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1. Functional genomics identifies N-acetyllactosamine extension of complex N-glycans as a mechanism to evade lysis by natural killer cells

Author

Xiaoxuan Zhuang, James Woods, Yanlong Ji, Sebastian Scheich, Fei Mo, Sumati Rajagopalan, Zana A. Coulibaly, Matthias Voss, Henning Urlaub, Louis M. Staudt, Kuan-Ting Pan, and Eric O. Long

Subjects
CP: Cancer, Biology (General), QH301-705.5
Abstract

Summary: Natural killer (NK) cells are primary defenders against cancer precursors, but cancer cells can persist by evading immune surveillance. To investigate the genetic mechanisms underlying this evasion, we perform a genome-wide CRISPR screen using B lymphoblastoid cells. SPPL3, a peptidase that cleaves glycosyltransferases in the Golgi, emerges as a top hit facilitating evasion from NK cytotoxicity. SPPL3-deleted cells accumulate glycosyltransferases and complex N-glycans, disrupting not only binding of ligands to NK receptors but also binding of rituximab, a CD20 antibody approved for treating B cell cancers. Notably, inhibiting N-glycan maturation restores receptor binding and sensitivity to NK cells. A secondary CRISPR screen in SPPL3-deficient cells identifies B3GNT2, a transferase-mediating poly-LacNAc extension, as crucial for resistance. Mass spectrometry confirms enrichment of N-glycans bearing poly-LacNAc upon SPPL3 loss. Collectively, our study shows the essential role of SPPL3 and poly-LacNAc in cancer immune evasion, suggesting a promising target for cancer treatment.

Published
2024
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2. In vivo CRISPR screens reveal a HIF-1α-mTOR-network regulates T follicular helper versus Th1 cells

Author

Bonnie Huang, James D. Phelan, Silvia Preite, Julio Gomez-Rodriguez, Kristoffer H. Johansen, Hirofumi Shibata, Arthur L. Shaffer, Qin Xu, Brendan Jeffrey, Martha Kirby, Stacie Anderson, Yandan Yang, Selamawit Gossa, Dorian B. McGavern, Louis M. Staudt, and Pamela L. Schwartzberg

Subjects
Science
Abstract

T follicular helper (Tfh) and T help type 1 (Th1) cells both arise from naïve CD4 T cells, but detailed knowledge of their differentiation remains incomplete. Here the authors pursue an in vivo CRISPR screen to identify genes, focusing on druggable targets, regulating Tfh versus Th1 to provide a resource for related studies, while also implicating HIF-1α and VHL in this regulation.

Published
2022
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3. Survey of Lifestyle, Past Medical History and Complementary and Alternative Medicine Use Among Adult Patients Participating in the National Cancer Institute's Exceptional Responders Initiative

Author

Oluwadamilola Olaku, Barbara A. Conley, S. Percy Ivy, Lisa M. McShane, Louis M. Staudt, Sophie M. King, Megan Sansevere, Benjamin Kim, and Jeffrey D. White

Subjects
Exceptional response, Lifestyle, Complementary Alternative Medicine, Diet, Physical Activity, Neoplasms. Tumors. Oncology. Including cancer and carcinogens, RC254-282
Abstract

Introduction: The Exceptional Responders Initiative (ERI) at the National Cancer Institute attempts to correlate unusually good outcomes in patients with cancer with genetic targets in tumors and the therapies the patients received. It is not known if other factors might contribute to exceptional responses or outcomes. We explored aspects of the medical history, lifestyle changes, complementary and alternative medicine (CAM) use and communication between health care practitioners and patients who experienced an exceptional response following cancer treatment. Methods: All subjects whose case was submitted to the ERI were eligible to participate in the survey. A 121-question survey questionnaire was developed to assess aspects of the subject's past medical history, lifestyle (e.g., diet, exercise, spirituality) and use of CAM. Results: Thirty subjects completed and returned the questionnaire from approximately 88 patients invited to participate (approximate response rate = 34%). Approximately 68% were female and 32% were male. Fifty percent of subjects changed their diet after their cancer diagnosis. Eighteen patients (60%) reported using a CAM therapy (not including oral vitamins/minerals or spiritual practices) during their Exceptional Response (ER). Conclusion: Multiple factors, including features of the tumor itself, the patient, or the environment, could affect tumor response or patient survival, either solely or in combination with the treatments received. Many patients use other medications, change their diet or physical activity or use CAM interventions after their cancer diagnosis. Investigators attempting to understand the exceptional response phenomenon should acquire rich data sets of their subjects that include information about these factors.

Published
2022
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4. Uniform genomic data analysis in the NCI Genomic Data Commons

Author

Zhenyu Zhang, Kyle Hernandez, Jeremiah Savage, Shenglai Li, Dan Miller, Stuti Agrawal, Francisco Ortuno, Louis M. Staudt, Allison Heath, and Robert L. Grossman

Subjects
Science
Abstract

The Genomic Data Commons repository contains genomic, epigenomic, proteomic and clinical data from the TCGA and TARGET datasets. Here, the authors describe the analysis methods for how these divergent datasets were integrated together.

Published
2021
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5. MAPK and JAK-STAT pathways dysregulation in plasmablastic lymphoma

Author

Joan Enric Ramis-Zaldivar, Blanca Gonzalez-Farre, Alina Nicolae, Svetlana Pack, Guillem Clot, Ferran Nadeu, Anja Mottok, Heike Horn, Joo Y. Song, Kai Fu, George Wright, Randy D. Gascoyne, Wing C. Chan, David W. Scott, Andrew L. Feldman, Alexandra Valera, Anna Enjuanes, Rita M. Braziel, Erlend B. Smeland, Louis M. Staudt, Andreas Rosenwald, Lisa M. Rimsza, German Ott, Elaine S. Jaffe, Itziar Salaverria, and Elias Campo

Subjects
Diseases of the blood and blood-forming organs, RC633-647.5
Abstract

Plasmablastic lymphoma (PBL) is an aggressive B-cell lymphoma with an immunoblastic/large-cell morphology and terminal B-cell differentiation. The differential diagnosis from Burkitt lymphoma, plasma cell myeloma and some variants of diffuse large B-cell lymphoma may be challenging because of the overlapping morphological, genetic and immunophenotypic features. Furthermore, the genomic landscape in PBL is not well known. To characterize the genetic and molecular heterogeneity of these tumors, we investigated 34 cases of PBL using an integrated approach, including fluorescence in situ hybridization, targeted sequencing of 94 B-cell lymphoma-related genes, and copy-number arrays. PBL were characterized by high genetic complexity including MYC translocations (87%), gains of 1q21.1-q44, trisomy 7, 8q23.2- q24.21, 11p13-p11.2, 11q14.2-q25, 12p and 19p13.3-p13.13, losses of 1p33, 1p31.1-p22.3, 13q and 17p13.3-p11.2, and recurrent mutations of STAT3 (37%), NRAS and TP53 (33%), MYC and EP300 (19%) and CARD11, SOCS1 and TET2 (11%). Pathway enrichment analysis suggested a cooperative action between MYC alterations and MAPK (49%) and JAK-STAT (40%) signaling pathways. Of note, Epstein-Barr virus (EBV)-negative PBL cases had higher mutational and copy-number load and more frequent TP53, CARD11 and MYC mutations, whereas EBVpositive PBL tended to have more mutations affecting the JAK-STAT pathway. In conclusion, these findings further unravel the distinctive molecular heterogeneity of PBL identifying novel molecular targets and the different genetic profile of these tumors in relation to EBV infection.

