Homo sapiens strain:PBL1
Ontology highlight
ABSTRACT:
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| DRR063230.fastq.gz | Fastqsanger.gz | |||
| DRR063231.fastq.gz | Fastqsanger.gz |
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Project description:Plasmablastic lymphoma is a high grade B cell lymphoma with plasmablastic morphology and a terminally differentiated B cell immunophenotype, usually arising in the setting of immunodeficiency and often demonstrating Epstein Barr Virus positivity. The molecular and genetic mechanisms underlying the pathogenesis of PBL are largely unknown. To better understand its pathogenesis, herein we have analyzed global gene expression of PBL and compared that to gene expression profiles of diffuse large B cell lymphoma. While overlaps in transcriptomes between these malignancies were identified, we have shown that the gene expression profile of plasmablastic lymphoma is distinct, demonstrating striking downregulation of B cell receptor signaling genes, BCL6, BCL11A SPI-B, targets of NFKB1, and upregulation of mitochondrial genes, PRMT5, MYC and MYC targets and IL21, implicating these alterations in the pathogenesis of this lymphoma. In addition we show the usefulness of SWAP-70 immunohistochemistry in the differentiation of immunoblastic diffuse large B cell lymphoma and plasmablastic lymphoma. Our findings provide justification for considering plasmablastic lymphoma as a specific lymphoma entity and provide insight into the unique transcriptional aberrations occurring in this high-grade lymphoma.
2015-09-15 | GSE53117 | GEO
Project description:Plasmablastic lymphoma is a high grade B cell lymphoma with plasmablastic morphology and a terminally differentiated B cell immunophenotype, usually arising in the setting of immunodeficiency and often demonstrating Epstein Barr Virus positivity. The molecular and genetic mechanisms underlying the pathogenesis of PBL are largely unknown. To better understand its pathogenesis, herein we have analyzed global gene expression of PBL and compared that to gene expression profiles of diffuse large B cell lymphoma. While overlaps in transcriptomes between these malignancies were identified, we have shown that the gene expression profile of plasmablastic lymphoma is distinct, demonstrating striking downregulation of B cell receptor signaling genes, BCL6, BCL11A SPI-B, targets of NFKB1, and upregulation of mitochondrial genes, PRMT5, MYC and MYC targets and IL21, implicating these alterations in the pathogenesis of this lymphoma. In addition we show the usefulness of SWAP-70 immunohistochemistry in the differentiation of immunoblastic diffuse large B cell lymphoma and plasmablastic lymphoma. Our findings provide justification for considering plasmablastic lymphoma as a specific lymphoma entity and provide insight into the unique transcriptional aberrations occurring in this high-grade lymphoma. Expression profiles of 15 plasmablastic lymphomas and 10 diffuse large B-cell lymphomas were obtained using Afymmetrix U133A2 microarrays.
2015-09-15 | E-GEOD-53117 | biostudies-arrayexpress
Project description:Primary mediastinal B-cell lymphoma (PMBL) and classical Hodgkin lymphoma (cHL) share a frequent constitutive activation of Janus-activated kinase (JAK) / signal transducer and activator of transcription (STAT) signaling pathway. Due to complex non-linear relations within the pathway, key dynamic properties remained to be identified to predict possible strategies for intervention. To untangle these features, we used dynamic pathway modeling that employs model development and calibration based on extensive quantitative data generation. Quantitative data were collected on JAK/STAT pathway signaling components in two lymphoma-derived cell lines, MedB-1 and L1236, representative of PMBL and cHL, respectively. We showed that the amounts of STAT5 and STAT6 are higher whereas the amount of SHP1 is lower in the two lymphoma cell lines compared to B cells from healthy donors. Distinctively, L1236 cells harbor more JAK2 and less SHP1 molecules per cell than MedB-1 or control cells. In our experimental setting interleukin-13 (IL13) stimulation levels remained constant over time. In MedB-1 cells surface IL13 receptor alpha 2 had a strong IL13-sequestering/decoy function. In both lymphoma cell lines we observed IL13-induced activation of interleukin-4 receptor alpha, JAK2 and STAT5, but not of STAT6, which was highly phosphorylated even without stimulus. Furthermore, the known STAT-inducible negative regulators CISH and SOCS3 were up-regulated within 2 hours in MedB-1 but not in L1236 cells. Global transcription profiling revealed 11 early and 16 sustained common genes up-regulated by IL13 in both lymphoma cell lines. Based on this detailed information we established two individual mathematical models, MedB-1 and L1236 model, which were able to describe the respective experimental data. Sensitivity analysis of the model identified six possible therapeutic targets able to reduce gene expression levels in L1236 cells and three in MedB-1 cells. By inhibition of STAT5 phosphorylation we successfully validated one of the predicted targets demonstrating the potential of the approach in guiding target identification for highly deregulated signaling networks in cancer cells. We established mathematical models of the JAK/STAT pathway in two lymphoma cell types (PMBL and cHL), able to reproduce experimental data and to predict possible therapeutic targets. Cells from two lymphoma-derived cell lines, MedB-1 and L1236, were used for a time-course microarray analysis comprising stimulations with IL13 for 0, 0.5, 1, 1.5, 2, 3, 4, 6, 8, 12 h and unstimulated controls (0, 0.5, 1, 1.5, 2, 3, 4, 6, 8, 12 h), for a total of 20 microarrays per cell line.
