IgG4-ROD and orbital MALT lymphoma
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ABSTRACT:
PROVIDER: PRJNA648922 | ENA |
REPOSITORIES: ENA
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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 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.
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Project description:Immunoglobulin G4 (IgG4)-related disease (IgG4-RD) is a fibroinflammatory disorder signified by aberrant infiltration of IgG4-restricted plasma cells in a variety of organs. Clinical presentation is heterogeneous and pathophysiological mechanisms of IgG4-related autoimmunity remain elusive. Secondary parenchymal lesions of IgG4-RD in the central nervous system (CNS) are rare and there are very few cases of IgG4-RD with isolated CNS manifestation. Patients suffering from IgG4-RD frequently require prolonged treatment with glucocorticoids and are often unable to taper these medications. By leveraging single-cell sequencing of the cerebrospinal fluid (CSF) of a patient with an unusual inflammatory intracranial pseudotumor we provide novel insights into the immuno-pathophysiology of IgG4-RD by illustrating an IgG4-RD-associated polyclonal T cell response in the CSF and multifaceted cell-cell interaction between immune cell subsets and pathogenic B cells.
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Project description:Comparison of gene expression profiling analysis of bone marrow isolated CD34+ cells from patients with MALT lymphoma vs. healthy individuals revealed a large number of differentially expressed genes that included NF-kB target genes, genes involved in inflamatory signalling and immunoglobulin genes, suggesting an early lymphoid B-cell priming. Chromosomal translocations involving MALT1 gene are hallmarks of mucosa-associated lymphoid tissue (MALT) lymphoma. However, targeting these translocations to mouse B-cells has failed to reproduce human disease. Here, we induced MALT1 expression in mouse Sca1+Lin- hematopoietic stem/progenitor cells (HS/PCs), leading to the development of tumors recapitulating the clinical, histopathological and molecular features of human MALT lymphomas. Ablation of the p53 gene induced transformation of MALT lymphoma to diffuse large-cell lymphoma of activated B-cell type (ABC-DLBCL). Human CD34+ cells isolated from MALT lymphoma patients displayed an abnormal transcriptional program that was shared by MALT lymphoma cells, transgenic mouse Sca1+Lin- cells and Sca1-MALT1-induced lymphomas. Our study shows that MALT lymphoma can be modeled in mice by targeting MALT1 oncogene to HS/PCs.
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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. 5 human fresh frozen MALT lymphoma samples were analysed and 4 human tonsil tissue samples were used as the non-tumour control
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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
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