Published
2021
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6. Most non-canonical proteins uniquely populate the proteome or immunopeptidome

Author

Maria Virginia Ruiz Cuevas, Marie-Pierre Hardy, Jaroslav Hollý, Éric Bonneil, Chantal Durette, Mathieu Courcelles, Joël Lanoix, Caroline Côté, Louis M. Staudt, Sébastien Lemieux, Pierre Thibault, Claude Perreault, and Jonathan W. Yewdell

Subjects
computational biology, defective ribosomal products, major histocompatibility complex, mass spectrometry, non-canonical translation, peptides, Biology (General), QH301-705.5
Abstract

Summary: Combining RNA sequencing, ribosome profiling, and mass spectrometry, we elucidate the contribution of non-canonical translation to the proteome and major histocompatibility complex (MHC) class I immunopeptidome. Remarkably, of 14,498 proteins identified in three human B cell lymphomas, 2,503 are non-canonical proteins. Of these, 28% are novel isoforms and 72% are cryptic proteins encoded by ostensibly non-coding regions (60%) or frameshifted canonical genes (12%). Cryptic proteins are translated as efficiently as canonical proteins, have more predicted disordered residues and lower stability, and critically generate MHC-I peptides 5-fold more efficiently per translation event. Translating 5′ “untranslated” regions hinders downstream translation of genes involved in transcription, translation, and antiviral responses. Novel protein isoforms show strong enrichment for signaling pathways deregulated in cancer. Only a small fraction of cryptic proteins detected in the proteome contribute to the MHC-I immunopeptidome, demonstrating the high preferential access of cryptic defective ribosomal products to the class I pathway.

Published
2021
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7. Reliable subtype classification of diffuse large B-cell lymphoma samples from GELA LNH2003 trials using the Lymph2Cx gene expression assay

Author

Jean-Philippe Jais, Thierry Jo Molina, Philippe Ruminy, David Gentien, Cecile Reyes, David W. Scott, Lisa M. Rimsza, George Wright, Randy D. Gascoyne, Louis M. Staudt, Corinne Haioun, Herve Tilly, Philippe Gaulard, Gilles A. Salles, Fabrice Jardin, and Karen Leroy

Subjects
Diseases of the blood and blood-forming organs, RC633-647.5
Published
2017
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9. Methylation profiling of mediastinal gray zone lymphoma reveals a distinctive signature with elements shared by classical Hodgkin’s lymphoma and primary mediastinal large B-cell lymphoma

Author

Franziska C. Eberle, Jaime Rodriguez-Canales, Lai Wei, Jeffrey C. Hanson, J. Keith Killian, Hong-Wei Sun, Lisa G. Adams, Stephen M. Hewitt, Wyndham H. Wilson, Stefania Pittaluga, Paul S. Meltzer, Louis M. Staudt, Michael R. Emmert-Buck, and Elaine S. Jaffe

Subjects
Diseases of the blood and blood-forming organs, RC633-647.5
Abstract

Background Mediastinal gray zone lymphoma is a newly recognized entity with transitional morphological and immunophenotypic features between the nodular sclerosis subtype of Hodgkin’s lymphoma and primary mediastinal large B-cell lymphoma. Diagnostic criteria for mediastinal gray zone lymphoma are still challenging, and the optimal therapy is as yet undetermined. Epigenetic changes have been implicated in the loss of the B-cell program in classical Hodgkin’s lymphoma, and might provide a basis for the immunophenotypic alterations seen in mediastinal gray zone lymphoma.Design and Methods We performed a large-scale DNA methylation analysis of microdissected tumor cells to investigate the biological underpinnings of mediastinal gray zone lymphoma and its association with the related entities classical Hodgkin’s lymphoma and primary mediastinal large B-cell lymphoma, making comparisons with the presumptively less related diffuse large B-cell lymphoma.Results Principal component analysis demonstrated that mediastinal gray zone lymphoma has a distinct epigenetic profile intermediate between classical Hodgkin’s lymphoma and primary mediastinal large B-cell lymphoma but remarkably different from that of diffuse large B-cell lymphoma. Analysis of common hypo- and hypermethylated CpG targets in mediastinal gray zone lymphoma, classical Hodgkin’s lymphoma, primary mediastinal large B-cell lymphoma and diffuse large B-cell lymphoma was performed and confirmed the findings of the principal component analysis. Based on the epigenetic profiles we were able to establish class prediction models utilizing genes such as HOXA5, MMP9, EPHA7 and DAPK1 which could distinguish between mediastinal gray zone lymphoma, classical Hodgkin’s lymphoma and primary mediastinal large B-cell lymphoma with a final combined prediction of 100%.Conclusions Our data confirm a close relationship between mediastinal gray zone lymphoma and both classical Hodgkin’s lymphoma and primary mediastinal large B-cell lymphoma. However, important differences were observed as well, allowing a clear distinction from both parent entities. Thus, mediastinal gray zone lymphoma cannot be assigned to either classical Hodgkin’s lymphoma or primary mediastinal large B-cell lymphoma, validating the decision to create an intermediate category in the World Health Organization classification.

Published
2011
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10. SOX11 expression is highly specific for mantle cell lymphoma and identifies the cyclin D1-negative subtype

Author

Ana Mozos, Cristina Royo, Elena Hartmann, Daphne De Jong, Cristina Baró, Alexandra Valera, Kai Fu, Dennis D. Weisenburger, Jan Delabie, Shih-Sung Chuang, Elaine S. Jaffe, Carmen Ruiz-Marcellan, Sandeep Dave, Lisa Rimsza, Rita Braziel, Randy D. Gascoyne, Francisco Solé, Armando López-Guillermo, Dolors Colomer, Louis M. Staudt, Andreas Rosenwald, German Ott, Pedro Jares, and Elias Campo

Subjects
Diseases of the blood and blood-forming organs, RC633-647.5
Abstract

Background Cyclin D1-negative mantle cell lymphoma is difficult to distinguish from other small B-cell lymphomas. The clinical and pathological characteristics of patients with this form of lymphoma have not been well defined. Overexpression of the transcription factor SOX11 has been observed in conventional mantle cell lymphoma. The aim of this study was to determine whether this gene is expressed in cyclin D1-negative mantle cell lymphoma and whether its detection may be useful to identify these tumors.Design and Methods The microarray database of 238 mature B-cell neoplasms was re-examined. SOX11 protein expression was investigated immunohistochemically in 12 cases of cyclin D1-negative mantle cell lymphoma, 54 cases of conventional mantle cell lymphoma, and 209 additional lymphoid neoplasms.Results SOX11 mRNA was highly expressed in conventional and cyclin D1-negative mantle cell lymphoma and in 33% of the cases of Burkitt’s lymphoma but not in any other mature lymphoid neoplasm. SOX11 nuclear protein was detected in 50 cases (93%) of conventional mantle cell lymphoma and also in the 12 cyclin D1-negative cases of mantle cell lymphoma, the six cases of lymphoblastic lymphomas, in two of eight cases of Burkitt’s lymphoma, and in two of three T-prolymphocytic leukemias but was negative in the remaining lymphoid neoplasms. Cyclin D2 and D3 mRNA levels were significantly higher in cyclin D1-negative mantle cell lymphoma than in conventional mantle cell lymphoma but the protein expression was not discriminative. The clinico-pathological features and outcomes of the patients with cyclin D1-negative mantle cell lymphoma identified by SOX11 expression were similar to those of patients with conventional mantle cell lymphoma.Conclusions SOX11 mRNA and nuclear protein expression is a highly specific marker for both cyclin D1-positive and negative mantle cell lymphoma.

