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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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The miRNA expression signature of human MALT lymphoma

ABSTRACT: To identify key tumour supressor miRNAs involed in MALT lymphoma pathogenesis Gastric mucosa-associated lymphoid tissue lymphoma develops in the chronically inflamed mucosa of Helicobacter pylori-infected patients. MicroRNA expression profiling of human MALT lymphoma revealed a 10-fold down-regulation of miR-203, which resulted from promoter hypermethylation and coincided with the dysregulation of the miR-203 target ABL1. Demethylating treatment of lymphoma B-cells led to an increase in miR-203 expression and concomitant ABL1 down-regulation. The lentiviral delivery of miR-203, as well as treatment with various ABL inhibitors, prevented primary MALT lymphoma cell proliferation in vitro. Finally, the treatment of tumor-bearing mice with imatinib induced MALT lymphoma regression in vivo. Our results show that MALT lymphomagenesis is epigenetically induced by miR-203 promoter methylation and identify ABL1 as a novel target for the treatment of this malignancy. 5 human fresh frozen MALT lymphoma samples were analysed and 4 human tonsil tissue samples were used as the non-tumour control

ORGANISM(S): Homo sapiens

SUBMITTER: Vanessa Craig

PROVIDER: E-GEOD-23877 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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The miRNA expression signature of human MALT lymphoma

Project description:To identify key tumour supressor miRNAs involed in MALT lymphoma pathogenesis Gastric mucosa-associated lymphoid tissue lymphoma develops in the chronically inflamed mucosa of Helicobacter pylori-infected patients. MicroRNA expression profiling of human MALT lymphoma revealed a 10-fold down-regulation of miR-203, which resulted from promoter hypermethylation and coincided with the dysregulation of the miR-203 target ABL1. Demethylating treatment of lymphoma B-cells led to an increase in miR-203 expression and concomitant ABL1 down-regulation. The lentiviral delivery of miR-203, as well as treatment with various ABL inhibitors, prevented primary MALT lymphoma cell proliferation in vitro. Finally, the treatment of tumor-bearing mice with imatinib induced MALT lymphoma regression in vivo. Our results show that MALT lymphomagenesis is epigenetically induced by miR-203 promoter methylation and identify ABL1 as a novel target for the treatment of this malignancy.

2010-08-31 | GSE23877 | GEO

IgG4-ROD and orbital MALT lymphoma

Project description:The molecular pathogenesis of orbital lymphoproliferative disorders, such as immunoglobulin G4-related ophthalmic disease (IgG4-ROD) and orbital mucosa-associated lymphoid tissue (MALT) lymphoma, remains essentially unknown. Differentiation between the two disorders, which is important since work-up and treatment can vary greatly, is often challenging due to the lack of specific biomarkers. Although miRNAs play an important role in the regulation of carcinogenesis and inflammation, the relationship between miRNA and orbital lymphoproliferative diseases remains unknown. A comprehensive analysis of 2,565 miRNAs was performed in biopsied specimens and serum of 17 cases with IgG4-ROD and 21 cases with orbital MALT lymphoma. We identified specific miRNA signatures, their miRNA target pathways, and network analysis associated with IgG4-ROD and orbital MALT lymphoma. Machine-learning analysis identified miR-202-3p and miR-7112-3p as the best discriminators of IgG4-ROD and orbital MALT lymphoma, respectively. In the tissue pathway, Longevity regulating pathway in IgG4-ROD and MAPK signaling pathway in orbital MALT lymphoma were most enriched by downregulated miRNAs. This is the first evidence of the miRNA profile in biopsied specimens and serum of patients with IgG4-ROD and orbital MALT lymphoma. These data will be useful for developing diagnostic and therapeutic interventions, as well as elucidating of these disorders.

