Laura Pasqualucci

Summary

Affiliation: Columbia University
Country: USA

Publications

  1. pmc PKA-mediated phosphorylation regulates the function of activation-induced deaminase (AID) in B cells
    Laura 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
  2. ncbi request reprint Mutations of the BCL6 proto-oncogene disrupt its negative autoregulation in diffuse large B-cell lymphoma
    Laura Pasqualucci
    Institute for Cancer Genetics and the Department of Pathology, Columbia University, New York, NY 10032, USA
    Blood 101:2914-23. 2003
  3. ncbi request reprint A signaling pathway mediating downregulation of BCL6 in germinal center B cells is blocked by BCL6 gene alterations in B cell lymphoma
    Masumichi Saito
    Institute for Cancer Genetics, Herbert Irving Comprehensive Cancer Center, Columbia University, New York, NY 10032, USA
    Cancer Cell 12:280-92. 2007
  4. pmc Inactivating mutations of acetyltransferase genes in B-cell lymphoma
    Laura Pasqualucci
    Institute for Cancer Genetics, Herbert Irving Comprehensive Cancer Center, Columbia University, New York, New York 10032, USA
    Nature 471:189-95. 2011
  5. pmc Analysis of the coding genome of diffuse large B-cell lymphoma
    Laura Pasqualucci
    Institute for Cancer Genetics, Columbia University, New York, New York, USA
    Nat Genet 43:830-7. 2011
  6. ncbi request reprint Genetics of follicular lymphoma transformation
    Laura Pasqualucci
    Institute for Cancer Genetics, Columbia University, New York, NY 10032, USA Herbert Irving Comprehensive Cancer Center, Columbia University, New York, NY 10032, USA Department of Pathology and Cell Biology, Columbia University, New York, NY 10032, USA Electronic address
    Cell Rep 6:130-40. 2014
  7. doi request reprint The genetic basis of diffuse large B-cell lymphoma
    Laura Pasqualucci
    Institute for Cancer Genetics and the Department of Pathology and Cell Biology, Herbert Irving Comprehensive Cancer Center, Columbia University, New York, New York 10032, USA
    Curr Opin Hematol 20:336-44. 2013
  8. ncbi request reprint AID is required for germinal center-derived lymphomagenesis
    Laura 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
  9. ncbi request reprint Expression of the AID protein in normal and neoplastic B cells
    Laura Pasqualucci
    Institute for Cancer Genetics, Department of Pathology, Columbia University, 1150 St Nicholas Ave, New York, NY 10032, USA
    Blood 104:3318-25. 2004
  10. pmc BCL6 suppression of BCL2 via Miz1 and its disruption in diffuse large B cell lymphoma
    Masumichi 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

