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306 results on '"Basso, Katia"'

3. Genetic mechanisms of HLA-I loss and immune escape in diffuse large B cell lymphoma

Author

Fangazio, Marco, Ladewig, Erik, Gomez, Karen, Garcia-Ibanez, Laura, Kumar, Rahul, Teruya-Feldstein, Julie, Rossi, Davide, Filip, Ioan, Pan-Hammarström, Qiang, Inghirami, Giorgio, Boldorini, Renzo, Ott, German, Staiger, Annette M., Chapuy, Björn, Gaidano, Gianluca, Bhagat, Govind, Basso, Katia, Rabadan, Raul, Pasqualucci, Laura, and Dalla-Favera, Riccardo

Published
2021

5. Repurposing dasatinib for diffuse large B cell lymphoma

Author

Scuoppo, Claudio, Wang, Jiguang, Persaud, Mirjana, Mittan, Sandeep K., Basso, Katia, Pasqualucci, Laura, Rabadan, Raul, Inghirami, Giorgio, Grandori, Carla, Bosch, Francesc, and Dalla-Faver, Riccardo

Published
2019

7. Conditional Network Analysis Identifies Candidate Regulator Genes in Human B Cells

Author

Wang, Kai, Banerjee, Nilanjana, Margolin, Adam, Nemenman, Ilya, Basso, Katia, Favera, Riccardo, and Califano, Andrea

Subjects
Quantitative Biology - Molecular Networks, Quantitative Biology - Genomics, Quantitative Biology - Quantitative Methods
Abstract

Cellular phenotypes are determined by the dynamical activity of networks of co-regulated genes. Elucidating such networks is crucial for the understanding of normal cell physiology as well as for the dissection of complex pathologic phenotypes. Existing methods for such "reverse engineering" of genetic networks from microarray expression data have been successful only in prokaryotes (E. coli) and lower eukaryotes (S. cerevisiae) with relatively simple genomes. Additionally, they have mostly attempted to reconstruct average properties about the network connectivity without capturing the highly conditional nature of the interactions. In this paper we extend the ARACNE algorithm, which we recently introduced and successfully applied to the reconstruction of whole-genome transcriptional networks from mammalian cells, precisely to link the existence of specific network structures to the expression or lack thereof of specific regulator genes. This is accomplished by analyzing thousands of alternative network topologies generated by constraining the data set on the presence or absence of putative regulator genes. By considering interactions that are consistently supported across several such constraints, we identify many transcriptional interactions that would not have been detectable by the original method. By selecting genes that produce statistically significant changes in network topology, we identify novel candidate regulator genes. Further analysis shows that transcription factors, kinases, phosphatases, and other gene families known to effect biochemical interactions, are significantly overrepresented among the set of candidate regulator genes identified in silico, indirectly supporting the validity of the approach., Comment: Submitted to RECOMB 2005 (11 pages, 4 figures, 2 tables)

Published
2004

8. ARACNE: An Algorithm for the Reconstruction of Gene Regulatory Networks in a Mammalian Cellular Context

Author

Margolin, Adam A., Nemenman, Ilya, Basso, Katia, Klein, Ulf, Wiggins, Chris, Stolovitzky, Gustavo, Favera, Riccardo Dalla, and Califano, Andrea

Subjects
Quantitative Biology - Molecular Networks, Quantitative Biology - Genomics, Quantitative Biology - Quantitative Methods
Abstract

Background: Elucidating gene regulatory networks is crucial for understanding normal cell physiology and complex pathologic phenotypes. Existing computational methods for the genome-wide ``reverse engineering'' of such networks have been successful only for lower eukaryotes with simple genomes. Here we present ARACNE, a novel algorithm, using microarray expression profiles, specifically designed to scale up to the complexity of regulatory networks in mammalian cells, yet general enough to address a wider range of network deconvolution problems. This method uses an information theoretic approach to eliminate the majority of indirect interactions inferred by co-expression methods. Results: We prove that ARACNE reconstructs the network exactly (asymptotically) if the effect of loops in the network topology is negligible, and we show that the algorithm works well in practice, even in the presence of numerous loops and complex topologies. We assess ARACNE's ability to reconstruct transcriptional regulatory networks using both a realistic synthetic dataset and a microarray dataset from human B cells. On synthetic datasets ARACNE achieves very low error rates and outperforms established methods, such as Relevance Networks and Bayesian Networks. Application to the deconvolution of genetic networks in human B cells demonstrates ARACNE's ability to infer validated transcriptional targets of the c MYC proto-oncogene. We also study the effects of mis estimation of mutual information on network reconstruction, and show that algorithms based on mutual information ranking are more resilient to estimation errors., Comment: accepted version; minor revisions following referee suggestions; 28 pages, 9 figures; detailed version of q-bio.MN/0410036

