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189 results on '"ten Hacken, Elisa"'

1. T-bet suppresses proliferation of malignant B cells in chronic lymphocytic leukemia

Author

Roessner, Philipp M., Seufert, Isabelle, Chapaprieta, Vicente, Jayabalan, Ruparoshni, Briesch, Hannah, Massoni-Badosa, Ramon, Boskovic, Pavle, Benckendorff, Julian, Roider, Tobias, Arseni, Lavinia, Coelho, Mariana, Chakraborty, Supriya, Vaca, Alicia M., Sivina, Mariela, Muckenhuber, Markus, Rodriguez-Rodriguez, Sonia, Bonato, Alice, Herbst, Sophie A., Zapatka, Marc, Sun, Clare, Kretzmer, Helene, Naake, Thomas, Bruch, Peter-Martin, Czernilofsky, Felix, ten Hacken, Elisa, Schneider, Martin, Helm, Dominic, Yosifov, Deyan Y., Kauer, Joseph, Danilov, Alexey V., Bewarder, Moritz, Heyne, Kristina, Schneider, Christof, Stilgenbauer, Stephan, Wiestner, Adrian, Mallm, Jan-Philipp, Burger, Jan A., Efremov, Dimitar G., Lichter, Peter, Dietrich, Sascha, Martin-Subero, José I., Rippe, Karsten, and Seiffert, Martina

Published
2024
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2. Activation of Notch and Myc signaling via B cell-restricted depletion of Dnmt3a generates a consistent murine model of chronic lymphocytic leukemia

Author

Biran, Anat, Yin, Shanye, Kretzmer, Helene, Ten Hacken, Elisa, Parvin, Salma, Lucas, Fabienne, Uduman, Mohamed, Gutierrez, Catherine, Dangle, Nathan, Billington, Leah, Regis, Fara Faye, Rassenti, Laura Z, Mohammad, Arman, Hoffmann, Gabriela Brunsting, Stevenson, Kristen, Zheng, Mei, Witten, Elizabeth, Fernandes, Stacey M, Tausch, Eugen, Sun, Clare, Stilgenbauer, Stephan, Brown, Jennifer R, Kipps, Thomas J, Aster, John C, Gnirke, Andreas, Neuberg, Donna S, Letai, Anthony, Wang, Lili, Carrasco, Ruben D, Meissner, Alexander, and Wu, Catherine J

Subjects
Genetics, Lymphoma, Cancer, Rare Diseases, Hematology, Aetiology, 2.1 Biological and endogenous factors, Animals, Anti-Bacterial Agents, Apoptosis, Biomarkers, Tumor, Cell Proliferation, DNA Methyltransferase 3A, Daptomycin, Disease Models, Animal, Drug Resistance, Neoplasm, Female, Gene Expression Regulation, Neoplastic, Humans, Leukemia, Lymphocytic, Chronic, B-Cell, Male, Mice, Mice, Inbred NOD, Mice, Knockout, Mice, SCID, Prognosis, Proto-Oncogene Proteins c-myc, RNA-Seq, Receptors, Notch, Survival Rate, Tumor Cells, Cultured, Xenograft Model Antitumor Assays, Oncology and Carcinogenesis, Oncology & Carcinogenesis
Abstract

Chronic lymphocytic leukemia (CLL) is characterized by disordered DNA methylation, suggesting these epigenetic changes might play a critical role in disease onset and progression. The methyltransferase DNMT3A is a key regulator of DNA methylation. Although DNMT3A somatic mutations in CLL are rare, we found that low DNMT3A expression is associated with more aggressive disease. A conditional knockout mouse model showed that homozygous depletion of Dnmt3a from B cells results in the development of CLL with 100% penetrance at a median age of onset of 5.3 months, and heterozygous Dnmt3a depletion yields a disease penetrance of 89% with a median onset at 18.5 months, confirming its role as a haploinsufficient tumor suppressor. B1a cells were confirmed as the cell of origin of disease in this model, and Dnmt3a depletion resulted in focal hypomethylation and activation of Notch and Myc signaling. Amplification of chromosome 15 containing the Myc gene was detected in all CLL mice tested, and infiltration of high-Myc-expressing CLL cells in the spleen was observed. Notably, hyperactivation of Notch and Myc signaling was exclusively observed in the Dnmt3a CLL mice, but not in three other CLL mouse models tested (Sf3b1-Atm, Ikzf3, and MDR), and Dnmt3a-depleted CLL were sensitive to pharmacologic inhibition of Notch signaling in vitro and in vivo. Consistent with these findings, human CLL samples with lower DNMT3A expression were more sensitive to Notch inhibition than those with higher DNMT3A expression. Altogether, these results suggest that Dnmt3a depletion induces CLL that is highly dependent on activation of Notch and Myc signaling. SIGNIFICANCE: Loss of DNMT3A expression is a driving event in CLL and is associated with aggressive disease, activation of Notch and Myc signaling, and enhanced sensitivity to Notch inhibition.