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Project description:Plasmablastic lymphoma is an aggressive B-cell lymphoma with an immunoblastic/large cell morphology anda plasmacytic differentiation. The differential diagnosis with Burkitt lymphoma, plasma cell myeloma and some variants of diffuse large B-cell lymphoma may be challenging due to the overlapping morphological, genetic and immunophenotypic features. Furthermore, the profile of chromosomal alterations is not well known.
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Project description:Primary mediastinal B-cell lymphoma (PMBL) and classical Hodgkin lymphoma (cHL) share a frequent constitutive activation of Janus-activated kinase (JAK) / signal transducer and activator of transcription (STAT) signaling pathway. Due to complex non-linear relations within the pathway, key dynamic properties remained to be identified to predict possible strategies for intervention. To untangle these features, we used dynamic pathway modeling that employs model development and calibration based on extensive quantitative data generation. Quantitative data were collected on JAK/STAT pathway signaling components in two lymphoma-derived cell lines, MedB-1 and L1236, representative of PMBL and cHL, respectively. We showed that the amounts of STAT5 and STAT6 are higher whereas the amount of SHP1 is lower in the two lymphoma cell lines compared to B cells from healthy donors. Distinctively, L1236 cells harbor more JAK2 and less SHP1 molecules per cell than MedB-1 or control cells. In our experimental setting interleukin-13 (IL13) stimulation levels remained constant over time. In MedB-1 cells surface IL13 receptor alpha 2 had a strong IL13-sequestering/decoy function. In both lymphoma cell lines we observed IL13-induced activation of interleukin-4 receptor alpha, JAK2 and STAT5, but not of STAT6, which was highly phosphorylated even without stimulus. Furthermore, the known STAT-inducible negative regulators CISH and SOCS3 were up-regulated within 2 hours in MedB-1 but not in L1236 cells. Global transcription profiling revealed 11 early and 16 sustained common genes up-regulated by IL13 in both lymphoma cell lines. Based on this detailed information we established two individual mathematical models, MedB-1 and L1236 model, which were able to describe the respective experimental data. Sensitivity analysis of the model identified six possible therapeutic targets able to reduce gene expression levels in L1236 cells and three in MedB-1 cells. By inhibition of STAT5 phosphorylation we successfully validated one of the predicted targets demonstrating the potential of the approach in guiding target identification for highly deregulated signaling networks in cancer cells. We established mathematical models of the JAK/STAT pathway in two lymphoma cell types (PMBL and cHL), able to reproduce experimental data and to predict possible therapeutic targets.
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Project description:We produced and analyzed the transcriptomic profiles of agressive plasmablastic lymphomas to describe their "immune escape" profile, depending on their viral status (HIV, EBV, ...). We used microarrays to compare the global gene expression profile between EBV+ and EBV- PL subtypes. This analysis unveiled the interest of treating EBV+ PL patients by immune checkpoint blockade strategies. Plasmablastic lymphoma (PL) is a subtype of diffuse large B-cell lymphoma occurring frequently in HIV-positive individuals and most often associated with Epstein Barr Virus infection. Despite recent therapeutic progress, PL still is an aggressive lymphoma with adverse prognosis. The aim of this study was to investigate whether the emerging strategies of immune checkpoint blockade could be efficient for PL patients. Here, we produced and analyzed the transcriptomic profiles of such tumors to address this question. Unsupervised hierarchical analysis of PL samples showed that PL segregated according to their EBV-status. Moreover, we report that EBV+ PL displayed a significant association with abundant leucocyte infiltrate and selective T-cell activation signatures, together with high level of inhibitory receptors and immune checkpoint markers. We propose that EBV infection induced an anti-viral cytotoxic immunity which progressively exhausted and promoted the tolerogenic tumor microenvironment of PL. Hence, most EBV+ PL patients presenting an early stage of cancer immune-editing process appear eligible for ICB immunotherapies.
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