Research Topics
Genomes and Genes | Laura PasqualucciSummaryAffiliation: Columbia University Country: USA Publications
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Publications
PKA-mediated phosphorylation regulates the function of activation-induced deaminase (AID) in B cellsLaura Pasqualucci
Institute for Cancer Genetics and the Herbert Irving Comprehensive Cancer Center and Department of Microbiology, Columbia University, 1150 Saint Nicholas Avenue, New York, NY 10032, USA
Proc Natl Acad Sci U S A 103:395-400. 2006..These findings implicate PKA in the regulation of AID function and suggest that the control of T cell-dependent immune responses may be modulated, via AID, by signals that activate PKA...
Mutations of the BCL6 proto-oncogene disrupt its negative autoregulation in diffuse large B-cell lymphomaLaura Pasqualucci
Institute for Cancer Genetics and the Department of Pathology, Columbia University, New York, NY 10032, USA
Blood 101:2914-23. 2003..This study establishes a novel mechanism for BCL6 deregulation and reveals a broader involvement of this gene in DLBCL pathogenesis...- A signaling pathway mediating downregulation of BCL6 in germinal center B cells is blocked by BCL6 gene alterations in B cell lymphomaMasumichi Saito
Institute for Cancer Genetics, Herbert Irving Comprehensive Cancer Center, Columbia University, New York, NY 10032, USA
Cancer Cell 12:280-92. 2007..A subset of DLBCL displays chromosomal translocations or mutations that disrupt the IRF4-responsive region in the BCL6 promoter and block its downregulation by CD40 signaling... - Inactivating mutations of acetyltransferase genes in B-cell lymphomaLaura Pasqualucci
Institute for Cancer Genetics, Herbert Irving Comprehensive Cancer Center, Columbia University, New York, New York 10032, USA
Nature 471:189-95. 2011..These results identify CREBBP/EP300 mutations as a major pathogenetic mechanism shared by common forms of B-cell non-Hodgkin's lymphoma, with direct implications for the use of drugs targeting acetylation/deacetylation mechanisms... - Analysis of the coding genome of diffuse large B-cell lymphomaLaura Pasqualucci
Institute for Cancer Genetics, Columbia University, New York, New York, USA
Nat Genet 43:830-7. 2011..These results provide initial data on the complexity of the DLBCL coding genome and identify novel dysregulated pathways underlying its pathogenesis... - AID is required for germinal center-derived lymphomagenesisLaura Pasqualucci
Institute for Cancer Genetics, the Departments of Pathology and Genetics and Development, and The Herbert Irving Comprehensive Cancer Center, Columbia University, New York, New York 10032, USA
Nat Genet 40:108-12. 2008..These results show that AID is required for GC-derived lymphomagenesis, supporting the notion that errors in AID-mediated antigen-receptor gene modification processes are principal contributors to the pathogenesis of human B-NHL... - Expression of the AID protein in normal and neoplastic B cellsLaura Pasqualucci
Institute for Cancer Genetics, Department of Pathology, Columbia University, 1150 St Nicholas Ave, New York, NY 10032, USA
Blood 104:3318-25. 2004.... - BCL6 suppression of BCL2 via Miz1 and its disruption in diffuse large B cell lymphomaMasumichi Saito
Institute for Cancer Genetics, Herbert Irving Comprehensive Cancer Center, Columbia University, New York, NY 10032, USA
Proc Natl Acad Sci U S A 106:11294-9. 2009..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... 