Published
2021

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

Author

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

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

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

Published
2021

4. A hotspot mutation in transcription factor IKZF3 drives B cell neoplasia via transcriptional dysregulation

Author

Lazarian, Gregory, Yin, Shanye, Ten Hacken, Elisa, Sewastianik, Tomasz, Uduman, Mohamed, Font-Tello, Alba, Gohil, Satyen H, Li, Shuqiang, Kim, Ekaterina, Joyal, Heather, Billington, Leah, Witten, Elizabeth, Zheng, Mei, Huang, Teddy, Severgnini, Mariano, Lefebvre, Valerie, Rassenti, Laura Z, Gutierrez, Catherine, Georgopoulos, Katia, Ott, Christopher J, Wang, Lili, Kipps, Thomas J, Burger, Jan A, Livak, Kenneth J, Neuberg, Donna S, Baran-Marszak, Fanny, Cymbalista, Florence, Carrasco, Ruben D, and Wu, Catherine J

Subjects
Biochemistry and Cell Biology, Biological Sciences, Hematology, Lymphoma, Rare Diseases, Genetics, Cancer, 2.1 Biological and endogenous factors, Aetiology, Animals, B-Lymphocytes, Humans, Ikaros Transcription Factor, Leukemia, Lymphocytic, Chronic, B-Cell, Mice, Mice, Inbred C57BL, Mice, Inbred NOD, Mutation, NF-kappa B, Receptors, Antigen, B-Cell, Signal Transduction, Transcription, Genetic, BCR signaling, CLL, IKZF3, NF-κB, murine mode, Neurosciences, Oncology and Carcinogenesis, Oncology & Carcinogenesis, Biochemistry and cell biology, Oncology and carcinogenesis
Abstract

Hotspot mutation of IKZF3 (IKZF3-L162R) has been identified as a putative driver of chronic lymphocytic leukemia (CLL), but its function remains unknown. Here, we demonstrate its driving role in CLL through a B cell-restricted conditional knockin mouse model. Mutant Ikzf3 alters DNA binding specificity and target selection, leading to hyperactivation of B cell receptor (BCR) signaling, overexpression of nuclear factor κB (NF-κB) target genes, and development of CLL-like disease in elderly mice with a penetrance of ~40%. Human CLL carrying either IKZF3 mutation or high IKZF3 expression was associated with overexpression of BCR/NF-κB pathway members and reduced sensitivity to BCR signaling inhibition by ibrutinib. Our results thus highlight IKZF3 oncogenic function in CLL via transcriptional dysregulation and demonstrate that this pro-survival function can be achieved by either somatic mutation or overexpression of this CLL driver. This emphasizes the need for combinatorial approaches to overcome IKZF3-mediated BCR inhibitor resistance.

Published
2021

6. Functional Differences between IgM and IgD Signaling in Chronic Lymphocytic Leukemia

Author

Ten Hacken, Elisa, Sivina, Mariela, Kim, Ekaterina, O'Brien, Susan, Wierda, William G, Ferrajoli, Alessandra, Estrov, Zeev, Keating, Michael J, Oellerich, Thomas, Scielzo, Cristina, Ghia, Paolo, Caligaris-Cappio, Federico, and Burger, Jan A

Subjects
Biochemistry and Cell Biology, Medical Physiology, Biomedical and Clinical Sciences, Biological Sciences, Lymphoma, Clinical Research, Cancer, Rare Diseases, Hematology, Adaptor Proteins, Signal Transducing, B-Lymphocytes, Blood Proteins, Cell Survival, Cells, Cultured, Cellular Microenvironment, Chemokine CCL3, Chemokine CCL4, Gene Expression Regulation, Humans, Immunoglobulin D, Immunoglobulin M, Intracellular Signaling Peptides and Proteins, Leukemia, Lymphocytic, Chronic, B-Cell, Lymph Nodes, Protein-Tyrosine Kinases, Proto-Oncogene Proteins c-bcl-6, Receptors, Antigen, B-Cell, Signal Transduction, Immunology, Biochemistry and cell biology
Abstract

BCR signaling is a central pathogenetic pathway in chronic lymphocytic leukemia (CLL). Most CLL cells express BCRs of IgM and IgD isotypes, but the contribution of these isotypes to functional responses remains incompletely defined. We therefore investigated differences between IgM and IgD signaling in freshly isolated peripheral blood CLL cells and in CLL cells cultured with nurselike cells, a model that mimics the lymph node microenvironment. IgM signaling induced prolonged activation of ERK kinases and promoted CLL cell survival, CCL3 and CCL4 chemokine secretion, and downregulation of BCL6, the transcriptional repressor of CCL3 In contrast, IgD signaling induced activation of the cytoskeletal protein HS1, along with F-actin polymerization, which resulted in rapid receptor internalization and failure to support downstream responses, including CLL cell survival and chemokine secretion. IgM and IgD receptor downmodulation, HS1 and ERK activation, chemokine secretion, and BCL6 downregulation were also observed when CLL cells were cocultured with nurselike cells. The Bruton's tyrosine kinase inhibitor ibrutinib effectively inhibited both IgM and IgD isotype signaling. In conclusion, through a variety of functional readouts, we demonstrate very distinct outcomes of IgM and IgD isotype activation in CLL cells, providing novel insight into the regulation of BCR signaling in CLL.

