujan, Orcutt-Jahns, Brian, Li, Peng, Mou, Jody, Chung, Liam, Kuo, Yun-Huai, Ali, Yasmin, Meyer, Aaron, Grayson, Warren, Heller, Nicola, Garcia, K, Leonard, Warren, Silva, Daniel-Adriano, Elisseeff, Jennifer, Baker, David, and Spangler, Jamie

Subjects
Animals, Interleukin-4, Cytokines, Signal Transduction
Abstract

The interleukin-4 (IL-4) cytokine plays a critical role in modulating immune homeostasis. Although there is great interest in harnessing this cytokine as a therapeutic in natural or engineered formats, the clinical potential of native IL-4 is limited by its instability and pleiotropic actions. Here, we design IL-4 cytokine mimetics (denoted Neo-4) based on a de novo engineered IL-2 mimetic scaffold and demonstrate that these cytokines can recapitulate physiological functions of IL-4 in cellular and animal models. In contrast with natural IL-4, Neo-4 is hyperstable and signals exclusively through the type I IL-4 receptor complex, providing previously inaccessible insights into differential IL-4 signaling through type I versus type II receptors. Because of their hyperstability, our computationally designed mimetics can directly incorporate into sophisticated biomaterials that require heat processing, such as three-dimensional-printed scaffolds. Neo-4 should be broadly useful for interrogating IL-4 biology, and the design workflow will inform targeted cytokine therapeutic development.

Published
2023

6. Potentiating adoptive cell therapy using synthetic IL-9 receptors

Author

Kalbasi, Anusha, Siurala, Mikko, Su, Leon L, Tariveranmoshabad, Mito, Picton, Lora K, Ravikumar, Pranali, Li, Peng, Lin, Jian-Xin, Escuin-Ordinas, Helena, Da, Tong, Kremer, Sarah V, Sun, Amy L, Castelli, Sofia, Agarwal, Sangya, Scholler, John, Song, Decheng, Rommel, Philipp C, Radaelli, Enrico, Young, Regina M, Leonard, Warren J, Ribas, Antoni, June, Carl H, and Garcia, K Christopher

Subjects
Biochemistry and Cell Biology, Biomedical and Clinical Sciences, Biological Sciences, Immunology, Oncology and Carcinogenesis, Cancer, Biotechnology, Vaccine Related, Immunization, Animals, Cell- and Tissue-Based Therapy, Immunotherapy, Adoptive, Interleukin Receptor Common gamma Subunit, Interleukins, Melanoma, Mice, Neoplasms, Pancreatic Neoplasms, Receptors, Interleukin-9, Recombinant Fusion Proteins, STAT Transcription Factors, T-Lymphocytes, General Science & Technology
Abstract

Synthetic receptor signalling has the potential to endow adoptively transferred T cells with new functions that overcome major barriers in the treatment of solid tumours, including the need for conditioning chemotherapy1,2. Here we designed chimeric receptors that have an orthogonal IL-2 receptor extracellular domain (ECD) fused with the intracellular domain (ICD) of receptors for common γ-chain (γc) cytokines IL-4, IL-7, IL-9 and IL-21 such that the orthogonal IL-2 cytokine elicits the corresponding γc cytokine signal. Of these, T cells that signal through the chimeric orthogonal IL-2Rβ-ECD-IL-9R-ICD (o9R) are distinguished by the concomitant activation of STAT1, STAT3 and STAT5 and assume characteristics of stem cell memory and effector T cells. Compared to o2R T cells, o9R T cells have superior anti-tumour efficacy in two recalcitrant syngeneic mouse solid tumour models of melanoma and pancreatic cancer and are effective even in the absence of conditioning lymphodepletion. Therefore, by repurposing IL-9R signalling using a chimeric orthogonal cytokine receptor, T cells gain new functions, and this results in improved anti-tumour activity for hard-to-treat solid tumours.