Collaborators

Detail Information

Publications35

  1. pmc PKA-mediated phosphorylation regulates the function of activation-induced deaminase (AID) in B cells
    Laura 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...
  2. ncbi request reprint Mutations of the BCL6 proto-oncogene disrupt its negative autoregulation in diffuse large B-cell lymphoma
    Laura 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...
  3. ncbi request reprint A signaling pathway mediating downregulation of BCL6 in germinal center B cells is blocked by BCL6 gene alterations in B cell lymphoma
    Masumichi 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...
  4. pmc Inactivating mutations of acetyltransferase genes in B-cell lymphoma
    Laura 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...
  5. pmc Analysis of the coding genome of diffuse large B-cell lymphoma
    Laura 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...
  6. ncbi request reprint Genetics of follicular lymphoma transformation
    Laura Pasqualucci
    Institute for Cancer Genetics, Columbia University, New York, NY 10032, USA Herbert Irving Comprehensive Cancer Center, Columbia University, New York, NY 10032, USA Department of Pathology and Cell Biology, Columbia University, New York, NY 10032, USA Electronic address
    Cell Rep 6:130-40. 2014
    ..The genomic profile of tFL shares similarities with that of germinal center B cell-type de novo DLBCL but also displays unique combinations of altered genes with diagnostic and therapeutic implications. ..
  7. doi request reprint The genetic basis of diffuse large B-cell lymphoma
    Laura Pasqualucci
    Institute for Cancer Genetics and the Department of Pathology and Cell Biology, Herbert Irving Comprehensive Cancer Center, Columbia University, New York, New York 10032, USA
    Curr Opin Hematol 20:336-44. 2013
    ....
  8. ncbi request reprint AID is required for germinal center-derived lymphomagenesis
    Laura 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...
  9. ncbi request reprint Expression of the AID protein in normal and neoplastic B cells
    Laura Pasqualucci
    Institute for Cancer Genetics, Department of Pathology, Columbia University, 1150 St Nicholas Ave, New York, NY 10032, USA
    Blood 104:3318-25. 2004
    ....
  10. pmc BCL6 suppression of BCL2 via Miz1 and its disruption in diffuse large B cell lymphoma
    Masumichi 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...
  11. pmc Inactivation of the PRDM1/BLIMP1 gene in diffuse large B cell lymphoma
    Laura 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...
  12. pmc Mutations of multiple genes cause deregulation of NF-kappaB in diffuse large B-cell lymphoma
    Mara 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...
  13. doi request reprint Genetic and phenotypic analysis of B-cell post-transplant lymphoproliferative disorders provides insights into disease biology
    Efsevia 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...
  14. ncbi request reprint Molecular pathogenesis of non-Hodgkin's lymphoma: the role of Bcl-6
    Laura 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...
  15. ncbi request reprint Deregulated BCL6 expression recapitulates the pathogenesis of human diffuse large B cell lymphomas in mice
    Giorgio 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...
  16. doi request reprint MEF2B mutations lead to deregulated expression of the oncogene BCL6 in diffuse large B cell lymphoma
    Carol Y Ying
    Institute for Cancer Genetics, Columbia University, New York, New York, USA
    Nat Immunol 14:1084-92. 2013
    ..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. ..
  17. pmc The NF-{kappa}B negative regulator TNFAIP3 (A20) is inactivated by somatic mutations and genomic deletions in marginal zone lymphomas
    Urban 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...
  18. pmc Analysis of the chronic lymphocytic leukemia coding genome: role of NOTCH1 mutational activation
    Giulia 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...
  19. pmc Genetic lesions associated with chronic lymphocytic leukemia transformation to Richter syndrome
    Giulia Fabbri
    Institute for Cancer Genetics, Herbert Irving Comprehensive Cancer Center, 2 Department of Pathology and Cell Biology, 3 Departments of Genetics and Development and of Microbiology and Immunology and 4 Department of Biomedical Informatics and Center for Computational Biology and Bioinformatics, Columbia University, New York, NY 10032
    J Exp Med 210:2273-88. 2013
    ..These results provide insights into RS pathogenesis, and identify dysregulated pathways of potential diagnostic and therapeutic relevance. ..
  20. ncbi request reprint Aberrant somatic hypermutation in multiple subtypes of AIDS-associated non-Hodgkin lymphoma
    Gianluca 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...
  21. pmc Targeted disruption of the S1P2 sphingosine 1-phosphate receptor gene leads to diffuse large B-cell lymphoma formation
    Giorgio 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...
  22. pmc Combined genetic inactivation of β2-Microglobulin and CD58 reveals frequent escape from immune recognition in diffuse large B cell lymphoma
    Madhavi 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...
  23. pmc MutComFocal: an integrative approach to identifying recurrent and focal genomic alterations in tumor samples
    Vladimir Trifonov
    Department of Biomedical Informatics, New York, NY 10032, USA
    BMC Syst Biol 7:25. 2013
    ..Current large-scale genomic projects provide high throughput genomic data in a large number of well-characterized tumor samples...
  24. pmc BLIMP1 is a tumor suppressor gene frequently disrupted in activated B cell-like diffuse large B cell lymphoma
    Jonathan 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...
  25. pmc Fractal-like distributions over the rational numbers in high-throughput biological and clinical data
    Vladimir Trifonov
    Department of Biomedical Informatics, Center for Computational Biology and Bioinformatics, Columbia University, New York, NY 10032, USA
    Sci Rep 1:191. 2011
    ..The distributions are also relevant to identification of subclonal populations in tumors and the study of quasi-species and intrahost diversity of viral populations...
  26. doi request reprint Genomic analysis of non-splenic marginal zone lymphomas (MZL) indicates similarities between nodal and extranodal MZL and supports their derivation from memory B-cells
    Urban 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...
  27. ncbi request reprint 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, NY
    Nyla 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...
  28. pmc Molecular pathogenesis of diffuse large B-cell lymphoma
    Christof 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...
  29. ncbi request reprint Aberrant somatic hypermutation in tumor cells of nodular-lymphocyte-predominant and classic Hodgkin lymphoma
    Arcangelo 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...
  30. ncbi request reprint Aberrant somatic hypermutation in transformation of follicular lymphoma and chronic lymphocytic leukemia to diffuse large B-cell lymphoma
    Davide 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...
  31. ncbi request reprint Aberrant somatic hypermutation in post-transplant lymphoproliferative disorders
    Michaela Cerri
    Br J Haematol 127:362-4. 2004
  32. ncbi request reprint 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...
  33. ncbi request reprint Cytoplasmic nucleophosmin in acute myelogenous leukemia with a normal karyotype
    Brunangelo 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...
  34. ncbi request reprint Molecular profiling of diffuse large B-cell lymphoma identifies robust subtypes including one characterized by host inflammatory response
    Stefano 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...
  35. ncbi request reprint Both carboxy-terminus NES motif and mutated tryptophan(s) are crucial for aberrant nuclear export of nucleophosmin leukemic mutants in NPMc+ AML
    Brunangelo 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...