Published
2009
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12. Chromosomal alterations detected by comparative genomic hybridization in subgroups of gene expression-defined Burkitt’s lymphoma

Author

Itziar Salaverria, Andreas Zettl, Silvia Beà, Elena M. Hartmann, Sandeep S. Dave, George W. Wright, Evert-Jan Boerma, Philip M. Kluin, German Ott, Wing C. Chan, Dennis D. Weisenburger, Armando Lopez-Guillermo, Randy D. Gascoyne, Jan Delabie, Lisa M. Rimsza, Rita M. Braziel, Elaine S. Jaffe, Louis M. Staudt, Hans Konrad Müller-Hermelink, Elias Campo, Andreas Rosenwald, and for the Leukemia and Lymphoma Molecular Profiling Project (LLMPP)

Subjects
Diseases of the blood and blood-forming organs, RC633-647.5
Abstract

Background Burkitt’s lymphoma is an aggressive B-cell lymphoma characterized by typical morphological, immunophenotypic and molecular features. Gene expression profiling provided a molecular signature of Burkitt’s lymphoma, but also demonstrated that a subset of aggressive B-cell lymphomas not fulfilling the current World Health Organization criteria for the diagnosis of Burkitt’s lymphoma nonetheless show a molecular signature of Burkitt’s lymphoma (‘discrepant Burkitt’s lymphoma’). Given the different treatment of Burkitt’s lymphoma and diffuse large B-cell lymphomas we investigated molecular differences within gene expression-defined Burkitt’s lymphoma.Design and Methods We studied tumors from 51 Burkitt’s lymphoma patients, comprising 26 with classic Burkitt’s lymphoma, 17 with atypical Burkitt’s lymphoma and 8 with ‘discrepant Burkitt’s lymphoma’, by comparative genomic hybridization and gene expression profiling.Results Classic and atypical Burkitt’s lymphoma (excluding ‘discrepant Burkitt’s lymphoma’), in adult and pediatric cases do not differ in underlying genomic imbalances or gene expression suggesting that these subgroups are molecularly homogeneous. ‘Discrepant Burkitt’s lymphoma’, however, differ dramatically in the absolute number of alterations from classic/atypical Burkitt’s lymphoma and from diffuse large B-cell lymphoma. Moreover, this category includes lymphomas that carry both the t(14;18) and t(8;14) translocations and are clinically characterized by presentation in adult patients and an aggressive course.Conclusions Pediatric and adult Burkitt’s lymphoma are molecularly homogeneous, whereas ‘discrepant Burkitt’s lymphoma’ differ in underlying genetic and clinical features from typical/atypical Burkitt’s lymphoma. ‘Discrepant Burkitt’s lymphoma’ may therefore form a distinct genetic subgroup of aggressive B-cell lymphomas, which show poor response to multi-agent chemotherapy.

Published
2008
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13. Burkitt’s Lymphoma

Author

Mark Roschewski, Louis M. Staudt, and Wyndham H. Wilson

Subjects
Diagnosis, Differential, Humans, General Medicine, Burkitt Lymphoma
Published
2022

14. Targeting N-linked Glycosylation for the Therapy of Aggressive Lymphomas

Author

Sebastian Scheich, Jiji Chen, Jiamin Liu, Frank Schnutgen, Julius C. Enssle, Michele Ceribelli, Craig J. Thomas, Jaewoo Choi, Vivian Morris, Tony Hsiao, Hang Nguyen, Boya Wang, Arnold Bolomsky, James D. Phelan, Sean Corcoran, Henning Urlaub, Ryan M. Young, Bjorn Haupl, George W. Wright, Da Wei Huang, Yanlong Ji, Xin Yu, Weihong Xu, Yandan Yang, Hong Zhao, Jagan Muppidi, Kuan-Ting Pan, Thomas Oellerich, and Louis M. Staudt

Subjects
Oncology
Abstract

Diffuse large B-cell lymphoma (DLBCL) can be subdivided into activated B-cell like (ABC) and germinal center B-cell-like (GCB) DLCBL. Self-antigen engagement of B-cell receptors (BCRs) in ABC tumors induces their clustering, thereby initiating chronic active signaling and activation of NF-kB and PI3 kinase. Constitutive BCR signaling is essential in some GCB tumors but primarily activates PI3 kinase. We devised genome-wide CRISPR-Cas9 screens to identify regulators of IRF4, a direct transcriptional target of NF-kB and an indicator of proximal BCR signaling in ABC DLBCL. Unexpectedly, inactivation of N-linked protein glycosylation by the oligosaccharyltransferase-B (OST-B) complex reduced IRF4 expression. OST-B inhibition of BCR glycosylation reduced BCR clustering and internalization while promoting its association with CD22, which attenuated PI3 kinase and NF-kB activation. By directly interfering with proximal BCR signaling, OST-B inactivation killed models of ABC and GCB DLBCL, supporting the development of selective OST-B inhibitors for the treatment of these aggressive cancers.

Published
2023

15. Supplementary Table 7 from Overcoming Acquired Epigenetic Resistance to BTK Inhibitors

Author

Louis M. Staudt, Adrian Wiestner, Wyndham H. Wilson, Erika M. Gaglione, Clare Sun, Inhye E. Ahn, Michael C. Kelly, Zachary Rae, Thomas Oellerich, Björn Häupl, Craig J. Thomas, Carleen Klumpp-Thomas, Crystal McKnight, Lu Chen, Kelli M. Wilson, Xiaohu Zhang, Michele Ceribelli, Sandrine Roulland, Weihong Xu, Xin Yu, Hong Zhao, Yandan Yang, Daniel E. Webster, Ryan M. Young, Jaewoo Choi, Monica Kasbekar, George W. Wright, DaWei Huang, James Q. Wang, James D. Phelan, and Arthur L. Shaffer

Abstract

Supplemental Table 7. Targeting epigenetic resistance to BTK inhibitor treatment in ABC DLBCL, relates to Fig7