Published
2022

8. Cushing syndrome and glucocorticoids: T-cell lymphopenia, apoptosis, and rescue by IL-21.

Author

Hwang, SuJin, Tatsi, Christina, Kuehn, Hye, Niemela, Julie, Stoddard, Jennifer, Su, Yan, Lodish, Maya, Uzel, Gulbu, Spolski, Rosanne, Leonard, Warren, Holland, Steven, Fleisher, Thomas, Stratakis, Constantine, and Rosenzweig, Sergio

Subjects
BCL2, NF-κB, PI3K, cytokines, infections, interleukins, Adolescent, Apoptosis, Child, Cushing Syndrome, Cytokines, Female, Glucocorticoids, Humans, Leukocyte Count, Lymphopenia, Male, T-Lymphocytes
Abstract

BACKGROUND: Pediatric endogenous Cushing syndrome (eCs) is mainly caused by pituitary corticotropin-producing adenomas, and most glucocorticoid-dependent effects progressively regress upon tumor removal. eCs reproduces long-term, high-dose glucocorticoid therapy, representing a clean, natural, and unbiased model in which to study glucocorticoid bona fide effects on immunity. OBJECTIVE: We performed extensive immunologic studies in otherwise healthy pediatric patients with eCs before and 6 to 13 months after tumor resection, as well as in in vitro glucocorticoid-treated control cells. METHODS: Flow cytometry, immunoblotting, enzyme-linked immunosorbent assay, real-time quantitative PCR, and RNA-Seq techniques were used to characterize patients and in vitro glucocorticoid treated cells. RESULTS: Reduced thymic output, decreased naive T cells, diminished proliferation, and increased T-cell apoptosis were detected before surgery; all these defects eventually normalized after tumor removal in patients. In vitro studies also showed increased T-cell apoptosis, with correspondingly diminished NF-κB signaling and IL-21 levels. In this setting, IL-21 addition upregulated antiapoptotic BCL2 expression and rescued T-cell apoptosis in a PI3K pathway-dependent manner. Similar and reproducible findings were confirmed in eCs patient cells as well. CONCLUSIONS: We identified decreased thymic output and lymphocyte proliferation, together with increased apoptosis, as the underlying causes to T-cell lymphopenia in eCs patients. IL-21 was decreased in both natural and in vitro long-term, high-dose glucocorticoid environments, and in vitro addition of IL-21 counteracted the proapoptotic effects of glucocorticoid therapy. Thus, our results suggest that administration of IL-21 in patients receiving long-term, high-dose glucocorticoid therapy may contribute to ameliorate lymphopenia and the complications associated to it.

Published
2022

9. Investigation of the causal etiology in a patient with T-B+NK+ immunodeficiency

Author

Sertori, Robert, Lin, Jian-Xin, Martinez, Esteban, Rana, Sadhna, Sharo, Andrew, Kazemian, Majid, Sunderam, Uma, Andrake, Mark, Shinton, Susan, Truong, Billy, Dunbrack, Roland M, Liu, Chengyu, Srinivasan, Rajgopol, Brenner, Steven E, Seroogy, Christine M, Puck, Jennifer M, Leonard, Warren J, and Wiest, David L

Subjects
Biological Sciences, Biomedical and Clinical Sciences, Cardiovascular Medicine and Haematology, Immunology, Stem Cell Research, Pediatric, Rare Diseases, Transplantation, Genetics, 2.1 Biological and endogenous factors, Animals, Humans, Infant, Infant, Newborn, Lymphopenia, Male, Mice, Neonatal Screening, Severe Combined Immunodeficiency, T-Lymphocytes, Zebrafish, immunodeficiency, newborn screening, zebrafish, thymus, MED14, T cell lymphopenia, severe combined immunodeficiency, Medical Microbiology, Biochemistry and cell biology
Abstract