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Project description:To clarify the molecular pathogenesis of DFL pathogenesis using GEP. DFL shares characteristics of both NFL and MALT lymphoma. 55 total samples were examined; 10 DFL, 18 NFL, 10 gastric MALT lymphoma, 5 normal duodenal mucosa, 8 nodal reactive lymphoid hyperplasia, and 4 normal gastric mucosa.

2014-03-01 | E-GEOD-48047 | biostudies-arrayexpress

Expression of MALT1 oncogene in mouse hematopoietic stem/progenitor cells recapitulates the pathogenesis of human MALT lymphoma

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Inhibition of BCL6-dependent gene expression in Philadelphia chromosome positive acute lymphoblastic leukemia

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Genome-wide DNA Methylation Analysis along the Progression of Gastric Marginal Zone B-cell Lymphoma of MALT Type

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A mouse model of deregulation of the malt1 oncogene recapitulates the pathogenesis of human malt lymphoma [MALT dataset]

Project description:Attempts at modeling chromosomal translocations involving MALT1 gene, hallmarks of human mucosa-associated lymphoid tissue (MALT) lymphoma, have failed to reproduce the disease in mice. Here we describe a transgenic model in which MALT1 expression was targeted to mouse hematopoietic stem/progenitor cells. In Sca1-MALT1 mice, MALT1 deregulation activated the NF-kappaB pathway in Sca1+ cells, promoting selective B-cell differentiation and mature lymphocyte accumulation in extranodal tissues, progressively leading to the development of clonal B-cell lymphomas. These tumors recapitulated the histopathological features of human MALT lymphomas, presenting typical lymphoepithelial lesions and plasmacytic differentiation. Transcriptional profiling of Sca1-MALT1 murine lymphomas revealed overlapping molecular signatures with human MALT lymphomas, including MALT1-mediated NF-kappaB activation, pro-inflammatory signaling and XBP1-induced plasmacytic differentiation. Moreover, murine Malt1 showed proteolytic activity by cleaving Bcl10 in Sca1-MALT1 lymphomas. Our novel technological approach has allowed modeling human MALT lymphoma in mice, which represent unique tools study MALT lymphoma biology and evaluate anti-MALT1 therapies. Keywords: lymphoma profiling, MALT lymphoma

2012-07-10 | GSE25638 | GEO

A mouse model of deregulation of the malt1 oncogene recapitulates the pathogenesis of human malt lymphoma [Spleen dataset]

Project description:Attempts at modeling chromosomal translocations involving MALT1 gene, hallmarks of human mucosa-associated lymphoid tissue (MALT) lymphoma, have failed to reproduce the disease in mice. Here we describe a transgenic model in which MALT1 expression was targeted to mouse hematopoietic stem/progenitor cells. In Sca1-MALT1 mice, MALT1 deregulation activated the NF-kappaB pathway in Sca1+ cells, promoting selective B-cell differentiation and mature lymphocyte accumulation in extranodal tissues, progressively leading to the development of clonal B-cell lymphomas. These tumors recapitulated the histopathological features of human MALT lymphomas, presenting typical lymphoepithelial lesions and plasmacytic differentiation. Transcriptional profiling of Sca1-MALT1 murine lymphomas revealed overlapping molecular signatures with human MALT lymphomas, including MALT1-mediated NFkappaB activation, pro-inflammatory signaling and XBP1-induced plasmacytic differentiation. Moreover, murine Malt1 showed proteolytic activity by cleaving Bcl10 in Sca1-MALT1 lymphomas. Our novel technological approach has allowed modeling human MALT lymphoma in mice, which represent unique tools study MALT lymphoma biology and evaluate anti-MALT1 therapies. Keywords: Genetic modification, wt vs. transgenic, disease analysis, MALT lymphoma

2012-07-10 | GSE25637 | GEO

Expression of MALT1 oncogene in mouse hematopoietic stem/progenitor cells recapitulates the pathogenesis of human MALT lymphoma

2012-07-09 | E-GEOD-34015 | biostudies-arrayexpress

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