Inactivation of the PRDM1/BLIMP1 gene in diffuse large B cell lymphomaLaura Pasqualucci
Institute for Cancer Genetics and 2The Herbert Irving Comprehensive Cancer Center, Columbia University, New York, NY 10032, USA
J Exp Med 203:311-7. 2006..These findings point to a role for BLIMP1 as a tumor suppressor gene, whose inactivation may contribute to lymphomagenesis by blocking post-GC differentiation of B cells toward plasma cells...- Deregulated BCL6 expression recapitulates the pathogenesis of human diffuse large B cell lymphomas in miceGiorgio Cattoretti
Institute for Cancer Genetics, Columbia University, New York, New York 10032, USA
Cancer Cell 7:445-55. 2005..These results define the oncogenic role of BCL6 in the pathogenesis of DLBCL and provide a faithful mouse model of this common disease... - Mutations of multiple genes cause deregulation of NF-kappaB in diffuse large B-cell lymphomaMara Compagno
Institute for Cancer Genetics and the Herbert Irving Comprehensive Cancer Center, Columbia University, New York, New York 10032, USA
Nature 459:717-21. 2009..Thus, our results demonstrate that NF-kappaB activation in DLBCL is caused by genetic lesions affecting multiple genes, the loss or activation of which may promote lymphomagenesis by leading to abnormally prolonged NF-kappaB responses... - Molecular pathogenesis of non-Hodgkin's lymphoma: the role of Bcl-6Laura Pasqualucci
Institute for Cancer Genetics, Columbia University, 1150 St Nicholas Avenue, New York, NY 10032, USA
Leuk Lymphoma 44:S5-12. 2003..These studies also indicate a novel mechanism by which acetylation promotes transcription, not only by modifying histones and activating transcriptional activators, but also by inhibiting transcriptional repressors... 
Genetic and phenotypic analysis of B-cell post-transplant lymphoproliferative disorders provides insights into disease biologyEfsevia Vakiani
Department of Pathology, Columbia University, New York, NY 10032, USA
Hematol Oncol 26:199-211. 2008..Together, our results suggest that PTLD represent a distinct type of B-NHL deriving from an antigen experienced B-cell, whose evolution is associated with accrual of genetic lesions...- The NF-{kappa}B negative regulator TNFAIP3 (A20) is inactivated by somatic mutations and genomic deletions in marginal zone lymphomasUrban Novak
Institute for Cancer Genetics, Departments of Pathology and Genetics and Development, and The Herbert Irving Comprehensive Cancer Center, Columbia University, New York, NY 10032, USA
Blood 113:4918-21. 2009..Thus, A20 inactivation by either somatic mutation and/or deletion represents a common genetic aberration across all MZL subtypes, which may contribute to lymphomagenesis by inducing constitutive NF-kappaB activation... - Targeted disruption of the S1P2 sphingosine 1-phosphate receptor gene leads to diffuse large B-cell lymphoma formationGiorgio Cattoretti
Institute for Cancer Genetics and the Department of Pathology, Herbert Irving Comprehensive Cancer Center, Columbia University, New York, New York, USA
Cancer Res 69:8686-92. 2009..The high incidence of DLBCL in S1P(2)(-/-) mice, its onset at old age, and the relative lack of other neoplasms identify these mice as a novel, and potentially valuable, model for this highly prevalent and aggressive human malignancy... - Aberrant somatic hypermutation in multiple subtypes of AIDS-associated non-Hodgkin lymphomaGianluca Gaidano
Institute for Cancer Genetics, Columbia University, Russ Berrie Science Pavilion, 1150 St Nicholas Ave, Rm 303B, New York, NY 10032, USA
Blood 102:1833-41. 2003..These data indicate that aberrant hypermutation is associated with various subtypes of AIDS-NHL and may represent a major contributor to their pathogenesis... - BLIMP1 is a tumor suppressor gene frequently disrupted in activated B cell-like diffuse large B cell lymphomaJonathan Mandelbaum
Institute for Cancer Genetics, Herbert Irving Comprehensive Cancer Center, Columbia University, New York, NY 10032, USA
Cancer Cell 18:568-79. 2010..These results demonstrate that BLIMP1 is a bona fide tumor-suppressor gene whose loss contributes to lymphomagenesis by blocking plasma cell differentiation... - Analysis of the chronic lymphocytic leukemia coding genome: role of NOTCH1 mutational activationGiulia Fabbri
Institute for Cancer Genetics and the Herbert Irving Comprehensive Cancer Center, Columbia University, New York, NY 10032, USA
J Exp Med 208:1389-401. 2011..These results provide initial data on the complexity of the CLL coding genome and identify a dysregulated pathway of diagnostic and therapeutic relevance... - Combined genetic inactivation of β2-Microglobulin and CD58 reveals frequent escape from immune recognition in diffuse large B cell lymphomaMadhavi Challa-Malladi