Newborn screening for severe combined immunodeficiency (SCID) has not only accelerated diagnosis and improved treatment for affected infants, but also led to identification of novel genes required for human T cell development. A male proband had SCID newborn screening showing very low T cell receptor excision circles (TRECs), a biomarker for thymic output of nascent T cells. He had persistent profound T lymphopenia, but normal numbers of B and natural killer (NK) cells. Despite an allogeneic hematopoietic stem cell transplant from his brother, he failed to develop normal T cells. Targeted resequencing excluded known SCID genes; however, whole exome sequencing (WES) of the proband and parents revealed a maternally inherited X-linked missense mutation in MED14 (MED14V763A), a component of the mediator complex. Morpholino (MO)-mediated loss of MED14 function attenuated T cell development in zebrafish. Moreover, this arrest was rescued by ectopic expression of cDNA encoding the wild type human MED14 ortholog, but not by MED14V763A , suggesting that the variant impaired MED14 function. Modeling of the equivalent mutation in mouse (Med14V769A) did not disrupt T cell development at baseline. However, repopulation of peripheral T cells upon competitive bone marrow transplantation was compromised, consistent with the incomplete T cell reconstitution experienced by the proband upon transplantation with bone marrow from his healthy male sibling, who was found to have the same MED14V763A variant. Suspecting that the variable phenotypic expression between the siblings was influenced by further mutation(s), we sought to identify genetic variants present only in the affected proband. Indeed, WES revealed a mutation in the L1 cell adhesion molecule (L1CAMQ498H); however, introducing that mutation in vivo in mice did not disrupt T cell development. Consequently, immunodeficiency in the proband may depend upon additional, unidentified gene variants.

Published
2022

11. Transcription factor EGR2 controls homing and pathogenicity of TH17 cells in the central nervous system

Author

Gao, Yuanyuan, Wang, Yan, Chauss, Daniel, Villarino, Alejandro V., Link, Verena M., Nagashima, Hiroyuki, Spinner, Camille A., Koparde, Vishal N., Bouladoux, Nicolas, Abers, Michael S., Break, Timothy J., Chopp, Laura B., Park, Jung-Hyun, Zhu, Jinfang, Wiest, David L., Leonard, Warren J., Lionakis, Michail S., O’Shea, John J., Afzali, Behdad, Belkaid, Yasmine, and Lazarevic, Vanja

Published
2023
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18. PD-1 combination therapy with IL-2 modifies CD8+ T cell exhaustion program

Author

Hashimoto, Masao, Araki, Koichi, Cardenas, Maria A., Li, Peng, Jadhav, Rohit R., Kissick, Haydn T., Hudson, William H., McGuire, Donald J., Obeng, Rebecca C., Wieland, Andreas, Lee, Judong, McManus, Daniel T., Ross, James L., Im, Se Jin, Lee, Junghwa, Lin, Jian-Xin, Hu, Bin, West, Erin E., Scharer, Christopher D., Freeman, Gordon J., Sharpe, Arlene H., Ramalingam, Suresh S., Pellerin, Alex, Teichgräber, Volker, Greenleaf, William J., Klein, Christian, Goronzy, Jorg J., Umaña, Pablo, Leonard, Warren J., Smith, Kendall A., and Ahmed, Rafi

Published
2022
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22. Lactate dehydrogenase inhibition synergizes with IL-21 to promote CD8⁺ T cell stemness and antitumor immunity

Author

Hermans, Dalton, Gautam, Sanjivan, García-Cañaveras, Juan C., Gromer, Daniel, Mitra, Suman, Spolski, Rosanne, Li, Peng, Christensen, Stephen, Nguyen, Rosa, Lin, Jian-Xin, Oh, Jangsuk, Du, Ning, Veenbergen, Sharon, Fioravanti, Jessica, Ebina-Shibuya, Risa, Bleck, Christopher, Neckers, Leonard M., Rabinowitz, Joshua D., Gattinoni, Luca, and Leonard, Warren J.