Published
2016

8. CRISPR/Cas9-generated models uncover therapeutic vulnerabilities of del(11q) CLL cells to dual BCR and PARP inhibition

Author

Quijada-Álamo, Miguel, Hernández-Sánchez, María, Alonso-Pérez, Verónica, Rodríguez-Vicente, Ana E., García-Tuñón, Ignacio, Martín-Izquierdo, Marta, Hernández-Sánchez, Jesús María, Herrero, Ana B., Bastida, José María, San Segundo, Laura, Gruber, Michaela, García, Juan Luis, Yin, Shanye, ten Hacken, Elisa, Benito, Rocío, Ordóñez, José Luis, Wu, Catherine J., and Hernández-Rivas, Jesús María

Published
2020
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12. Data from In Vivo Modeling of CLL Transformation to Richter Syndrome Reveals Convergent Evolutionary Paths and Therapeutic Vulnerabilities

Author

ten Hacken, Elisa, primary, Sewastianik, Tomasz, primary, Yin, Shanye, primary, Hoffmann, Gabriela Brunsting, primary, Gruber, Michaela, primary, Clement, Kendell, primary, Penter, Livius, primary, Redd, Robert A., primary, Ruthen, Neil, primary, Hergalant, Sébastien, primary, Sholokhova, Alanna, primary, Fell, Geoffrey, primary, Parry, Erin M., primary, Broséus, Julien, primary, Guieze, Romain, primary, Lucas, Fabienne, primary, Hernández-Sánchez, María, primary, Baranowski, Kaitlyn, primary, Southard, Jackson, primary, Joyal, Heather, primary, Billington, Leah, primary, Regis, Fara Faye D., primary, Witten, Elizabeth, primary, Uduman, Mohamed, primary, Knisbacher, Binyamin A., primary, Li, Shuqiang, primary, Lyu, Haoxiang, primary, Vaisitti, Tiziana, primary, Deaglio, Silvia, primary, Inghirami, Giorgio, primary, Feugier, Pierre, primary, Stilgenbauer, Stephan, primary, Tausch, Eugen, primary, Davids, Matthew S., primary, Getz, Gad, primary, Livak, Kenneth J., primary, Bozic, Ivana, primary, Neuberg, Donna S., primary, Carrasco, Ruben D., primary, and Wu, Catherine J., primary

Published
2023
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13. Supplementary Tables and Figures from SLAMF6 as a Regulator of Exhausted CD8+ T Cells in Cancer

Author

Yigit, Burcu, primary, Wang, Ninghai, primary, ten Hacken, Elisa, primary, Chen, Shih-Shih, primary, Bhan, Atul K., primary, Suarez-Fueyo, Abel, primary, Katsuyama, Eri, primary, Tsokos, George C., primary, Chiorazzi, Nicholas, primary, Wu, Catherine J., primary, Burger, Jan A., primary, Herzog, Roland W., primary, Engel, Pablo, primary, and Terhorst, Cox, primary

Published
2023
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14. Data from SLAMF6 as a Regulator of Exhausted CD8+ T Cells in Cancer

Author

Yigit, Burcu, primary, Wang, Ninghai, primary, ten Hacken, Elisa, primary, Chen, Shih-Shih, primary, Bhan, Atul K., primary, Suarez-Fueyo, Abel, primary, Katsuyama, Eri, primary, Tsokos, George C., primary, Chiorazzi, Nicholas, primary, Wu, Catherine J., primary, Burger, Jan A., primary, Herzog, Roland W., primary, Engel, Pablo, primary, and Terhorst, Cox, primary

Published
2023
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15. Supplementary Legends from SLAMF6 as a Regulator of Exhausted CD8+ T Cells in Cancer

Author

Yigit, Burcu, primary, Wang, Ninghai, primary, ten Hacken, Elisa, primary, Chen, Shih-Shih, primary, Bhan, Atul K., primary, Suarez-Fueyo, Abel, primary, Katsuyama, Eri, primary, Tsokos, George C., primary, Chiorazzi, Nicholas, primary, Wu, Catherine J., primary, Burger, Jan A., primary, Herzog, Roland W., primary, Engel, Pablo, primary, and Terhorst, Cox, primary

Published
2023
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16. Supplementary Figures from In Vivo Modeling of CLL Transformation to Richter Syndrome Reveals Convergent Evolutionary Paths and Therapeutic Vulnerabilities

Author

ten Hacken, Elisa, primary, Sewastianik, Tomasz, primary, Yin, Shanye, primary, Hoffmann, Gabriela Brunsting, primary, Gruber, Michaela, primary, Clement, Kendell, primary, Penter, Livius, primary, Redd, Robert A., primary, Ruthen, Neil, primary, Hergalant, Sébastien, primary, Sholokhova, Alanna, primary, Fell, Geoffrey, primary, Parry, Erin M., primary, Broséus, Julien, primary, Guieze, Romain, primary, Lucas, Fabienne, primary, Hernández-Sánchez, María, primary, Baranowski, Kaitlyn, primary, Southard, Jackson, primary, Joyal, Heather, primary, Billington, Leah, primary, Regis, Fara Faye D., primary, Witten, Elizabeth, primary, Uduman, Mohamed, primary, Knisbacher, Binyamin A., primary, Li, Shuqiang, primary, Lyu, Haoxiang, primary, Vaisitti, Tiziana, primary, Deaglio, Silvia, primary, Inghirami, Giorgio, primary, Feugier, Pierre, primary, Stilgenbauer, Stephan, primary, Tausch, Eugen, primary, Davids, Matthew S., primary, Getz, Gad, primary, Livak, Kenneth J., primary, Bozic, Ivana, primary, Neuberg, Donna S., primary, Carrasco, Ruben D., primary, and Wu, Catherine J., primary

Published
2023
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17. Supplementary Tables from In Vivo Modeling of CLL Transformation to Richter Syndrome Reveals Convergent Evolutionary Paths and Therapeutic Vulnerabilities