Published
2023

16. Supplementary Table 1 from Overcoming Acquired Epigenetic Resistance to BTK Inhibitors

Author

Louis M. Staudt, Adrian Wiestner, Wyndham H. Wilson, Erika M. Gaglione, Clare Sun, Inhye E. Ahn, Michael C. Kelly, Zachary Rae, Thomas Oellerich, Björn Häupl, Craig J. Thomas, Carleen Klumpp-Thomas, Crystal McKnight, Lu Chen, Kelli M. Wilson, Xiaohu Zhang, Michele Ceribelli, Sandrine Roulland, Weihong Xu, Xin Yu, Hong Zhao, Yandan Yang, Daniel E. Webster, Ryan M. Young, Jaewoo Choi, Monica Kasbekar, George W. Wright, DaWei Huang, James Q. Wang, James D. Phelan, and Arthur L. Shaffer

Abstract

Supplemental Table 1. Epigenetic Ibrutinib Resistance in ABC DLBCL lines, , relates to Fig. 1

Published
2023

17. Supplementary Figures and Legends from Overcoming Acquired Epigenetic Resistance to BTK Inhibitors

Author

Louis M. Staudt, Adrian Wiestner, Wyndham H. Wilson, Erika M. Gaglione, Clare Sun, Inhye E. Ahn, Michael C. Kelly, Zachary Rae, Thomas Oellerich, Björn Häupl, Craig J. Thomas, Carleen Klumpp-Thomas, Crystal McKnight, Lu Chen, Kelli M. Wilson, Xiaohu Zhang, Michele Ceribelli, Sandrine Roulland, Weihong Xu, Xin Yu, Hong Zhao, Yandan Yang, Daniel E. Webster, Ryan M. Young, Jaewoo Choi, Monica Kasbekar, George W. Wright, DaWei Huang, James Q. Wang, James D. Phelan, and Arthur L. Shaffer

Abstract

Supplemental Information- Figures & Legends (Supplemental Tables loaded separately)

Published
2023

18. Supplementary Table 6 from Overcoming Acquired Epigenetic Resistance to BTK Inhibitors

Author

Louis M. Staudt, Adrian Wiestner, Wyndham H. Wilson, Erika M. Gaglione, Clare Sun, Inhye E. Ahn, Michael C. Kelly, Zachary Rae, Thomas Oellerich, Björn Häupl, Craig J. Thomas, Carleen Klumpp-Thomas, Crystal McKnight, Lu Chen, Kelli M. Wilson, Xiaohu Zhang, Michele Ceribelli, Sandrine Roulland, Weihong Xu, Xin Yu, Hong Zhao, Yandan Yang, Daniel E. Webster, Ryan M. Young, Jaewoo Choi, Monica Kasbekar, George W. Wright, DaWei Huang, James Q. Wang, James D. Phelan, and Arthur L. Shaffer

Abstract

Supplemental Table 6. RAC2 protein interactions are a marker of epigenetic ibrutinib resistance

Published
2023

19. Supplementary Table 4 from Overcoming Acquired Epigenetic Resistance to BTK Inhibitors

Author

Louis M. Staudt, Adrian Wiestner, Wyndham H. Wilson, Erika M. Gaglione, Clare Sun, Inhye E. Ahn, Michael C. Kelly, Zachary Rae, Thomas Oellerich, Björn Häupl, Craig J. Thomas, Carleen Klumpp-Thomas, Crystal McKnight, Lu Chen, Kelli M. Wilson, Xiaohu Zhang, Michele Ceribelli, Sandrine Roulland, Weihong Xu, Xin Yu, Hong Zhao, Yandan Yang, Daniel E. Webster, Ryan M. Young, Jaewoo Choi, Monica Kasbekar, George W. Wright, DaWei Huang, James Q. Wang, James D. Phelan, and Arthur L. Shaffer

Abstract

Supplemental Table 4. Altered dependencies in ibrutinib resistant ABC DLBCL, relates to Fig. 4

Published
2023

20. Supplementary Methods from Overcoming Acquired Epigenetic Resistance to BTK Inhibitors

Author

Louis M. Staudt, Adrian Wiestner, Wyndham H. Wilson, Erika M. Gaglione, Clare Sun, Inhye E. Ahn, Michael C. Kelly, Zachary Rae, Thomas Oellerich, Björn Häupl, Craig J. Thomas, Carleen Klumpp-Thomas, Crystal McKnight, Lu Chen, Kelli M. Wilson, Xiaohu Zhang, Michele Ceribelli, Sandrine Roulland, Weihong Xu, Xin Yu, Hong Zhao, Yandan Yang, Daniel E. Webster, Ryan M. Young, Jaewoo Choi, Monica Kasbekar, George W. Wright, DaWei Huang, James Q. Wang, James D. Phelan, and Arthur L. Shaffer

Abstract

Supplementary Methods

Published
2023

21. Supplementary Table 2 from Overcoming Acquired Epigenetic Resistance to BTK Inhibitors

Author

Louis M. Staudt, Adrian Wiestner, Wyndham H. Wilson, Erika M. Gaglione, Clare Sun, Inhye E. Ahn, Michael C. Kelly, Zachary Rae, Thomas Oellerich, Björn Häupl, Craig J. Thomas, Carleen Klumpp-Thomas, Crystal McKnight, Lu Chen, Kelli M. Wilson, Xiaohu Zhang, Michele Ceribelli, Sandrine Roulland, Weihong Xu, Xin Yu, Hong Zhao, Yandan Yang, Daniel E. Webster, Ryan M. Young, Jaewoo Choi, Monica Kasbekar, George W. Wright, DaWei Huang, James Q. Wang, James D. Phelan, and Arthur L. Shaffer

Abstract

Supplemental Table2. Tracking the evolution of ibrutinib resistance phenotypes, relates to Fig. 2

Published
2023

22. Oligos and Primers - related to Methods from Overcoming Acquired Epigenetic Resistance to BTK Inhibitors

Author

Louis M. Staudt, Adrian Wiestner, Wyndham H. Wilson, Erika M. Gaglione, Clare Sun, Inhye E. Ahn, Michael C. Kelly, Zachary Rae, Thomas Oellerich, Björn Häupl, Craig J. Thomas, Carleen Klumpp-Thomas, Crystal McKnight, Lu Chen, Kelli M. Wilson, Xiaohu Zhang, Michele Ceribelli, Sandrine Roulland, Weihong Xu, Xin Yu, Hong Zhao, Yandan Yang, Daniel E. Webster, Ryan M. Young, Jaewoo Choi, Monica Kasbekar, George W. Wright, DaWei Huang, James Q. Wang, James D. Phelan, and Arthur L. Shaffer

Abstract

Oligo and Primer Tables

Published
2023

23. Supplementary Table 5 from Overcoming Acquired Epigenetic Resistance to BTK Inhibitors

Author

Louis M. Staudt, Adrian Wiestner, Wyndham H. Wilson, Erika M. Gaglione, Clare Sun, Inhye E. Ahn, Michael C. Kelly, Zachary Rae, Thomas Oellerich, Björn Häupl, Craig J. Thomas, Carleen Klumpp-Thomas, Crystal McKnight, Lu Chen, Kelli M. Wilson, Xiaohu Zhang, Michele Ceribelli, Sandrine Roulland, Weihong Xu, Xin Yu, Hong Zhao, Yandan Yang, Daniel E. Webster, Ryan M. Young, Jaewoo Choi, Monica Kasbekar, George W. Wright, DaWei Huang, James Q. Wang, James D. Phelan, and Arthur L. Shaffer