Published
2020

23. An engineered IL-2 partial agonist promotes CD8+ T cell stemness

Author

Mo, Fei, Yu, Zhiya, Li, Peng, Oh, Jangsuk, Spolski, Rosanne, Zhao, Liang, Glassman, Caleb R., Yamamoto, Tori N., Chen, Yun, Golebiowski, Filip M., Hermans, Dalton, Majri-Morrison, Sonia, Picton, Lora K., Liao, Wei, Ren, Min, Zhuang, Xiaoxuan, Mitra, Suman, Lin, Jian-Xin, Gattinoni, Luca, Powell, Jonathan D., Restifo, Nicholas P., Garcia, K. Christopher, and Leonard, Warren J.

Published
2021
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27. Publisher Correction: Potentiating adoptive cell therapy using synthetic IL-9 receptors

Author

Kalbasi, Anusha, Siurala, Mikko, Su, Leon L., Tariveranmoshabad, Mito, Picton, Lora K., Ravikumar, Pranali, Li, Peng, Lin, Jian-Xin, Escuin-Ordinas, Helena, Da, Tong, Kremer, Sarah V., Sun, Amy L., Castelli, Sofia, Agarwal, Sangya, Scholler, John, Song, Decheng, Rommel, Philipp C., Radaelli, Enrico, Young, Regina M., Leonard, Warren J., Ribas, Antoni, June, Carl H., and Garcia, K. Christopher

Published
2022
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31. Supplementary Table 1 from Transcriptional Heterogeneity Overcomes Super-Enhancer Disrupting Drug Combinations in Multiple Myeloma

Author

Welsh, Seth J., primary, Barwick, Benjamin G., primary, Meermeier, Erin W., primary, Riggs, Daniel L., primary, Shi, Chang-Xin, primary, Zhu, Yuan Xiao, primary, Sharik, Meaghen E., primary, Du, Megan T., primary, Abrego Rocha, Leslie D., primary, Garbitt, Victoria M., primary, Stein, Caleb K., primary, Petit, Joachim L., primary, Meurice, Nathalie, primary, Tafoya Alvarado, Yuliza, primary, Fonseca, Rodrigo, primary, Todd, Kennedi T., primary, Brown, Sochilt, primary, Hammond, Zachery J., primary, Cuc, Nicklus H., primary, Wittenberg, Courtney, primary, Herzog, Camille, primary, Roschke, Anna V., primary, Demchenko, Yulia N., primary, Chen, Wei-dong D., primary, Li, Peng, primary, Liao, Wei, primary, Leonard, Warren J., primary, Lonial, Sagar, primary, Bahlis, Nizar J., primary, Neri, Paola, primary, Boise, Lawrence H., primary, Chesi, Marta, primary, and Bergsagel, P. Leif, primary

Published
2024
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32. Supplementary Data 4 from Transcriptional Heterogeneity Overcomes Super-Enhancer Disrupting Drug Combinations in Multiple Myeloma

Author

Welsh, Seth J., primary, Barwick, Benjamin G., primary, Meermeier, Erin W., primary, Riggs, Daniel L., primary, Shi, Chang-Xin, primary, Zhu, Yuan Xiao, primary, Sharik, Meaghen E., primary, Du, Megan T., primary, Abrego Rocha, Leslie D., primary, Garbitt, Victoria M., primary, Stein, Caleb K., primary, Petit, Joachim L., primary, Meurice, Nathalie, primary, Tafoya Alvarado, Yuliza, primary, Fonseca, Rodrigo, primary, Todd, Kennedi T., primary, Brown, Sochilt, primary, Hammond, Zachery J., primary, Cuc, Nicklus H., primary, Wittenberg, Courtney, primary, Herzog, Camille, primary, Roschke, Anna V., primary, Demchenko, Yulia N., primary, Chen, Wei-dong D., primary, Li, Peng, primary, Liao, Wei, primary, Leonard, Warren J., primary, Lonial, Sagar, primary, Bahlis, Nizar J., primary, Neri, Paola, primary, Boise, Lawrence H., primary, Chesi, Marta, primary, and Bergsagel, P. Leif, primary

Published
2024
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33. Supplementary Data 3 from Transcriptional Heterogeneity Overcomes Super-Enhancer Disrupting Drug Combinations in Multiple Myeloma