Author

ten Hacken, Elisa, primary, Sewastianik, Tomasz, primary, Yin, Shanye, primary, Hoffmann, Gabriela Brunsting, primary, Gruber, Michaela, primary, Clement, Kendell, primary, Penter, Livius, primary, Redd, Robert A., primary, Ruthen, Neil, primary, Hergalant, Sébastien, primary, Sholokhova, Alanna, primary, Fell, Geoffrey, primary, Parry, Erin M., primary, Broséus, Julien, primary, Guieze, Romain, primary, Lucas, Fabienne, primary, Hernández-Sánchez, María, primary, Baranowski, Kaitlyn, primary, Southard, Jackson, primary, Joyal, Heather, primary, Billington, Leah, primary, Regis, Fara Faye D., primary, Witten, Elizabeth, primary, Uduman, Mohamed, primary, Knisbacher, Binyamin A., primary, Li, Shuqiang, primary, Lyu, Haoxiang, primary, Vaisitti, Tiziana, primary, Deaglio, Silvia, primary, Inghirami, Giorgio, primary, Feugier, Pierre, primary, Stilgenbauer, Stephan, primary, Tausch, Eugen, primary, Davids, Matthew S., primary, Getz, Gad, primary, Livak, Kenneth J., primary, Bozic, Ivana, primary, Neuberg, Donna S., primary, Carrasco, Ruben D., primary, and Wu, Catherine J., primary

Published
2023
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18. HIF-1α regulates the interaction of chronic lymphocytic leukemia cells with the tumor microenvironment

Author

Valsecchi, Roberta, Coltella, Nadia, Belloni, Daniela, Ponente, Manfredi, ten Hacken, Elisa, Scielzo, Cristina, Scarfò, Lydia, Bertilaccio, Maria Teresa Sabrina, Brambilla, Paola, Lenti, Elisa, Martinelli Boneschi, Filippo, Brendolan, Andrea, Ferrero, Elisabetta, Ferrarini, Marina, Ghia, Paolo, Tonon, Giovanni, Ponzoni, Maurilio, Caligaris-Cappio, Federico, and Bernardi, Rosa

Published
2016
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20. Supplementary Tables 1,2,3,4 from Ofatumumab and Lenalidomide for Patients with Relapsed or Refractory Chronic Lymphocytic Leukemia: Correlation between Responses and Immune Characteristics

Author

Vitale, Candida, primary, Falchi, Lorenzo, primary, ten Hacken, Elisa, primary, Gao, Hui, primary, Shaim, Hila, primary, Van Roosbroeck, Katrien, primary, Calin, George, primary, O'Brien, Susan, primary, Faderl, Stefan, primary, Wang, Xuemei, primary, Wierda, William G., primary, Rezvani, Katayoun, primary, Reuben, James M., primary, Burger, Jan A., primary, Keating, Michael J., primary, and Ferrajoli, Alessandra, primary

Published
2023
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21. Supplementary Figures 1,2,3,4,5 from Ofatumumab and Lenalidomide for Patients with Relapsed or Refractory Chronic Lymphocytic Leukemia: Correlation between Responses and Immune Characteristics

Author

Vitale, Candida, primary, Falchi, Lorenzo, primary, ten Hacken, Elisa, primary, Gao, Hui, primary, Shaim, Hila, primary, Van Roosbroeck, Katrien, primary, Calin, George, primary, O'Brien, Susan, primary, Faderl, Stefan, primary, Wang, Xuemei, primary, Wierda, William G., primary, Rezvani, Katayoun, primary, Reuben, James M., primary, Burger, Jan A., primary, Keating, Michael J., primary, and Ferrajoli, Alessandra, primary

Published
2023
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22. Supplementary Data from Activation of Notch and Myc Signaling via B-cell–Restricted Depletion of Dnmt3a Generates a Consistent Murine Model of Chronic Lymphocytic Leukemia

Author

Biran, Anat, primary, Yin, Shanye, primary, Kretzmer, Helene, primary, ten Hacken, Elisa, primary, Parvin, Salma, primary, Lucas, Fabienne, primary, Uduman, Mohamed, primary, Gutierrez, Catherine, primary, Dangle, Nathan, primary, Billington, Leah, primary, Regis, Fara Faye, primary, Rassenti, Laura Z., primary, Mohammad, Arman, primary, Hoffmann, Gabriela Brunsting, primary, Stevenson, Kristen, primary, Zheng, Mei, primary, Witten, Elizabeth, primary, Fernandes, Stacey M., primary, Tausch, Eugen, primary, Sun, Clare, primary, Stilgenbauer, Stephan, primary, Brown, Jennifer R., primary, Kipps, Thomas J., primary, Aster, John C., primary, Gnirke, Andreas, primary, Neuberg, Donna S., primary, Letai, Anthony, primary, Wang, Lili, primary, Carrasco, Ruben D., primary, Meissner, Alexander, primary, and Wu, Catherine J., primary

Published
2023
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23. Data from Activation of Notch and Myc Signaling via B-cell–Restricted Depletion of Dnmt3a Generates a Consistent Murine Model of Chronic Lymphocytic Leukemia

Author

Biran, Anat, primary, Yin, Shanye, primary, Kretzmer, Helene, primary, ten Hacken, Elisa, primary, Parvin, Salma, primary, Lucas, Fabienne, primary, Uduman, Mohamed, primary, Gutierrez, Catherine, primary, Dangle, Nathan, primary, Billington, Leah, primary, Regis, Fara Faye, primary, Rassenti, Laura Z., primary, Mohammad, Arman, primary, Hoffmann, Gabriela Brunsting, primary, Stevenson, Kristen, primary, Zheng, Mei, primary, Witten, Elizabeth, primary, Fernandes, Stacey M., primary, Tausch, Eugen, primary, Sun, Clare, primary, Stilgenbauer, Stephan, primary, Brown, Jennifer R., primary, Kipps, Thomas J., primary, Aster, John C., primary, Gnirke, Andreas, primary, Neuberg, Donna S., primary, Letai, Anthony, primary, Wang, Lili, primary, Carrasco, Ruben D., primary, Meissner, Alexander, primary, and Wu, Catherine J., primary