Abstract

Supplemental Table 5. RAC2 as a mediator of epigenetic ibrutinib resistance, , relates to Fig5

Published
2023

24. Data from Overcoming Acquired Epigenetic Resistance to BTK Inhibitors

Author

Louis M. Staudt, Adrian Wiestner, Wyndham H. Wilson, Erika M. Gaglione, Clare Sun, Inhye E. Ahn, Michael C. Kelly, Zachary Rae, Thomas Oellerich, Björn Häupl, Craig J. Thomas, Carleen Klumpp-Thomas, Crystal McKnight, Lu Chen, Kelli M. Wilson, Xiaohu Zhang, Michele Ceribelli, Sandrine Roulland, Weihong Xu, Xin Yu, Hong Zhao, Yandan Yang, Daniel E. Webster, Ryan M. Young, Jaewoo Choi, Monica Kasbekar, George W. Wright, DaWei Huang, James Q. Wang, James D. Phelan, and Arthur L. Shaffer

Abstract

The use of Bruton tyrosine kinase (BTK) inhibitors to block B-cell receptor (BCR)–dependent NF-κB activation in lymphoid malignancies has been a major clinical advance, yet acquired therapeutic resistance is a recurring problem. We modeled the development of resistance to the BTK inhibitor ibrutinib in the activated B-cell (ABC) subtype of diffuse large B-cell lymphoma, which relies on chronic active BCR signaling for survival. The primary mode of resistance was epigenetic, driven in part by the transcription factor TCF4. The resultant phenotypic shift altered BCR signaling such that the GTPase RAC2 substituted for BTK in the activation of phospholipase Cγ2, thereby sustaining NF-κB activity. The interaction of RAC2 with phospholipase Cγ2 was also increased in chronic lymphocytic leukemia cells from patients with persistent or progressive disease on BTK inhibitor treatment. We identified clinically available drugs that can treat epigenetic ibrutinib resistance, suggesting combination therapeutic strategies.Significance:In diffuse large B-cell lymphoma, we show that primary resistance to BTK inhibitors is due to epigenetic rather than genetic changes that circumvent the BTK blockade. We also observed this resistance mechanism in chronic lymphocytic leukemia, suggesting that epigenetic alterations may contribute more to BTK inhibitor resistance than currently thought.See related commentary by Pasqualucci, p. 555.This article is highlighted in the In This Issue feature, p. 549

Published
2023

25. Supplementary Table 3 from Overcoming Acquired Epigenetic Resistance to BTK Inhibitors

Author

Louis M. Staudt, Adrian Wiestner, Wyndham H. Wilson, Erika M. Gaglione, Clare Sun, Inhye E. Ahn, Michael C. Kelly, Zachary Rae, Thomas Oellerich, Björn Häupl, Craig J. Thomas, Carleen Klumpp-Thomas, Crystal McKnight, Lu Chen, Kelli M. Wilson, Xiaohu Zhang, Michele Ceribelli, Sandrine Roulland, Weihong Xu, Xin Yu, Hong Zhao, Yandan Yang, Daniel E. Webster, Ryan M. Young, Jaewoo Choi, Monica Kasbekar, George W. Wright, DaWei Huang, James Q. Wang, James D. Phelan, and Arthur L. Shaffer

Abstract

Supplemental Table 3. Epigenetic retuning of oncogenic signaling in ibrutinib resistance, relates to Fig. 3

Published
2023

26. Supplementary Table 8 from TYK2–STAT1–BCL2 Pathway Dependence in T-cell Acute Lymphoblastic Leukemia

Author

A. Thomas Look, Brian J. Druker, Louis M. Staudt, Andrew P. Weng, Catriona H.M. Jamieson, Nathanael S. Gray, Mathias Müller, Richard Moriggl, Ross L. Levine, Donna S. Neuberg, Michelle A. Kelliher, Jessica Tatarek, Yebin Ahn, Maria Kleppe, Yandan Yang, Wenjun Zhou, Angela G. Fleischman, Wenxue Ma, Arla Yost, Bill H. Chang, Jason Glover, Vu N. Ngo, Alejandro Gutierrez, Jeffrey W. Tyner, and Takaomi Sanda

Abstract

XLSX file - 24K, PCR Primer sequences.

Published
2023

27. Supplementary Figure 9 from TYK2–STAT1–BCL2 Pathway Dependence in T-cell Acute Lymphoblastic Leukemia

Author

A. Thomas Look, Brian J. Druker, Louis M. Staudt, Andrew P. Weng, Catriona H.M. Jamieson, Nathanael S. Gray, Mathias Müller, Richard Moriggl, Ross L. Levine, Donna S. Neuberg, Michelle A. Kelliher, Jessica Tatarek, Yebin Ahn, Maria Kleppe, Yandan Yang, Wenjun Zhou, Angela G. Fleischman, Wenxue Ma, Arla Yost, Bill H. Chang, Jason Glover, Vu N. Ngo, Alejandro Gutierrez, Jeffrey W. Tyner, and Takaomi Sanda

Abstract

PDF file - 113K, Bcl2 protein expression in wild-type and Tyk2 knockout mice.

Published
2023

28. Supplementary Figure 4 from TYK2–STAT1–BCL2 Pathway Dependence in T-cell Acute Lymphoblastic Leukemia

Author

A. Thomas Look, Brian J. Druker, Louis M. Staudt, Andrew P. Weng, Catriona H.M. Jamieson, Nathanael S. Gray, Mathias Müller, Richard Moriggl, Ross L. Levine, Donna S. Neuberg, Michelle A. Kelliher, Jessica Tatarek, Yebin Ahn, Maria Kleppe, Yandan Yang, Wenjun Zhou, Angela G. Fleischman, Wenxue Ma, Arla Yost, Bill H. Chang, Jason Glover, Vu N. Ngo, Alejandro Gutierrez, Jeffrey W. Tyner, and Takaomi Sanda

Abstract

PDF file - 74K, Knockdown efficiency and BCL2 expression in JURKAT cells.

Published
2023

29. Supplementary Table 2 from TYK2–STAT1–BCL2 Pathway Dependence in T-cell Acute Lymphoblastic Leukemia

Author

A. Thomas Look, Brian J. Druker, Louis M. Staudt, Andrew P. Weng, Catriona H.M. Jamieson, Nathanael S. Gray, Mathias Müller, Richard Moriggl, Ross L. Levine, Donna S. Neuberg, Michelle A. Kelliher, Jessica Tatarek, Yebin Ahn, Maria Kleppe, Yandan Yang, Wenjun Zhou, Angela G. Fleischman, Wenxue Ma, Arla Yost, Bill H. Chang, Jason Glover, Vu N. Ngo, Alejandro Gutierrez, Jeffrey W. Tyner, and Takaomi Sanda

Abstract

XLSX file - 525K, Summary of inducible shRNA screen on three T-ALL cell lines.