Author

Welsh, Seth J., primary, Barwick, Benjamin G., primary, Meermeier, Erin W., primary, Riggs, Daniel L., primary, Shi, Chang-Xin, primary, Zhu, Yuan Xiao, primary, Sharik, Meaghen E., primary, Du, Megan T., primary, Abrego Rocha, Leslie D., primary, Garbitt, Victoria M., primary, Stein, Caleb K., primary, Petit, Joachim L., primary, Meurice, Nathalie, primary, Tafoya Alvarado, Yuliza, primary, Fonseca, Rodrigo, primary, Todd, Kennedi T., primary, Brown, Sochilt, primary, Hammond, Zachery J., primary, Cuc, Nicklus H., primary, Wittenberg, Courtney, primary, Herzog, Camille, primary, Roschke, Anna V., primary, Demchenko, Yulia N., primary, Chen, Wei-dong D., primary, Li, Peng, primary, Liao, Wei, primary, Leonard, Warren J., primary, Lonial, Sagar, primary, Bahlis, Nizar J., primary, Neri, Paola, primary, Boise, Lawrence H., primary, Chesi, Marta, primary, and Bergsagel, P. Leif, primary

Published
2024
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34. Data from Transcriptional Heterogeneity Overcomes Super-Enhancer Disrupting Drug Combinations in Multiple Myeloma

Author

Welsh, Seth J., primary, Barwick, Benjamin G., primary, Meermeier, Erin W., primary, Riggs, Daniel L., primary, Shi, Chang-Xin, primary, Zhu, Yuan Xiao, primary, Sharik, Meaghen E., primary, Du, Megan T., primary, Abrego Rocha, Leslie D., primary, Garbitt, Victoria M., primary, Stein, Caleb K., primary, Petit, Joachim L., primary, Meurice, Nathalie, primary, Tafoya Alvarado, Yuliza, primary, Fonseca, Rodrigo, primary, Todd, Kennedi T., primary, Brown, Sochilt, primary, Hammond, Zachery J., primary, Cuc, Nicklus H., primary, Wittenberg, Courtney, primary, Herzog, Camille, primary, Roschke, Anna V., primary, Demchenko, Yulia N., primary, Chen, Wei-dong D., primary, Li, Peng, primary, Liao, Wei, primary, Leonard, Warren J., primary, Lonial, Sagar, primary, Bahlis, Nizar J., primary, Neri, Paola, primary, Boise, Lawrence H., primary, Chesi, Marta, primary, and Bergsagel, P. Leif, primary

Published
2024
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35. Supplementary Table 2 from Transcriptional Heterogeneity Overcomes Super-Enhancer Disrupting Drug Combinations in Multiple Myeloma

Author

Welsh, Seth J., primary, Barwick, Benjamin G., primary, Meermeier, Erin W., primary, Riggs, Daniel L., primary, Shi, Chang-Xin, primary, Zhu, Yuan Xiao, primary, Sharik, Meaghen E., primary, Du, Megan T., primary, Abrego Rocha, Leslie D., primary, Garbitt, Victoria M., primary, Stein, Caleb K., primary, Petit, Joachim L., primary, Meurice, Nathalie, primary, Tafoya Alvarado, Yuliza, primary, Fonseca, Rodrigo, primary, Todd, Kennedi T., primary, Brown, Sochilt, primary, Hammond, Zachery J., primary, Cuc, Nicklus H., primary, Wittenberg, Courtney, primary, Herzog, Camille, primary, Roschke, Anna V., primary, Demchenko, Yulia N., primary, Chen, Wei-dong D., primary, Li, Peng, primary, Liao, Wei, primary, Leonard, Warren J., primary, Lonial, Sagar, primary, Bahlis, Nizar J., primary, Neri, Paola, primary, Boise, Lawrence H., primary, Chesi, Marta, primary, and Bergsagel, P. Leif, primary

Published
2024
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36. Supplementary Data 1 from Transcriptional Heterogeneity Overcomes Super-Enhancer Disrupting Drug Combinations in Multiple Myeloma