Published
2023
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25. In VivoModeling of CLL Transformation to Richter Syndrome Reveals Convergent Evolutionary Paths and Therapeutic Vulnerabilities

Author

ten Hacken, Elisa, primary, Sewastianik, Tomasz, additional, Yin, Shanye, additional, Hoffmann, Gabriela Brunsting, additional, Gruber, Michaela, additional, Clement, Kendell, additional, Penter, Livius, additional, Redd, Robert A., additional, Ruthen, Neil, additional, Hergalant, Sébastien, additional, Sholokhova, Alanna, additional, Fell, Geoffrey, additional, Parry, Erin M., additional, Broséus, Julien, additional, Guieze, Romain, additional, Lucas, Fabienne, additional, Hernández-Sánchez, María, additional, Baranowski, Kaitlyn, additional, Southard, Jackson, additional, Joyal, Heather, additional, Billington, Leah, additional, Regis, Fara Faye D., additional, Witten, Elizabeth, additional, Uduman, Mohamed, additional, Knisbacher, Binyamin A., additional, Li, Shuqiang, additional, Lyu, Haoxiang, additional, Vaisitti, Tiziana, additional, Deaglio, Silvia, additional, Inghirami, Giorgio, additional, Feugier, Pierre, additional, Stilgenbauer, Stephan, additional, Tausch, Eugen, additional, Davids, Matthew S., additional, Getz, Gad, additional, Livak, Kenneth J., additional, Bozic, Ivana, additional, Neuberg, Donna S., additional, Carrasco, Ruben D., additional, and Wu, Catherine J., additional

Published
2022
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31. Dissecting Richter's Syndrome in a Multiplexed CRISPR-Based Mouse Model Reveals Key Changes in MYC, Interferon and BCR Signaling Underlying Transformation

Author

Ten Hacken, Elisa, primary, Yin, Shanye, additional, Sewastianik, Tomasz, additional, Penter, Livius, additional, Ruthen, Neil, additional, Gruber, Michaela, additional, Parry, Erin Michelle, additional, Guieze, Romain, additional, Redd, Robert A., additional, Uduman, Mohamed, additional, Li, Shuqiang, additional, Southard, Jackson, additional, Hernandez-Sanchez, Maria, additional, Parvin, Salma, additional, Zhu, Fen, additional, Brunsting Hoffmann, Gabriela, additional, Witten, Elizabeth, additional, Livak, Kenneth J., additional, Davids, Matthew S., additional, Letai, Anthony G., additional, Neuberg, Donna S., additional, Carrasco, Ruben D., additional, and Wu, Catherine J., additional

Published
2021
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33. IKZF3 Overexpression Phenocopies Gain-of-Function Mutation in Chronic Lymphocytic Leukemia

Author

Yin, Shanye, primary, Lazarian, Gregory, additional, Ten Hacken, Elisa, additional, Sewastianik, Tomasz, additional, Gohil, Satyen, additional, Li, Shuqiang, additional, Rassenti, Laura Z., additional, Billington, Leah, additional, Witten, Elizabeth, additional, Huang, Teddy, additional, Livak, Kenneth J., additional, Neuberg, Donna S., additional, Baran-Marszak, Fanny, additional, Kipps, Thomas J., additional, Cymbalista, Florence, additional, Carrasco, Ruben D., additional, and Wu, Catherine J., additional

Published
2020
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34. Expression of Sf3b1-K700E accelerates the Development of Chronic Lymphocytic Leukemia in a Del(13q) Murine Model

Author

Zhang, Bo, primary, Iyer, Prajish, additional, Jin, Meiling, additional, Ten Hacken, Elisa, additional, Cartun, Zachary, additional, Hart, Kevyn, additional, Rassenti, Laura Z., additional, Kipps, Thomas J., additional, Neuberg, Donna S., additional, Carrasco, Ruben D., additional, Wu, Catherine J., additional, and Wang, Lili, additional

Published
2020
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35. Multiplexed CRISPR In Vivo Editing of CLL Loss-of-Function Lesions Models Transformation of Chronic Lymphocytic Leukemia into Richter's Syndrome

Author

Ten Hacken, Elisa, primary, Sewastianik, Tomasz, additional, Redd, Robert A., additional, Fell, Geoffrey, additional, Uduman, Mohamed, additional, Gruber, Michaela, additional, Yin, Shanye, additional, Clement, Kendell, additional, Parry, Erin Michelle, additional, Li, Shuqiang, additional, Hernandez-Sanchez, Maria, additional, Billington, Leah, additional, Witten, Elizabeth, additional, Baranowski, Kaitlyn J, additional, Wang, Lili, additional, Pinello, Luca, additional, Livak, Kenneth J., additional, Neuberg, Donna S., additional, Carrasco, Ruben D., additional, and Wu, Catherine J., additional

Published
2020
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36. RPS15 and TP53 Co-Mutation Drives B Cell Malignancy through Altered Translation and MYC Activation in a Murine Model