Published
2023

30. Data from Essential Role of the Linear Ubiquitin Chain Assembly Complex in Lymphoma Revealed by Rare Germline Polymorphisms

Author

Louis M. Staudt, Federico Bernal, Kazuhiro Iwai, Michael J. Kruhlak, Adrian Wiestner, Wing C. Chan, Dennis D. Weisenburger, James R. Cook, Raymond R. Tubbs, Rita M. Braziel, Erlend B. Smeland, Jan Delabie, Elaine S. Jaffe, Elias Campo, Lisa M. Rimsza, Joseph M. Connors, Randy D. Gascoyne, German Ott, Andreas Rosenwald, Weihong Xu, Yandan Yang, Hong Zhao, George W. Wright, Michele Ceribelli, Wenming Xiao, Amanda Whiting, Joseph Mitala, Roland Schmitz, and Yibin Yang

Abstract

Constitutive activation of NF-κB is a hallmark of the activated B cell–like (ABC) subtype of diffuse large B-cell lymphoma (DLBCL), owing to upstream signals from the B-cell receptor (BCR) and MYD88 pathways. The linear polyubiquitin chain assembly complex (LUBAC) attaches linear polyubiquitin chains to IκB kinase-γ, a necessary event in some pathways that engage NF-κB. Two germline polymorphisms affecting the LUBAC subunit RNF31 are rare among healthy individuals (∼1%) but enriched in ABC DLBCL (7.8%). These polymorphisms alter RNF31 α-helices that mediate binding to the LUBAC subunit RBCK1, thereby increasing RNF31–RBCK1 association, LUBAC enzymatic activity, and NF-κB engagement. In the BCR pathway, LUBAC associates with the CARD11–MALT1–BCL10 adapter complex and is required for ABC DLBCL viability. A stapled RNF31 α-helical peptide based on the ABC DLBCL–associated Q622L polymorphism inhibited RNF31–RBCK1 binding, decreased NF-κB activation, and killed ABC DLBCL cells, credentialing this protein–protein interface as a therapeutic target.Significance: We provide genetic, biochemical, and functional evidence that the LUBAC ubiquitin ligase is a therapeutic target in ABC DLBCL, the DLBCL subtype that is most refractory to current therapy. More generally, our findings highlight the role of rare germline-encoded protein variants in cancer pathogenesis. Cancer Discov; 4(4); 480–93. ©2014 AACR.See related commentary by Grumati and Dikic, p. 394This article is highlighted in the In This Issue feature, p. 377

Published
2023

31. Supplementary Figure Legend and Methods from TYK2–STAT1–BCL2 Pathway Dependence in T-cell Acute Lymphoblastic Leukemia

Author

A. Thomas Look, Brian J. Druker, Louis M. Staudt, Andrew P. Weng, Catriona H.M. Jamieson, Nathanael S. Gray, Mathias Müller, Richard Moriggl, Ross L. Levine, Donna S. Neuberg, Michelle A. Kelliher, Jessica Tatarek, Yebin Ahn, Maria Kleppe, Yandan Yang, Wenjun Zhou, Angela G. Fleischman, Wenxue Ma, Arla Yost, Bill H. Chang, Jason Glover, Vu N. Ngo, Alejandro Gutierrez, Jeffrey W. Tyner, and Takaomi Sanda

Abstract

PDF file - 138K

Published
2023

32. Supplementary Figure 6 from TYK2–STAT1–BCL2 Pathway Dependence in T-cell Acute Lymphoblastic Leukemia

Author

A. Thomas Look, Brian J. Druker, Louis M. Staudt, Andrew P. Weng, Catriona H.M. Jamieson, Nathanael S. Gray, Mathias Müller, Richard Moriggl, Ross L. Levine, Donna S. Neuberg, Michelle A. Kelliher, Jessica Tatarek, Yebin Ahn, Maria Kleppe, Yandan Yang, Wenjun Zhou, Angela G. Fleischman, Wenxue Ma, Arla Yost, Bill H. Chang, Jason Glover, Vu N. Ngo, Alejandro Gutierrez, Jeffrey W. Tyner, and Takaomi Sanda

Abstract

PDF file - 32K, Expressions of IL-10 and IL-10 receptors, and effect of an anti-IL10 neutralizing antibody on growth of T-ALL cell lines.

Published
2023

33. Supplementary Table 3 from TYK2–STAT1–BCL2 Pathway Dependence in T-cell Acute Lymphoblastic Leukemia

Author

A. Thomas Look, Brian J. Druker, Louis M. Staudt, Andrew P. Weng, Catriona H.M. Jamieson, Nathanael S. Gray, Mathias Müller, Richard Moriggl, Ross L. Levine, Donna S. Neuberg, Michelle A. Kelliher, Jessica Tatarek, Yebin Ahn, Maria Kleppe, Yandan Yang, Wenjun Zhou, Angela G. Fleischman, Wenxue Ma, Arla Yost, Bill H. Chang, Jason Glover, Vu N. Ngo, Alejandro Gutierrez, Jeffrey W. Tyner, and Takaomi Sanda

Abstract

XLSX file - 30K, Targeting sequences for shRNAs.

Published
2023

34. Supplementary Table 2 from Essential Role of the Linear Ubiquitin Chain Assembly Complex in Lymphoma Revealed by Rare Germline Polymorphisms

Author

Louis M. Staudt, Federico Bernal, Kazuhiro Iwai, Michael J. Kruhlak, Adrian Wiestner, Wing C. Chan, Dennis D. Weisenburger, James R. Cook, Raymond R. Tubbs, Rita M. Braziel, Erlend B. Smeland, Jan Delabie, Elaine S. Jaffe, Elias Campo, Lisa M. Rimsza, Joseph M. Connors, Randy D. Gascoyne, German Ott, Andreas Rosenwald, Weihong Xu, Yandan Yang, Hong Zhao, George W. Wright, Michele Ceribelli, Wenming Xiao, Amanda Whiting, Joseph Mitala, Roland Schmitz, and Yibin Yang

Abstract

PDF file 42K, Co-occurrence of RNF31 SNPs with other genetic lesions in ABC DLBCL cases

Published
2023

35. Supplementary Figure 2 from TYK2–STAT1–BCL2 Pathway Dependence in T-cell Acute Lymphoblastic Leukemia

Author

A. Thomas Look, Brian J. Druker, Louis M. Staudt, Andrew P. Weng, Catriona H.M. Jamieson, Nathanael S. Gray, Mathias Müller, Richard Moriggl, Ross L. Levine, Donna S. Neuberg, Michelle A. Kelliher, Jessica Tatarek, Yebin Ahn, Maria Kleppe, Yandan Yang, Wenjun Zhou, Angela G. Fleischman, Wenxue Ma, Arla Yost, Bill H. Chang, Jason Glover, Vu N. Ngo, Alejandro Gutierrez, Jeffrey W. Tyner, and Takaomi Sanda

Abstract

PDF file - 68K, Cell cycle distribution after TYK2 knockdown in T-ALL cells.