Author

Welsh, Seth J., primary, Barwick, Benjamin G., primary, Meermeier, Erin W., primary, Riggs, Daniel L., primary, Shi, Chang-Xin, primary, Zhu, Yuan Xiao, primary, Sharik, Meaghen E., primary, Du, Megan T., primary, Abrego Rocha, Leslie D., primary, Garbitt, Victoria M., primary, Stein, Caleb K., primary, Petit, Joachim L., primary, Meurice, Nathalie, primary, Tafoya Alvarado, Yuliza, primary, Fonseca, Rodrigo, primary, Todd, Kennedi T., primary, Brown, Sochilt, primary, Hammond, Zachery J., primary, Cuc, Nicklus H., primary, Wittenberg, Courtney, primary, Herzog, Camille, primary, Roschke, Anna V., primary, Demchenko, Yulia N., primary, Chen, Wei-dong D., primary, Li, Peng, primary, Liao, Wei, primary, Leonard, Warren J., primary, Lonial, Sagar, primary, Bahlis, Nizar J., primary, Neri, Paola, primary, Boise, Lawrence H., primary, Chesi, Marta, primary, and Bergsagel, P. Leif, primary

Published
2024
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37. Supplementary Data 2 from Transcriptional Heterogeneity Overcomes Super-Enhancer Disrupting Drug Combinations in Multiple Myeloma

Author

Welsh, Seth J., primary, Barwick, Benjamin G., primary, Meermeier, Erin W., primary, Riggs, Daniel L., primary, Shi, Chang-Xin, primary, Zhu, Yuan Xiao, primary, Sharik, Meaghen E., primary, Du, Megan T., primary, Abrego Rocha, Leslie D., primary, Garbitt, Victoria M., primary, Stein, Caleb K., primary, Petit, Joachim L., primary, Meurice, Nathalie, primary, Tafoya Alvarado, Yuliza, primary, Fonseca, Rodrigo, primary, Todd, Kennedi T., primary, Brown, Sochilt, primary, Hammond, Zachery J., primary, Cuc, Nicklus H., primary, Wittenberg, Courtney, primary, Herzog, Camille, primary, Roschke, Anna V., primary, Demchenko, Yulia N., primary, Chen, Wei-dong D., primary, Li, Peng, primary, Liao, Wei, primary, Leonard, Warren J., primary, Lonial, Sagar, primary, Bahlis, Nizar J., primary, Neri, Paola, primary, Boise, Lawrence H., primary, Chesi, Marta, primary, and Bergsagel, P. Leif, primary

Published
2024
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38. Supplementary Data 5 from Transcriptional Heterogeneity Overcomes Super-Enhancer Disrupting Drug Combinations in Multiple Myeloma

Author

Welsh, Seth J., primary, Barwick, Benjamin G., primary, Meermeier, Erin W., primary, Riggs, Daniel L., primary, Shi, Chang-Xin, primary, Zhu, Yuan Xiao, primary, Sharik, Meaghen E., primary, Du, Megan T., primary, Abrego Rocha, Leslie D., primary, Garbitt, Victoria M., primary, Stein, Caleb K., primary, Petit, Joachim L., primary, Meurice, Nathalie, primary, Tafoya Alvarado, Yuliza, primary, Fonseca, Rodrigo, primary, Todd, Kennedi T., primary, Brown, Sochilt, primary, Hammond, Zachery J., primary, Cuc, Nicklus H., primary, Wittenberg, Courtney, primary, Herzog, Camille, primary, Roschke, Anna V., primary, Demchenko, Yulia N., primary, Chen, Wei-dong D., primary, Li, Peng, primary, Liao, Wei, primary, Leonard, Warren J., primary, Lonial, Sagar, primary, Bahlis, Nizar J., primary, Neri, Paola, primary, Boise, Lawrence H., primary, Chesi, Marta, primary, and Bergsagel, P. Leif, primary

Published
2024
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39. Supplementary Figures S1-S11 from Transcriptional Heterogeneity Overcomes Super-Enhancer Disrupting Drug Combinations in Multiple Myeloma