Author

Gutierrez, Catherine, primary, Ouspenskaia, Tamara, additional, Fu, Doris, additional, Waddicor, Peyton, additional, Biran, Anat, additional, Liani, Aviv, additional, Lazarian, Gregory, additional, Ten Hacken, Elisa, additional, Witten, Elizabeth, additional, Regis, Fara Faye, additional, Joyal, Heather, additional, Billington, Leah, additional, Lucas, Fabienne, additional, Zheng, Mei, additional, Tye, Blake, additional, Hernandez-Sanchez, Maria, additional, Quijada Álamo, Miguel, additional, Li, Shuqiang, additional, Knisbacher, Binyamin A., additional, Lin, Ziao, additional, Al'Khafaji, Aziz, additional, Wang, Lili, additional, Livak, Kenneth J., additional, Neuberg, Donna S., additional, Cymbalista, Florence, additional, Getz, Gad, additional, Churchman, Stirling, additional, Carrasco, Ruben D., additional, Shao, Sichen, additional, Regev, Aviv, additional, and Wu, Catherine J., additional

Published
2020
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37. A Murine Model of Chronic Lymphocytic Leukemia Based on B Cell-Restricted Expression of Sf3b1 Mutation and Atm Deletion.

Author

Yin, Shanye, Yin, Shanye, Gambe, Rutendo G, Sun, Jing, Martinez, Aina Zurita, Cartun, Zachary J, Regis, Fara Faye D, Wan, Youzhong, Fan, Jean, Brooks, Angela N, Herman, Sarah EM, Ten Hacken, Elisa, Taylor-Weiner, Amaro, Rassenti, Laura Z, Ghia, Emanuela M, Kipps, Thomas J, Obeng, Esther A, Cibulskis, Carrie L, Neuberg, Donna, Campagna, Dean R, Fleming, Mark D, Ebert, Benjamin L, Wiestner, Adrian, Leshchiner, Ignaty, DeCaprio, James A, Getz, Gad, Reed, Robin, Carrasco, Ruben D, Wu, Catherine J, Wang, Lili, Yin, Shanye, Yin, Shanye, Gambe, Rutendo G, Sun, Jing, Martinez, Aina Zurita, Cartun, Zachary J, Regis, Fara Faye D, Wan, Youzhong, Fan, Jean, Brooks, Angela N, Herman, Sarah EM, Ten Hacken, Elisa, Taylor-Weiner, Amaro, Rassenti, Laura Z, Ghia, Emanuela M, Kipps, Thomas J, Obeng, Esther A, Cibulskis, Carrie L, Neuberg, Donna, Campagna, Dean R, Fleming, Mark D, Ebert, Benjamin L, Wiestner, Adrian, Leshchiner, Ignaty, DeCaprio, James A, Getz, Gad, Reed, Robin, Carrasco, Ruben D, Wu, Catherine J, and Wang, Lili

Abstract

SF3B1 is recurrently mutated in chronic lymphocytic leukemia (CLL), but its role in the pathogenesis of CLL remains elusive. Here, we show that conditional expression of Sf3b1-K700E mutation in mouse B cells disrupts pre-mRNA splicing, alters cell development, and induces a state of cellular senescence. Combination with Atm deletion leads to the overcoming of cellular senescence and the development of CLL-like disease in elderly mice. These CLL-like cells show genome instability and dysregulation of multiple CLL-associated cellular processes, including deregulated B cell receptor signaling, which we also identified in human CLL cases. Notably, human CLLs harboring SF3B1 mutations exhibit altered response to BTK inhibition. Our murine model of CLL thus provides insights into human CLL disease mechanisms and treatment.

Published
2019

38. Mitochondrial Reprogramming Underlies Resistance to BCL-2 Inhibition in Lymphoid Malignancies

Author

Swiss National Science Foundation, Sociedad Española de Hematología y Hemoterapia, Leukemia and Lymphoma Society of Canada, American Society of Hematology, National Institutes of Health (US), National Cancer Institute (US), Howard Hughes Medical Institute, Guièze, Romain, Liu, Vivian M., Rosebrock, Daniel, Jourdain, Alexis A., Hernández-Sánchez, María, Martinez Zurita, Aina, Sun, Jing, Ten Hacken, Elisa, Baranowski, Kaitlyn, Thompson, Philip A., Heo, Jin-Mi, Cartun, Zachary, Aygün, Ozan, Iorgulescu, J. Bryan, Zhang, Wandi, Notarangelo, Giulia, Livitz, Dimitri, Li, Shuqiang, Davids, Matthew S., Biran, Anat, Fernandes, Stacey M., Brown, Jennifer R., Lako, Ana, Ciantra, Zoe B., Lawlor, Matthew A., Keskin, Derin B., Udeshi, Namrata D., Wierda, William G., Livak, Kenneth J., Letai, Anthony G., Neuberg, Donna, Wade Harper, J., Carr, Steven A., Piccioni, Federica, Ott, Christopher J., Leshchiner, Ignaty, Johannessen, Cory M., Doench, John, Mootha, Vamsi K., Getz, Gad, Wu, Catherine J., Swiss National Science Foundation, Sociedad Española de Hematología y Hemoterapia, Leukemia and Lymphoma Society of Canada, American Society of Hematology, National Institutes of Health (US), National Cancer Institute (US), Howard Hughes Medical Institute, Guièze, Romain, Liu, Vivian M., Rosebrock, Daniel, Jourdain, Alexis A., Hernández-Sánchez, María, Martinez Zurita, Aina, Sun, Jing, Ten Hacken, Elisa, Baranowski, Kaitlyn, Thompson, Philip A., Heo, Jin-Mi, Cartun, Zachary, Aygün, Ozan, Iorgulescu, J. Bryan, Zhang, Wandi, Notarangelo, Giulia, Livitz, Dimitri, Li, Shuqiang, Davids, Matthew S., Biran, Anat, Fernandes, Stacey M., Brown, Jennifer R., Lako, Ana, Ciantra, Zoe B., Lawlor, Matthew A., Keskin, Derin B., Udeshi, Namrata D., Wierda, William G., Livak, Kenneth J., Letai, Anthony G., Neuberg, Donna, Wade Harper, J., Carr, Steven A., Piccioni, Federica, Ott, Christopher J., Leshchiner, Ignaty, Johannessen, Cory M., Doench, John, Mootha, Vamsi K., Getz, Gad, and Wu, Catherine J.