Institute for Cancer Genetics, Columbia University, New York, NY 10032, USA
Cancer Cell 20:728-40. 2011..These two events are significantly associated in this disease, suggesting that they are coselected during lymphomagenesis for their combined role in escape from immune-surveillance... - Genomic analysis of non-splenic marginal zone lymphomas (MZL) indicates similarities between nodal and extranodal MZL and supports their derivation from memory B-cellsUrban Novak
Departments of Pathology and Cell Biology Genetics and Development Herbert Irving Comprehensive Cancer Center Institute for Cancer Genetics, Columbia University Medical Center and New York Presbyterian Hospital, New York, NY, USA
Br J Haematol 155:362-5. 2011..Furthermore, the expression profiles of non-splenic MZL were similar to memory B cells... - State of the Art and Future Needs in Cytogenetic/Molecular Genetics/Arrays in childhood lymphoma: summary report of workshop at the First International Symposium on childhood and adolescent non-Hodgkin lymphoma, April 9, 2003, New York City, NYNyla A Heerema
Department of Pathology, The Ohio State University, Columbus, OH 43210, USA
Pediatr Blood Cancer 45:616-22. 2005..A significant number of studies describe the cytogenetics and molecular genetics of adult non-Hodgkin lymphoma (NHL); however, similar knowledge is lacking regarding pediatric NHL... - Molecular pathogenesis of diffuse large B-cell lymphomaChristof Schneider
Institute for Cancer Genetics and the Herbert Irving Comprehensive Cancer Center, and Department of Clinical Pathology and Cell Biology, Columbia University, New York, New York 10032, USA
Semin Diagn Pathol 28:167-77. 2011..This review focuses on the diversity of genetic lesions identified in the different subtypes of diffuse large B-cell lymphoma... - Expression of the IRTA1 receptor identifies intraepithelial and subepithelial marginal zone B cells of the mucosa-associated lymphoid tissue (MALT)Brunangelo Falini
Institute of Hematology, University of Perugia, 06122 Perugia, Italy
Blood 102:3684-92. 2003..Collectively, these results suggest a role of IRTA1 in the immune function of B cells within epithelia... - Aberrant somatic hypermutation in post-transplant lymphoproliferative disordersMichaela Cerri
Br J Haematol 127:362-4. 2004 - Molecular profiling of diffuse large B-cell lymphoma identifies robust subtypes including one characterized by host inflammatory responseStefano Monti
The Broad Institute, Cambridge, MA, USA
Blood 105:1851-61. 2005..These studies identify tumor microenvironment and host inflammatory response as defining features in DLBCL and suggest rational treatment targets in specific DLBCL subsets... - Cytoplasmic nucleophosmin in acute myelogenous leukemia with a normal karyotypeBrunangelo Falini
Institute of Hematology, University of Perugia, Perugia, Italy
N Engl J Med 352:254-66. 2005..Nucleophosmin (NPM), a nucleocytoplasmic shuttling protein with prominent nucleolar localization, regulates the ARF-p53 tumor-suppressor pathway. Translocations involving the NPM gene cause cytoplasmic dislocation of the NPM protein... - Both carboxy-terminus NES motif and mutated tryptophan(s) are crucial for aberrant nuclear export of nucleophosmin leukemic mutants in NPMc+ AMLBrunangelo Falini
Institute of Hematology, University of Perugia, 06122 Perugia, Italy
Blood 107:4514-23. 2006..These findings indicate that potential therapeutic strategies aimed to retarget NPM to its physiological sites will have to overcome 2 obstacles, the new NES motif and the mutated tryptophan(s) at the NPM mutant C-terminus... - Aberrant somatic hypermutation in tumor cells of nodular-lymphocyte-predominant and classic Hodgkin lymphomaArcangelo Liso
Institute of Hematology, University of Perugia, Policlinico, Monteluce, 06122 Perugia, Italy
Blood 108:1013-20. 2006..Our finding that NLPHL and cHL are targeted by aberrant SHM, as is DLBCL, suggests that these lymphomas may share common molecular pathogenetic events... - Aberrant somatic hypermutation in transformation of follicular lymphoma and chronic lymphocytic leukemia to diffuse large B-cell lymphomaDavide Rossi
Division of Hematology, Department of Clinical and Experimental Medicine and IRCAD, Amedeo Avogadro University of Eastern Piedmont, Via Solaroli 17, 28100 Novara, Italy
Haematologica 91:1405-9. 2006..Our findings demonstrate that acquisition of novel mutations due to aberrant somatic hypermutation was associated with DLBCL transformation in 5/9 (55.5%) cases of FL and 2/9 (22.2%) cases of B-CLL...