Published
2004
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9. Data from The CREBBP Acetyltransferase Is a Haploinsufficient Tumor Suppressor in B-cell Lymphoma

Author

Zhang, Jiyuan, primary, Vlasevska, Sofija, primary, Wells, Victoria A., primary, Nataraj, Sarah, primary, Holmes, Antony B., primary, Duval, Romain, primary, Meyer, Stefanie N., primary, Mo, Tongwei, primary, Basso, Katia, primary, Brindle, Paul K., primary, Hussein, Shafinaz, primary, Dalla-Favera, Riccardo, primary, and Pasqualucci, Laura, primary

Published
2023
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10. Supplementary Figure Legends, Figures S1 - S7, Tables S1 - S8 from The CREBBP Acetyltransferase Is a Haploinsufficient Tumor Suppressor in B-cell Lymphoma

Author

Zhang, Jiyuan, primary, Vlasevska, Sofija, primary, Wells, Victoria A., primary, Nataraj, Sarah, primary, Holmes, Antony B., primary, Duval, Romain, primary, Meyer, Stefanie N., primary, Mo, Tongwei, primary, Basso, Katia, primary, Brindle, Paul K., primary, Hussein, Shafinaz, primary, Dalla-Favera, Riccardo, primary, and Pasqualucci, Laura, primary

Published
2023
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11. KMT2D acetylation by CREBBP reveals a cooperative functional interaction at enhancers in normal and malignant germinal center B cells

Author

Vlasevska, Sofija, primary, Garcia-Ibanez, Laura, additional, Duval, Romain, additional, Holmes, Antony B., additional, Jahan, Rahat, additional, Cai, Bowen, additional, Kim, Andrew, additional, Mo, Tongwei, additional, Basso, Katia, additional, Soni, Rajesh K., additional, Bhagat, Govind, additional, Dalla-Favera, Riccardo, additional, and Pasqualucci, Laura, additional

Published
2023
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13. Single-cell transcriptomics of pediatric Burkitt lymphoma reveals intra-tumor heterogeneity and markers of therapy resistance

Author

Corinaldesi, Clarissa, Holmes, Antony B., Martire, Gaia, Tosato, Anna, Rizzato, Domenico, Lovisa, Federica, Gallingani, Ilaria, Shen, Qiong, Ferrone, Lavinia, Harris, Marian, Davies, Kimberly, Molinaro, Luca, Mortara, Umberto, Dei Tos, Angelo Paolo, Ofori, Kenneth, D’Amore, Emanuele S. G., Chiarle, Roberto, Ngan, Bo, Carraro, Elisa, Pillon, Marta, Hussein, Shafinaz, Bhagat, Govind, Pizzi, Marco, Mussolin, Lara, and Basso, Katia

Abstract

Burkitt lymphoma (BL) is the most frequent B-cell lymphoma in pediatric patients. While most patients are cured, a fraction of them are resistant to therapy. To investigate BL heterogeneity and the features distinguishing therapy responders (R) from non-responders (NR), we analyzed by single-cell (sc)-transcriptomics diagnostic EBV-negative BL specimens. Analysis of the non-tumor component revealed a predominance of immune cells and a small representation of fibroblasts, enriched in NR. Tumors displayed patient-specific features, as well as shared subpopulations that expressed transcripts related to cell cycle, signaling pathways and cell-of-origin signatures. Several transcripts were differentially expressed in R versus NR. The top candidate, Tropomyosin 2 (TPM2), a member of the tropomyosin actin filament binding protein family, was confirmed to be significantly higher in NR both at the transcript and protein level. Stratification of patients based on TPM2 expression at diagnosis significantly correlated with prognosis, independently of TP53mutations. These results indicate that BL displays transcriptional heterogeneity and identify candidate biomarkers of therapy resistance.