Abstract

Mitochondrial apoptosis can be effectively targeted in lymphoid malignancies with the FDA-approved B cell lymphoma 2 (BCL-2) inhibitor venetoclax, but resistance to this agent is emerging. We show that venetoclax resistance in chronic lymphocytic leukemia is associated with complex clonal shifts. To identify determinants of resistance, we conducted parallel genome-scale screens of the BCL-2-driven OCI-Ly1 lymphoma cell line after venetoclax exposure along with integrated expression profiling and functional characterization of drug-resistant and engineered cell lines. We identified regulators of lymphoid transcription and cellular energy metabolism as drivers of venetoclax resistance in addition to the known involvement by BCL-2 family members, which were confirmed in patient samples. Our data support the implementation of combinatorial therapy with metabolic modulators to address venetoclax resistance.Guièze et al. show that resistance to the BCL-2 inhibitor venetoclax in chronic lymphocytic leukemia is associated with complex clonal shifts and identify, in addition to the known involvement by BCL-2 family members, regulators of lymphoid transcription and cellular energy metabolism as resistance drivers.

Published
2019

39. The BET inhibitor GS-5829 targets chronic lymphocytic leukemia cells and their supportive microenvironment

Author

Kim, Ekaterina, primary, ten Hacken, Elisa, additional, Sivina, Mariela, additional, Clarke, Astrid, additional, Thompson, Philip A., additional, Jain, Nitin, additional, Ferrajoli, Alessandra, additional, Estrov, Zeev, additional, Keating, Michael J., additional, Wierda, William G., additional, Bhalla, Kapil N., additional, and Burger, Jan A., additional

Published
2019
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40. Interrogation of Individual CLL Loss-of-Function Lesions By CRISPR In Vivo Editing Reveals Common and Unique Pathway Alterations

Author

Ten Hacken, Elisa, primary, Yin, Shanye, primary, Clement, Kendell, primary, Redd, Robert A., primary, Hernandez-Sanchez, Maria, primary, Li, Shuqiang, primary, Gruber, Michaela, primary, Joyal, Heather, primary, Fell, Geoffrey, primary, Wang, Shu, primary, Jacob, Jose, primary, Flynn, James, primary, Ruff, David, primary, Jones, Keith W., primary, Wang, Lili, primary, Neuberg, Donna S, primary, Pinello, Luca, primary, Livak, Kenneth J., primary, Carrasco, Ruben D., primary, and Wu, Catherine J., primary

Published
2019
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41. Identification of Genotype-Specific Therapeutic Vulnerabilities By Comparative Dynamic BH3 Profiling Analysis of Human and Murine CLL

Author

Yin, Shanye, primary, Parvin, Salma, additional, Ten Hacken, Elisa, additional, Valentin, Rebecca, additional, Joyal, Heather, additional, Rassenti, Laura Z., additional, Ghia, Emanuela M., additional, Kipps, Thomas J., additional, Neuberg, Donna S, additional, Wang, Lili, additional, Davids, Matthew S., additional, Carrasco, Ruben D., additional, Letai, Anthony G., additional, and Wu, Catherine J., additional

Published
2019
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42. MCL-1 and PKA/AMPK Axis Fuel Venetoclax Resistance in Lymphoid Cancers

Author

Liu, Vivian M., primary, Guièze, Romain, additional, Rosebrock, Daniel, additional, Jourdain, Alexis A, additional, Hernández-Sánchez, María, additional, Martinez, Aina Zurita, additional, Ten Hacken, Elisa, additional, Thompson, Philip A., additional, Iorgulescu, Julian Bryan, additional, Li, Shuqiang, additional, Davids, Matthew S., additional, Brown, Jennifer R., additional, Lako, Ana, additional, Ciantra, Zoe B., additional, Lawlor, Matthew A., additional, Wierda, William G., additional, Letai, Anthony G., additional, Neuberg, Donna S, additional, Ott, Christopher J., additional, Leshchiner, Ignaty, additional, Mootha, Vamsi, additional, Getz, Gad, additional, and Wu, Catherine J., additional

Published
2019
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43. B Cell Restricted Expression of Mutated IKZF3 modulates BCR Signaling and Homing Pathways in a Mouse Model of CLL

Author

Lazarian, Gregory, primary, Yin, Shanye, primary, Ten Hacken, Elisa, primary, Sewastianik, Tomasz, primary, Font-tello, Alba, primary, Joyal, Heather, primary, Witten, Elizabeth, primary, Zheng, Mei, primary, Ott, Christopher J., primary, Neuberg, Donna S, primary, Wang, Lili, primary, Carrasco, Ruben D., primary, and Wu, Catherine J., primary

Published
2019
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44. Mitochondrial Reprogramming Underlies Resistance to BCL-2 Inhibition in Lymphoid Malignancies

