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.
2021-08-01 | GSE155177 | GEO
Project description:Purpose: MALT lymphoma orbital region and IgG4-related eye disease (IGG4ROD) account for the majority of mass lesions in the orbital region. They may show similar shadows on radiological images, and many cases are difficult to differentiate clinically. We investigated what kind of gene expression cluster(RNA-seq) and molecular differences are responsible for two diseases. Methods: Total RNA was extracted from fresh tissues in 20 cases which were histopathologically diagnosed from 20XX to 20XX, and a sequence library was created. Next-generation sequencing analysis (RNA-seq, NovaSeq6000) was performed to compare gene expression between the two groups, and principal component analysis and cluster hierarchy analysis were performed. Results: In principal component analysis, orbital MALT lymphoma and IgG4ROD were clustered in component 2in PCA analysis. Clear cluster differences were observed, except for one case that appeared to be IgG4-producing MALT lymphoma. In addition, cluster analysis showed that one case that appeared to be IgG4-producing MALT lymphoma was located just between the IGG4ROD and MALT lymphoma clusters. Furthermore, in a comparison of up regulator analysis between IgG4ROD and MALT lymphoma, 582 genes were identified as candidates(p<0.01). Pathway analysis of MALT lymphoma suggested that the Sting pathway be activated. Sting pathway-down-stream analysis were significant eight gene expression changes)P<0.05). In addition, STING immunohistochmical analysis were detected different formed staining pattern using quantitative evaluation in IgG4ROD and MALT(P<0.01). Conclusion: MALT lymphoma orbital and IgG4-related eye disease (IGG4ROD) can be divided into two clusters of gene expression. The Sting pathway may be a important pathway specific to orbital MALT lymphoma compared with orbital IgG4ROD.
2025-09-01 | GSE276421 | GEO
Project description:Gene expression clusters change and molecular correlation via STING pathway between orbital MALT lymphoma and orbital IgG4-related eye diseases
| PRJNA1157331 | ENA
Project description:Aim to investigate the pathogenesis of BLEL of the lacrimal gland, which is a kind of IgG4 related disease. A prospective study. Orbital Cavernous Hemangioma Tissues (nine continuous cases) vs. Benign Lymphoepithelial Lesions of the Lacrimal Gland tissues (nine continuous cases). Duplicate chips were used for each RNA sample.
2016-01-06 | E-GEOD-76497 | biostudies-arrayexpress
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
Project description:Comparison of t(11;18)-positive MALT lymphoma to t(11;18)-negative MALT lymphoma, with a special focus on the NF-KB pathway and it's targets
2010-11-25 | GSE25550 | GEO
Project description:Molecular pathways activated in MALT lymphoma are not well defined. In this study, we perform gene expression profiling on 35 pulmonary MALT lymphoma using fresh frozen biopsy samples Keywords: Cell type analysis and disease state analysis
2008-10-30 | GSE13314 | GEO
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.
2012-07-10 | GSE34015 | GEO
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.
2021-06-19 | E-MTAB-10479 | biostudies-arrayexpress
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
2010-08-31 | E-GEOD-23877 | biostudies-arrayexpress