Published
2024
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15. Abstract A12: Pervasive hypermutation of super-enhancer regions dysregulates oncogene expression in diffuse large B-cell lymphoma

Author

Bal, Elodie, primary, Kumar, Rahul, additional, Hadigol, Mohammad, additional, Holmes, Antony B., additional, Hilton, Laura K., additional, Loh, Jui Wan, additional, Dreval, Kostiantyn, additional, Wong, Jasper, additional, Vlasevska, Sofija, additional, Corinaldesi, Clarissa, additional, Soni, Rajesh Kumar Soni, additional, Basso, Katia, additional, Morin, Ryan D., additional, Khiabanian, Hossein, additional, Pasqualucci, Laura, additional, and Dalla-Favera, Riccardo, additional

Published
2022
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19. Disruption of KMT2D perturbs germinal center B cell development and promotes lymphomagenesis

Author

Zhang, Jiyuan, Dominguez-Sola, David, Hussein, Shafinaz, Lee, Ji-Eun, Holmes, Antony B., Bansal, Mukesh, Vlasevska, Sofija, Mo, Tongwei, Tang, Hongyan, Basso, Katia, Ge, Kai, Dalla-Favera, Riccardo, and Pasqualucci, Laura

Subjects
Gene mutations -- Physiological aspects -- Research, Lymphomas -- Development and progression -- Genetic aspects -- Research, B cells -- Physiological aspects -- Genetic aspects -- Research, Biological sciences, Health
Abstract

Mutations in the gene encoding the KMT2D (or MLL2) methyltransferase are highly recurrent and occur early during tumorigenesis in diffuse large B cell lymphoma (DLBCL) and follicular lymphoma (FL). However, the functional consequences of these mutations and their role in lymphomagenesis are unknown. Here we show that FL- and DLBCL-associated KMT2D mutations impair KMT2D enzymatic activity, leading to diminished global H3K4 methylation in germinal-center (GC) B cells and DLBCL cells. Conditional deletion of Kmt2d early during B cell development, but not after initiation of the GC reaction, results in an increase in GC B cells and enhances B cell proliferation in mice. Moreover, genetic ablation of Kmt2d in mice overexpressing Bcl2 increases the incidence of GC-derived lymphomas resembling human tumors. These findings suggest that KMT2D acts as a tumor suppressor gene whose early loss facilitates lymphomagenesis by remodeling the epigenetic landscape of the cancer precursor cells. Eradication of KMT2D-deficient cells may thus represent a rational therapeutic approach for targeting early tumorigenic events., B cell non-Hodgkin lymphomas (B-NHL) represent a heterogeneous group of malignancies that originate mostly from B cells in the GC and are driven by distinct genetic lesions disrupting key oncogenic [...]

Published
2015
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31. BCL6 suppression of BCL2 via Miz1 and its disruption in diffuse large B cell lymphoma

Author

Saito, Masumichi, Novak, Urban, Piovan, Erich, Basso, Katia, Sumazin, Pavel, Schneider, Christof, Crespo, Marta, Shen, Qiong, Bhagat, Govind, Califano, Andrea, Chadburn, Amy, Pasqualucci, Laura, and Dalla-Favera, Riccardo

Subjects
Oncogenes -- Research, Lymphomas -- Development and progression, Science and technology
Abstract

The BCL6 proto-oncogene encodes a transcriptional repressor that is required for germinal center (GC) formation and whose deregulation by genomic lesions is implicated in the pathogenesis of GC-derived diffuse large B cell lymphoma (DLBCL) and, less frequently, follicular lymphoma (FL). The biological function of BCL6 is only partially understood because no more than a few genes have been functionally characterized as direct targets of BCL6 transrepression activity. Here we report that the anti-apoptotic proto-oncogene BCL2 is a direct target of BCL6 in GC B cells. BCL6 binds to the BCL2 promoter region by interacting with the transcriptional activator Miz1 and suppresses Miz1-induced activation of BCL2 expression. BCL6-mediated suppression of BCL2 is lost in FL and DLBCL, where the 2 proteins are pathologically coexpressed, because of BCL2 chromosomal translocations and other mechanisms, including Miz1 deregulation and somatic mutations in the BCL2 promoter region. These results identify an important function for BCL6 in facilitating apoptosis of GC B cells via suppression of BCL2, and suggest that blocking this pathway is critical for lymphomagenesis. apoptosis | DLBCL | germinal center

Published
2009

32. Gene expression analysis of peripheral T cell lymphoma, unspecified, reveals distinct profiles and new potential therapeutic targets

Author

Piccaluga, Pier Paolo, Agostinelli, Claudio, Califano, Andrea, Rossi, Maura, Basso, Katia, Zupo, Simonetta, Went, Philip, Klein, Ulf, Zinzani, Pier Luigi, Baccarani, Michele, Favera, Riccardo Dalla, and Pileri, Stefano A.

Subjects
Lymphomas -- Care and treatment, T cells -- Diseases, Homeopathy -- Materia medica and therapeutics, Gene expression, Therapeutics
Abstract

Peripheral T cell lymphoma, unspecified (PTCL/U), the most common form of PTCL, displays heterogeneous morphology and phenotype, poor response to treatment, and poor prognosis. We demonstrate that PTCL/U shows a [...]

