Methylation Profiling of Splenic Marginal Zone Lymphomas
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ABSTRACT:
ORGANISM(S): Homo sapiens
SUBMITTER: helen Parker
PROVIDER: E-MTAB-15791 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
Similar Datasets
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: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
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. One hundred fourteen patients were included in this study: 46 MALT lymphomas (22 pulmonary, 11 salivary glands, 7 lacrimal glands and 6 gastrointestinal), 35 splenic marginal zone lymphomas, 20 nodal marginal zone lymphomas and 13 non-Waldenström’s Macroglobulinemia lymphoplasmacytic lymphomas. All cases were reviewed prior to study on paraffin sections with immunohistochemistry. Sections of each frozen tissue used for study were also reviewed by histological examination and immunohistochemistry before was submitted for the study.
2012-01-24 | E-GEOD-35278 | biostudies-arrayexpress
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:Array-based comparative genomic hybridization comparing splenic marginal zone lymphoma (SMZL) specimens with control DNA A custom high-definition oligonucleotide microarray (4x44K, Agilent) was designed for aCGH from the online application tool eArray (version 5.3) and HD-CGH probe library (sequence source UCSC hg18 / NCBI Build 36). This custom microarray combines the capability to scan human genome-wide with an average resolution of approximately 100 Kb and to focus on regions of interest for highest resolution tiling (11 Kb-resolution for either chromosomes 3q and 7q). The array contains about 8,500 and 9,000 oligonucleotides spanning 97 Mb and 105 Mb of the 7q and the 3q chromosomes respectively. Twenty-seven SMZL specimens (9 males, 18 females) were analyzed using a dye-swap methodology to confirm the copy number variations. Two samples (one male, one female, namely M-CTRL and F-CTRL) collected from healthy volunteers blood from national Etablissement FranM-CM-'ais du Sang were used as DNA reference for aCGH experiments.
2014-01-01 | E-GEOD-34768 | biostudies-arrayexpress
Project description:RNA microarray profiling analysis was performed on different ex-vivo human splenic B cell subsets (M-^SNaM-oveM-^T, marginal zone precursors or M-^SMZPM-^T, marginal zone B cells orM-^T MZBM-^T, M-^SMTG+CD45+M-^T cells) and on M-^Sp27M-^T cells, corresponding to the fraction of MZP cells that differentiated into CD27-expressing cells after culture on OP9-hDLL1 cells cultured with OP9-hDLL1 cells that differentiated into CD27-expressing cells
2014-03-26 | E-MTAB-2244 | 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 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: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:A single cell RNA-Seq study of splenic marginal zone lymphomas (SMZL)
| PRJNA733659 | ENA