Published
2023

36. Supplementary Table 5 from TYK2–STAT1–BCL2 Pathway Dependence in T-cell Acute Lymphoblastic Leukemia

Author

A. Thomas Look, Brian J. Druker, Louis M. Staudt, Andrew P. Weng, Catriona H.M. Jamieson, Nathanael S. Gray, Mathias Müller, Richard Moriggl, Ross L. Levine, Donna S. Neuberg, Michelle A. Kelliher, Jessica Tatarek, Yebin Ahn, Maria Kleppe, Yandan Yang, Wenjun Zhou, Angela G. Fleischman, Wenxue Ma, Arla Yost, Bill H. Chang, Jason Glover, Vu N. Ngo, Alejandro Gutierrez, Jeffrey W. Tyner, and Takaomi Sanda

Abstract

XLSX file - 14291K, TYK2 genotype in 17 T-ALL cell lines.

Published
2023

37. Supplementary Table 4 from TYK2–STAT1–BCL2 Pathway Dependence in T-cell Acute Lymphoblastic Leukemia

Author

A. Thomas Look, Brian J. Druker, Louis M. Staudt, Andrew P. Weng, Catriona H.M. Jamieson, Nathanael S. Gray, Mathias Müller, Richard Moriggl, Ross L. Levine, Donna S. Neuberg, Michelle A. Kelliher, Jessica Tatarek, Yebin Ahn, Maria Kleppe, Yandan Yang, Wenjun Zhou, Angela G. Fleischman, Wenxue Ma, Arla Yost, Bill H. Chang, Jason Glover, Vu N. Ngo, Alejandro Gutierrez, Jeffrey W. Tyner, and Takaomi Sanda

Abstract

XLSX file - 35K, Sensitivities to TYK2 knockdown and JAK Inhibitor I treatment, and phosphorylation status of downstream signaling molecules in T-ALL cell lines and Ba/F3 clones.

Published
2023

38. Supplementary Figure 1 from TYK2–STAT1–BCL2 Pathway Dependence in T-cell Acute Lymphoblastic Leukemia

Author

A. Thomas Look, Brian J. Druker, Louis M. Staudt, Andrew P. Weng, Catriona H.M. Jamieson, Nathanael S. Gray, Mathias Müller, Richard Moriggl, Ross L. Levine, Donna S. Neuberg, Michelle A. Kelliher, Jessica Tatarek, Yebin Ahn, Maria Kleppe, Yandan Yang, Wenjun Zhou, Angela G. Fleischman, Wenxue Ma, Arla Yost, Bill H. Chang, Jason Glover, Vu N. Ngo, Alejandro Gutierrez, Jeffrey W. Tyner, and Takaomi Sanda

Abstract

PDF file - 61K, Validation of shRNA constructs.

Published
2023

39. Supplementary Table 1 from TYK2–STAT1–BCL2 Pathway Dependence in T-cell Acute Lymphoblastic Leukemia

Author

A. Thomas Look, Brian J. Druker, Louis M. Staudt, Andrew P. Weng, Catriona H.M. Jamieson, Nathanael S. Gray, Mathias Müller, Richard Moriggl, Ross L. Levine, Donna S. Neuberg, Michelle A. Kelliher, Jessica Tatarek, Yebin Ahn, Maria Kleppe, Yandan Yang, Wenjun Zhou, Angela G. Fleischman, Wenxue Ma, Arla Yost, Bill H. Chang, Jason Glover, Vu N. Ngo, Alejandro Gutierrez, Jeffrey W. Tyner, and Takaomi Sanda

Abstract

XLSX file - 36K, Cell viability profile by RAPID assay.

Published
2023

40. Supplementary Table 1 from Essential Role of the Linear Ubiquitin Chain Assembly Complex in Lymphoma Revealed by Rare Germline Polymorphisms

Author

Louis M. Staudt, Federico Bernal, Kazuhiro Iwai, Michael J. Kruhlak, Adrian Wiestner, Wing C. Chan, Dennis D. Weisenburger, James R. Cook, Raymond R. Tubbs, Rita M. Braziel, Erlend B. Smeland, Jan Delabie, Elaine S. Jaffe, Elias Campo, Lisa M. Rimsza, Joseph M. Connors, Randy D. Gascoyne, German Ott, Andreas Rosenwald, Weihong Xu, Yandan Yang, Hong Zhao, George W. Wright, Michele Ceribelli, Wenming Xiao, Amanda Whiting, Joseph Mitala, Roland Schmitz, and Yibin Yang

Abstract

Supplementary Table 1 PDF file 53K, Enrichment of two rare SNPs among ABC DLBCL tumors

Published
2023

41. Supplementary Fig. 3 from Essential Role of the Linear Ubiquitin Chain Assembly Complex in Lymphoma Revealed by Rare Germline Polymorphisms

Author

Louis M. Staudt, Federico Bernal, Kazuhiro Iwai, Michael J. Kruhlak, Adrian Wiestner, Wing C. Chan, Dennis D. Weisenburger, James R. Cook, Raymond R. Tubbs, Rita M. Braziel, Erlend B. Smeland, Jan Delabie, Elaine S. Jaffe, Elias Campo, Lisa M. Rimsza, Joseph M. Connors, Randy D. Gascoyne, German Ott, Andreas Rosenwald, Weihong Xu, Yandan Yang, Hong Zhao, George W. Wright, Michele Ceribelli, Wenming Xiao, Amanda Whiting, Joseph Mitala, Roland Schmitz, and Yibin Yang

Abstract

PDF file 124K, Involvement of LUBAC in CBM complex mediated NF-kappaB activation, related to main figure 3

Published
2023

42. Supplementary Figure 5 from TYK2–STAT1–BCL2 Pathway Dependence in T-cell Acute Lymphoblastic Leukemia

Author

A. Thomas Look, Brian J. Druker, Louis M. Staudt, Andrew P. Weng, Catriona H.M. Jamieson, Nathanael S. Gray, Mathias Müller, Richard Moriggl, Ross L. Levine, Donna S. Neuberg, Michelle A. Kelliher, Jessica Tatarek, Yebin Ahn, Maria Kleppe, Yandan Yang, Wenjun Zhou, Angela G. Fleischman, Wenxue Ma, Arla Yost, Bill H. Chang, Jason Glover, Vu N. Ngo, Alejandro Gutierrez, Jeffrey W. Tyner, and Takaomi Sanda

Abstract

PDF file - 273K, Confirmation of CD3 expression on OP9 DL1 outgrowth cells.

Published
2023

43. Supplementary Figure 7 from TYK2–STAT1–BCL2 Pathway Dependence in T-cell Acute Lymphoblastic Leukemia

Author

A. Thomas Look, Brian J. Druker, Louis M. Staudt, Andrew P. Weng, Catriona H.M. Jamieson, Nathanael S. Gray, Mathias Müller, Richard Moriggl, Ross L. Levine, Donna S. Neuberg, Michelle A. Kelliher, Jessica Tatarek, Yebin Ahn, Maria Kleppe, Yandan Yang, Wenjun Zhou, Angela G. Fleischman, Wenxue Ma, Arla Yost, Bill H. Chang, Jason Glover, Vu N. Ngo, Alejandro Gutierrez, Jeffrey W. Tyner, and Takaomi Sanda

Abstract

PDF file - 24K, Effect of JAK kinase inhibitors with varying TYK2-specificity on growth and viability of T-ALL cells.