Published
2007

34. MicroRNA expression in HTLV-1 infection and pathogenesis

Author

Zanovello Paola, Corti Giorgio, De Bellis Gianluca, Guffanti Alessandro, Basso Katia, Corradin Alberto, Pise-Masison Cynthia A, Bortoluzzi Stefania, Biasiolo Marta, Ruggero Katia, D'Agostino Donna M, Bronte Vincenzo, and Ciminale Vincenzo

Subjects
Immunologic diseases. Allergy, RC581-607
Published
2011
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36. BCL6

Author

Basso, Katia, primary and Dalla-Favera, Riccardo, additional

Published
2010
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44. Unique and Shared Epigenetic Programs of the CREBBP and EP300 Acetyltransferases in Germinal Center B Cells Reveal Targetable Dependencies in Lymphoma

Author

Meyer, Stefanie N., primary, Scuoppo, Claudio, additional, Vlasevska, Sofija, additional, Bal, Elodie, additional, Holmes, Antony B., additional, Holloman, Mara, additional, Garcia-Ibanez, Laura, additional, Nataraj, Sarah, additional, Duval, Romain, additional, Vantrimpont, Thomas, additional, Basso, Katia, additional, Brooks, Nigel, additional, Dalla-Favera, Riccardo, additional, and Pasqualucci, Laura, additional

Published
2019
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48. MEF2B mutations lead to deregulated expression of the BCL6 oncogene in Diffuse Large B cell Lymphoma

Author

Ying, Carol Y., Dominguez-Sola, David, Fabi, Melissa, Lorenz, Ivo C., Hussein, Shafinaz, Bansal, Mukesh, Califano, Andrea, Pasqualucci, Laura, Basso, Katia, and Dalla-Favera, Riccardo

Subjects
Transcription, Genetic, Protein Conformation, MADS Domain Proteins, Proto-Oncogene Mas, Article, Mice, immune system diseases, hemic and lymphatic diseases, Animals, Cluster Analysis, Humans, Amino Acid Sequence, Lymphoma, Follicular, Adaptor Proteins, Signal Transducing, Cell Proliferation, B-Lymphocytes, MEF2 Transcription Factors, Gene Expression Profiling, Cell Cycle, Computational Biology, Sumoylation, Germinal Center, Cyclic AMP-Dependent Protein Kinases, Gene Expression Regulation, Neoplastic, Molecular Docking Simulation, Amino Acid Substitution, Myogenic Regulatory Factors, Mutation, Proto-Oncogene Proteins c-bcl-6, Lymphoma, Large B-Cell, Diffuse, Protein Binding
Abstract

MEF2B encodes a transcriptional activator and is mutated in ∼11% of diffuse large B cell lymphomas (DLBCLs) and ∼12% of follicular lymphomas (FLs). Here we found that MEF2B directly activated the transcription of the proto-oncogene BCL6 in normal germinal-center (GC) B cells and was required for DLBCL proliferation. Mutation of MEF2B resulted in enhanced transcriptional activity of MEF2B either through disruption of its interaction with the corepressor CABIN1 or by rendering it insensitive to inhibitory signaling events mediated by phosphorylation and sumoylation. Consequently, the transcriptional activity of Bcl-6 was deregulated in DLBCLs with MEF2B mutations. Thus, somatic mutations of MEF2B may contribute to lymphomagenesis by deregulating BCL6 expression, and MEF2B may represent an alternative target for blocking Bcl-6 activity in DLBCLs.

Published
2013

49. Clinical impact of miR-223 expression in pediatric T-Cell lymphoblastic lymphoma

Author

Pomari, Elena, primary, Lovisa, Federica, additional, Carraro, Elisa, additional, Primerano, Simona, additional, D’Amore, Emanuele S.G., additional, Bonvini, Paolo, additional, Nigro, Luca Lo, additional, Vito, Rita De, additional, Vinti, Luciana, additional, Farruggia, Piero, additional, Pillon, Marta, additional, Basso, Giuseppe, additional, Basso, Katia, additional, and Mussolin, Lara, additional

Published
2017
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50. The CREBBP Acetyltransferase Is a Haploinsufficient Tumor Suppressor in B-cell Lymphoma

Author

Zhang, Jiyuan, primary, Vlasevska, Sofija, additional, Wells, Victoria A., additional, Nataraj, Sarah, additional, Holmes, Antony B., additional, Duval, Romain, additional, Meyer, Stefanie N., additional, Mo, Tongwei, additional, Basso, Katia, additional, Brindle, Paul K., additional, Hussein, Shafinaz, additional, Dalla-Favera, Riccardo, additional, and Pasqualucci, Laura, additional

Published
2017
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