A single cell RNA-Seq 5’ study of splenic marginal zone lymphomas (SMZL) and spleen healthy donors
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PROVIDER: PRJNA947155 | ENA |
REPOSITORIES: ENA
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Project description:Purpose: Single cell RNA-Seq was used to characterize in depth splenic samples obtained from splenic marginal zone lymphomas Methods: 3 frozen samples of spleen and blood from SMZL patients, and healthy donors were selected and thawed for performing a 10X genomics single cell RNA-Sequencing 5' assay. Results: Tumor cells formed mainly patient specific-B cell clusters, while T-cells from the 3 patients and healthy donors clustered together. Conclusion: Single RNA-Seq unveils inter- and intra-patient heterogeneity.
2024-09-17 | GSE227833 | GEO
Project description:Purpose: Spatial transcriptomics was used to characterize in depth splenic samples obtained from splenic marginal zone lymphomas Methods: 4 frozen samples of spleen from SMZL patients, and 1 healthy donor were selected and thawed for performing a 10X genomics Visium Spatial assay. Results: Tumor cells formed mainly patient specific-B cell clusters, while T-cells from the 3 patients and healthy donors clustered together. Conclusion: Single RNA-Seq unveils inter- and intra-patient heterogeneity.
2024-09-17 | GSE228056 | GEO
Project description:Purpose: Single cell RNA-Seq was used to characterize in depth splenic samples obtained from splenic marginal zone lymphomas Methods: 3 frozen samples of spleen from SMZL patients were selected and thawed for performing a 10X genomics single cell RNA-Sequencing 3' assay. Results: Tumor cells formed mainly patient specific-B cell clusters, while T-cells from the 3 patients clustered together. Conclusion: Single RNA-Seq unveils the cellular composition of splenic tumors from SMZL patients.
2021-10-31 | GSE175785 | GEO
Project description:Splenic marginal zone lymphoma (SMZL) is a rare chronic B lymphoproliferative disease, whose molecular pathogenesis is still not well established. For the first time a proteomic approach was undertaken to analyse the protein profiles of SMZL tissue. Western blot, immunohistochemical analysis and functional data mining were also performed in order to validate results, classify proteins, and explore their potential relationships. We demonstrated that SMZL is characterized by modulation of proteins related to energetic metabolism and apoptosis pathways. We also reported specific proteins (such as biliverdin reductase A, manganese superoxide dismutase, beta-2 microglobulin, growth factor receptor-bound protein 2, acidic leucine-rich nuclear phosphoprotein 32 family member A, and SET nuclear oncogene) directly involved in NF-kBand BCR pathways, as well as in chromatin remodelling and cytoskeleton. Our findings shed new light on SMZL pathogenesis and provide a basis for the future development of novel biomarkers.
2015-04-23 | PXD001124 | Pride
Project description:Array-based comparative genomic hybridization comparing splenic marginal zone lymphoma (SMZL) specimens with control DNA
2014-01-01 | GSE34768 | GEO
Project description:A spatial transcriptomics study of splenic marginal zone lymphomas (SMZL) and spleen healthy donor
| PRJNA947959 | ENA
Project description:A single cell RNA-Seq study of splenic marginal zone lymphomas (SMZL)
| PRJNA733659 | ENA
Project description:Unique and shared cytogenetic abnormalities have been documented for marginal zone lymphomas (MZLs) arising at different sites. Recently, homozygous deletions of the chromosomal band 6q23, involving the tumor necrosis factor alpha-induced protein 3 (TNFAIP3, A20) gene, a negative regulator of NF-kappa B, were described in ocular adnexal MZL, suggesting a role for A20 as a tumor suppressor in this disease entity. Here, we investigated inactivation of A20 by DNA mutations or deletions in a panel of extranodal (EMZL), nodal (NMZL) and splenic (SMZL) MZLs. Inactivating mutations encoding truncated A20 proteins were identified in 6/32 (18.8%) MZLs, including 3/11 (27.3%) EMZLs, 2/9 (22.2%) NMZLs, and 1/12 (8.3%) SMZLs. Two additional unmutated non-splenic MZLs also showed mono- or biallelic A20 deletions by FISH and/or array-CGH. Thus, A20 loss by both somatic mutations and/or deletions represents a common genetic aberration across all MZL subtypes, which may contribute to lymphomagenesis by inducing constitutive NF-kappa B activation. Keywords: Genome variation profiling by SNP array 27 MZL samples. No technical replications.
2009-04-01 | E-GEOD-13989 | biostudies-arrayexpress
Project description:Unique and shared cytogenetic abnormalities have been documented for marginal zone lymphomas (MZLs) arising at different sites. Recently, homozygous deletions of the chromosomal band 6q23, involving the tumor necrosis factor alpha-induced protein 3 (TNFAIP3, A20) gene, a negative regulator of NF-kappa B, were described in ocular adnexal MZL, suggesting a role for A20 as a tumor suppressor in this disease entity. Here, we investigated inactivation of A20 by DNA mutations or deletions in a panel of extranodal (EMZL), nodal (NMZL) and splenic (SMZL) MZLs. Inactivating mutations encoding truncated A20 proteins were identified in 6/32 (18.8%) MZLs, including 3/11 (27.3%) EMZLs, 2/9 (22.2%) NMZLs, and 1/12 (8.3%) SMZLs. Two additional unmutated non-splenic MZLs also showed mono- or biallelic A20 deletions by FISH and/or array-CGH. Thus, A20 loss by both somatic mutations and/or deletions represents a common genetic aberration across all MZL subtypes, which may contribute to lymphomagenesis by inducing constitutive NF-kappa B activation. Keywords: Genome variation profiling by SNP array
2009-04-01 | GSE13989 | GEO
Project description:Lymphoplasmacytic lymphomas and marginal zone lymphomas of nodal, extra-nodal and splenic types account for 10% of non-Hodgkin lymphomas. They are similar at the cell differentiation level, sometimes making difficult to distinguish them from other indolent non-Hodgkin lymphomas. To better characterize their genetic basis, we performed array-based comparative genomic hybridization in 101 marginal zone lymphomas (46 MALT, 35 splenic and 20 nodal marginal zone lymphomas) and 13 lymphoplasmacytic lymphomas. Overall, 90.1% exhibited copy-number abnormalities. Lymphoplasmacytic lymphomas demonstrated the most complex karyotype (median=7 copy-number abnormalities), followed by MALT (4), nodal (3.5) and splenic marginal zone lymphomas (3). A comparative analysis exposed a group of copy-number abnormalities shared by several or all the entities with few disease-specific abnormalities. Gain of chromosomes 3, 12 and 18 and loss of 6q23-q24 (TNFAIP3) were identified in all entities. Losses of 13q14.3 (MIRN15A-MIRN16-1) and 17p13.3-p12 (TP53) were found in lymphoplasmacytic and splenic marginal zone lymphomas; loss of 11q21-q22 (ATM) in nodal, splenic marginal zone and lymphoplasmacytic lymphomas; loss of 7q32.1-q33 in MALT, splenic and lymphoplasmacytic lymphomas. Abnormalities affecting the NF-kB pathway were observed in 70% of MALT and lymphoplasmacytic lymphomas and 30% of splenic and nodal marginal zone lymphomas, suggesting distinct roles of this pathway in the pathogenesis/progression of these subtypes. Elucidation of the genetic alterations contributing to the pathogenesis of these lymphomas may guide to design specific therapeutic approaches.
2012-01-24 | GSE35278 | GEO