Published
2023

44. Supplementary Fig. 4 from Essential Role of the Linear Ubiquitin Chain Assembly Complex in Lymphoma Revealed by Rare Germline Polymorphisms

Author

Louis M. Staudt, Federico Bernal, Kazuhiro Iwai, Michael J. Kruhlak, Adrian Wiestner, Wing C. Chan, Dennis D. Weisenburger, James R. Cook, Raymond R. Tubbs, Rita M. Braziel, Erlend B. Smeland, Jan Delabie, Elaine S. Jaffe, Elias Campo, Lisa M. Rimsza, Joseph M. Connors, Randy D. Gascoyne, German Ott, Andreas Rosenwald, Weihong Xu, Yandan Yang, Hong Zhao, George W. Wright, Michele Ceribelli, Wenming Xiao, Amanda Whiting, Joseph Mitala, Roland Schmitz, and Yibin Yang

Abstract

PDF file 149K, RNF31 peptides internalized equivalently in ABC DLBCL cells

Published
2023

45. Supplementary Table 6 from TYK2–STAT1–BCL2 Pathway Dependence in T-cell Acute Lymphoblastic Leukemia

Author

A. Thomas Look, Brian J. Druker, Louis M. Staudt, Andrew P. Weng, Catriona H.M. Jamieson, Nathanael S. Gray, Mathias Müller, Richard Moriggl, Ross L. Levine, Donna S. Neuberg, Michelle A. Kelliher, Jessica Tatarek, Yebin Ahn, Maria Kleppe, Yandan Yang, Wenjun Zhou, Angela G. Fleischman, Wenxue Ma, Arla Yost, Bill H. Chang, Jason Glover, Vu N. Ngo, Alejandro Gutierrez, Jeffrey W. Tyner, and Takaomi Sanda

Abstract

XLSX file - 23K, Clinical, biologic and molecular characteristics of the T-ALL patient samples analyzed. See separate file.

Published
2023

46. Supplementary Fig. 2 from Essential Role of the Linear Ubiquitin Chain Assembly Complex in Lymphoma Revealed by Rare Germline Polymorphisms

Author

Louis M. Staudt, Federico Bernal, Kazuhiro Iwai, Michael J. Kruhlak, Adrian Wiestner, Wing C. Chan, Dennis D. Weisenburger, James R. Cook, Raymond R. Tubbs, Rita M. Braziel, Erlend B. Smeland, Jan Delabie, Elaine S. Jaffe, Elias Campo, Lisa M. Rimsza, Joseph M. Connors, Randy D. Gascoyne, German Ott, Andreas Rosenwald, Weihong Xu, Yandan Yang, Hong Zhao, George W. Wright, Michele Ceribelli, Wenming Xiao, Amanda Whiting, Joseph Mitala, Roland Schmitz, and Yibin Yang

Abstract

PDF file 73K, Constitutive linear ubiquitination of NEMO in ABC comparing to GCB DLBCL cells

Published
2023

47. Supplementary Figure 8 from TYK2–STAT1–BCL2 Pathway Dependence in T-cell Acute Lymphoblastic Leukemia

Author

A. Thomas Look, Brian J. Druker, Louis M. Staudt, Andrew P. Weng, Catriona H.M. Jamieson, Nathanael S. Gray, Mathias Müller, Richard Moriggl, Ross L. Levine, Donna S. Neuberg, Michelle A. Kelliher, Jessica Tatarek, Yebin Ahn, Maria Kleppe, Yandan Yang, Wenjun Zhou, Angela G. Fleischman, Wenxue Ma, Arla Yost, Bill H. Chang, Jason Glover, Vu N. Ngo, Alejandro Gutierrez, Jeffrey W. Tyner, and Takaomi Sanda

Abstract

PDF file - 105K, Signaling and cell cycle distribution after JAK inhibitor I treatment.

Published
2023

48. Supplementary Fig. 5 from Essential Role of the Linear Ubiquitin Chain Assembly Complex in Lymphoma Revealed by Rare Germline Polymorphisms

Author

Louis M. Staudt, Federico Bernal, Kazuhiro Iwai, Michael J. Kruhlak, Adrian Wiestner, Wing C. Chan, Dennis D. Weisenburger, James R. Cook, Raymond R. Tubbs, Rita M. Braziel, Erlend B. Smeland, Jan Delabie, Elaine S. Jaffe, Elias Campo, Lisa M. Rimsza, Joseph M. Connors, Randy D. Gascoyne, German Ott, Andreas Rosenwald, Weihong Xu, Yandan Yang, Hong Zhao, George W. Wright, Michele Ceribelli, Wenming Xiao, Amanda Whiting, Joseph Mitala, Roland Schmitz, and Yibin Yang

Abstract

PDF file 132K, Specificity of RNF31 stapled peptides in ABC DLBCL

Published
2023

49. Supplementary Fig. 1 from Essential Role of the Linear Ubiquitin Chain Assembly Complex in Lymphoma Revealed by Rare Germline Polymorphisms

Author

Louis M. Staudt, Federico Bernal, Kazuhiro Iwai, Michael J. Kruhlak, Adrian Wiestner, Wing C. Chan, Dennis D. Weisenburger, James R. Cook, Raymond R. Tubbs, Rita M. Braziel, Erlend B. Smeland, Jan Delabie, Elaine S. Jaffe, Elias Campo, Lisa M. Rimsza, Joseph M. Connors, Randy D. Gascoyne, German Ott, Andreas Rosenwald, Weihong Xu, Yandan Yang, Hong Zhao, George W. Wright, Michele Ceribelli, Wenming Xiao, Amanda Whiting, Joseph Mitala, Roland Schmitz, and Yibin Yang

Abstract

PDF file 283K, RNF31 DNA sequence electropherograms for the region corresponding to the single nucleotide polymorphisms (SNPs)

Published
2023

50. Supplementary Figure 1 from A Phase 2/3 Multicenter, Randomized, Open-Label Study to Compare the Efficacy and Safety of Lenalidomide Versus Investigator's Choice in Patients with Relapsed or Refractory Diffuse Large B-Cell Lymphoma

Author

Ian D. Lewis, Dale Song, Pierre Fustier, Patrick Hagner, Anjan Thakurta, Jacqueline Russo, Chih-Jian Lih, P. Mickey Williams, Yandan Yang, Louis M. Staudt, George W. Wright, Pier Luigi Zinzani, Thomas E. Witzig, Gilles Salles, Francisco J. Hernandez-Ilizaliturri, David A. Eberhard, Pierre Brousset, Graham W. Slack, Randy D. Gascoyne, Nina Wagner-Johnston, Kim M. Linton, Simon Rule, Andrew Davies, Marek Trněný, and Myron S. Czuczman

Abstract

DLC-001 Study Design (CONSORT diagram)

Published
2023

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