Author

Guièze, Romain, primary, Liu, Vivian M., additional, Rosebrock, Daniel, additional, Jourdain, Alexis A., additional, Hernández-Sánchez, María, additional, Martinez Zurita, Aina, additional, Sun, Jing, additional, Ten Hacken, Elisa, additional, Baranowski, Kaitlyn, additional, Thompson, Philip A., additional, Heo, Jin-Mi, additional, Cartun, Zachary, additional, Aygün, Ozan, additional, Iorgulescu, J. Bryan, additional, Zhang, Wandi, additional, Notarangelo, Giulia, additional, Livitz, Dimitri, additional, Li, Shuqiang, additional, Davids, Matthew S., additional, Biran, Anat, additional, Fernandes, Stacey M., additional, Brown, Jennifer R., additional, Lako, Ana, additional, Ciantra, Zoe B., additional, Lawlor, Matthew A., additional, Keskin, Derin B., additional, Udeshi, Namrata D., additional, Wierda, William G., additional, Livak, Kenneth J., additional, Letai, Anthony G., additional, Neuberg, Donna, additional, Harper, J. Wade, additional, Carr, Steven A., additional, Piccioni, Federica, additional, Ott, Christopher J., additional, Leshchiner, Ignaty, additional, Johannessen, Cory M., additional, Doench, John, additional, Mootha, Vamsi K., additional, Getz, Gad, additional, and Wu, Catherine J., additional

Published
2019
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45. SLAMF6 as a Regulator of Exhausted CD8+ T Cells in Cancer

Author

Yigit, Burcu, primary, Wang, Ninghai, additional, ten Hacken, Elisa, additional, Chen, Shih-Shih, additional, Bhan, Atul K., additional, Suarez-Fueyo, Abel, additional, Katsuyama, Eri, additional, Tsokos, George C., additional, Chiorazzi, Nicholas, additional, Wu, Catherine J., additional, Burger, Jan A., additional, Herzog, Roland W., additional, Engel, Pablo, additional, and Terhorst, Cox, additional

Published
2019
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46. A Murine Model of Chronic Lymphocytic Leukemia Based on B Cell-Restricted Expression of Sf3b1 Mutation and Atm Deletion

Author

Yin, Shanye, primary, Gambe, Rutendo G., additional, Sun, Jing, additional, Martinez, Aina Zurita, additional, Cartun, Zachary J., additional, Regis, Fara Faye D., additional, Wan, Youzhong, additional, Fan, Jean, additional, Brooks, Angela N., additional, Herman, Sarah E.M., additional, ten Hacken, Elisa, additional, Taylor-Weiner, Amaro, additional, Rassenti, Laura Z., additional, Ghia, Emanuela M., additional, Kipps, Thomas J., additional, Obeng, Esther A., additional, Cibulskis, Carrie L., additional, Neuberg, Donna, additional, Campagna, Dean R., additional, Fleming, Mark D., additional, Ebert, Benjamin L., additional, Wiestner, Adrian, additional, Leshchiner, Ignaty, additional, DeCaprio, James A., additional, Getz, Gad, additional, Reed, Robin, additional, Carrasco, Ruben D., additional, Wu, Catherine J., additional, and Wang, Lili, additional

Published
2019
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48. KZF-L162R Mutation Affects Splenic Mature B Cell Development and Alters Expression of Aiolos Target Genes

Author

Lazarian, Gregory, primary, Yin, Shanye, additional, Font-tello, Alba, additional, Ten Hacken, Elisa, additional, Sevastianik, Tomasz, additional, Tom, Daniel, additional, Regis, Fara Faye, additional, Gill, Amy, additional, Zheng, Mei, additional, Georgopoulos, Katia, additional, Neuberg, Donna S, additional, Wang, Lili, additional, Carrasco, Ruben D., additional, and Wu, Catherine J., additional

Published
2018
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49. Integrated Genomic and Proteomic Analysis of Murine CLL-like Cells Reveals SF3B1 Mutation to Impact DNA Damage Response and BCR Signaling

Author

Wang, Lili, primary, Yin, Shanye, additional, Martinez, Aina zurita, additional, Regis, Fara Faye, additional, Brooks, Angela, additional, Herman, Sarah E. M., additional, Ten Hacken, Elisa, additional, Obeng, Esther, additional, Campagna, Dean, additional, Fleming, Mark D., additional, Ebert, Benjamin L., additional, Wiestner, Adrian, additional, Leshchiner, Ignaty, additional, Getz, Gad, additional, Carrasco, Ruben D., additional, and Wu, Catherine J., additional

Published
2018
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50. Functional and clinical relevance of VLA-4 (CD49d/CD29) in ibrutinib-treated chronic lymphocytic leukemia

Author

Tissino, Erika, primary, Benedetti, Dania, additional, Herman, Sarah E.M., additional, ten Hacken, Elisa, additional, Ahn, Inhye E., additional, Chaffee, Kari G., additional, Rossi, Francesca Maria, additional, Dal Bo, Michele, additional, Bulian, Pietro, additional, Bomben, Riccardo, additional, Bayer, Elisabeth, additional, Härzschel, Andrea, additional, Gutjahr, Julia Christine, additional, Postorino, Massimiliano, additional, Santinelli, Enrico, additional, Ayed, Ayed, additional, Zaja, Francesco, additional, Chiarenza, Annalisa, additional, Pozzato, Gabriele, additional, Chigaev, Alexandre, additional, Sklar, Larry A., additional, Burger, Jan A., additional, Ferrajoli, Alessandra, additional, Shanafelt, Tait D., additional, Wiestner, Adrian, additional, Del Poeta, Giovanni, additional, Hartmann, Tanja Nicole, additional, Gattei, Valter, additional, and Zucchetto, Antonella, additional

Published
2018
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