Author

Welsh, Seth J., primary, Barwick, Benjamin G., primary, Meermeier, Erin W., primary, Riggs, Daniel L., primary, Shi, Chang-Xin, primary, Zhu, Yuan Xiao, primary, Sharik, Meaghen E., primary, Du, Megan T., primary, Abrego Rocha, Leslie D., primary, Garbitt, Victoria M., primary, Stein, Caleb K., primary, Petit, Joachim L., primary, Meurice, Nathalie, primary, Tafoya Alvarado, Yuliza, primary, Fonseca, Rodrigo, primary, Todd, Kennedi T., primary, Brown, Sochilt, primary, Hammond, Zachery J., primary, Cuc, Nicklus H., primary, Wittenberg, Courtney, primary, Herzog, Camille, primary, Roschke, Anna V., primary, Demchenko, Yulia N., primary, Chen, Wei-dong D., primary, Li, Peng, primary, Liao, Wei, primary, Leonard, Warren J., primary, Lonial, Sagar, primary, Bahlis, Nizar J., primary, Neri, Paola, primary, Boise, Lawrence H., primary, Chesi, Marta, primary, and Bergsagel, P. Leif, primary

Published
2024
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43. Defective B Cell Responses in the Absence of SH2D1A

Author

Morra, Massimo, Barrington, Robert A., Abadia-Molina, Ana C., Okamoto, Susumo, Julien, Aimee, Gullo, Charles, Kalsy, Anuj, Edwards, Matthew J., Chen, Gang, Spolski, Rosanne, Leonard, Warren J., Huber, Brigitte T., Borrow, Persephone, Biron, Christine A., Satoskar, Abhay R., Carroll, Michael C., Terhorst, Cox, and Fearon, Douglas T.

Published
2005

47. Distinct use of super-enhancer elements controls cell type–specific CD25 transcription and function

Author

Spolski, Rosanne, primary, Li, Peng, additional, Chandra, Vivek, additional, Shin, Boyoung, additional, Goel, Shubham, additional, Sakamoto, Keiko, additional, Liu, Chengyu, additional, Oh, Jangsuk, additional, Ren, Min, additional, Enomoto, Yutaka, additional, West, Erin E., additional, Christensen, Stephen M., additional, Wan, Edwin C. K., additional, Ge, Meili, additional, Lin, Jian-Xin, additional, Yan, Bingyu, additional, Kazemian, Majid, additional, Yu, Zu-Xi, additional, Nagao, Keisuke, additional, Vijayanand, Pandurangan, additional, Rothenberg, Ellen V., additional, and Leonard, Warren J., additional

Published
2023
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48. Transcriptional heterogeneity overcomes super-enhancer disrupting drug combinations in multiple myeloma

Author

Welsh, Seth J., primary, Barwick, Benjamin G., additional, Meermeier, Erin W., additional, Riggs, Daniel L., additional, Shi, Chang-Xin, additional, Zhu, Yuan Xiao, additional, Sharik, Meaghen E., additional, Du, Megan T., additional, Rocha, Leslie D Abrego., additional, Garbitt, Victoria M., additional, Stein, Caleb K., additional, Petit, Joachim L., additional, Meurice, Nathalie, additional, Tafoya Alvarado, Yuliza, additional, Fonseca, Rodrigo, additional, Todd, Kennedi T., additional, Brown, Sochilt, additional, Hammond, Zachary J., additional, Cuc, Nicklus H., additional, Wittenberg, Courtney, additional, Herzog, Camille, additional, Roschke, Anna V., additional, Demchenko, Yulia N., additional, Chen, Wei-dong D., additional, Li, Peng, additional, Liao, Wei, additional, Leonard, Warren J., additional, Lonial, Sagar, additional, Bahlis, Nizar J., additional, Neri, Paola, additional, Boise, Lawrence H., additional, Chesi, Marta, additional, and Bergsagel, P. Leif, additional

Published
2023
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