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Gene expression profiling of human peripheral T cell lymphoma cases vs. reactive lymph nodes

ABSTRACT: Peripheral T cell lymphoma (PTCL) is a very aggressive disease which currently lacks efficient targeted therapy. New therapeutic strategies are needed to improve the very poor outcome of these patients. However, little is known about the molecular pathogenesis of this disease. In this study, we performed a gene expression profiling analysis of a series of 38 PTCL cases in order to find deregulated pathways or genes that could become therapeutic agents for PTCL patients.

ORGANISM(S): Homo sapiens

PROVIDER: GSE36172 | GEO | 2012/08/01

SECONDARY ACCESSION(S): PRJNA152909

REPOSITORIES: GEO

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Gene expression profiling of human peripheral T cell lymphoma cases vs. reactive lymph nodes

Project description:Peripheral T cell lymphoma (PTCL) is a very aggressive disease which currently lacks efficient targeted therapy. New therapeutic strategies are needed to improve the very poor outcome of these patients. However, little is known about the molecular pathogenesis of this disease. In this study, we performed a gene expression profiling analysis of a series of 38 PTCL cases in order to find deregulated pathways or genes that could become therapeutic agents for PTCL patients. 38 PTCL cases and 6 reactive lymph nodes were hybridized with the Universal Human Reference RNA (Stratagene, La Jolla, CA), which served as the reference sample.

2012-07-31 | E-GEOD-36172 | biostudies-arrayexpress

BCL6 expression in AITL could be transcriptionally regulated

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Gene expression changes induced by the pan-PIM inhibitor ETP-39010 in 4 peripheral T cell lymphoma cell lines

Project description:Peripheral T cell lymphoma (PTCL) is a very aggressive disease which currently lacks efficient targeted therapy. New therapeutic strategies are needed to improve the very poor outcome of these patients. In these study we hypothesized that PIM kinases could be of therapeutic value in PTCL because we found an overexpression of PIM1 and PIM2, but not PIM3, in PTCL cases, cell lines and primary tumoral T cells from Sezary Syndrome patients, compared with reactive lymph nodes and normal T cells from healthy donors, respectively. In order to understand the mechanism of action of this pan-PIM inhibitor in PTCL, 4 cell lines (DERL7, HuT78, SR786 and MyLa) were treated with 10 Î¼M of ETP-39010 for 0, 2, 4, 6, 10 and 24 h, and gene expression profiling was performed. 4 PTCL cell lines (DERL7, HuT78, SR786 and MyLa) were treated with DMSO and 10 Î¼M of the pan-PIM inhibitor ETP-39010, and hybridized using the Universal Human Reference RNA (Stratagene, La Jolla, CA) as the reference sample.

2014-11-14 | E-GEOD-42595 | biostudies-arrayexpress

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Project description:Peripheral T cell lymphoma (PTCL) is a very aggressive disease which currently lacks efficient targeted therapy. New therapeutic strategies are needed to improve the very poor outcome of these patients. In these study we hypothesized that PIM kinases could be of therapeutic value in PTCL because we found an overexpression of PIM1 and PIM2, but not PIM3, in PTCL cases, cell lines and primary tumoral T cells from Sezary Syndrome patients, compared with reactive lymph nodes and normal T cells from healthy donors, respectively. In order to understand the mechanism of action of this pan-PIM inhibitor in PTCL, 4 cell lines (DERL7, HuT78, SR786 and MyLa) were treated with 10 μM of ETP-39010 for 0, 2, 4, 6, 10 and 24 h, and gene expression profiling was performed.

2014-11-14 | GSE42595 | GEO

Transcription Profiles of Regulatory T Cells in Follicular Lymphoma Lymph Nodes, Normal Lymph Nodes and Reactive Lymph Nodes

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Lymph nodes with follicular lymphoma or reactive hyperplasia

Project description:Comparison of gene expression profiles of follicular lymphoma vs. reactive lymph nodes.

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Activating Mutation in STAT5 Is Sufficient To Drive PTCL peripheral T-Cell Lymphoma (PTCL)

Project description:Recurrent gain-of-function mutations in the transcription factor STAT5 have been detected in PTCL, an aggressive, heterogeneous disease, for which currently no targeted therapy exists. Here we investigated whether constitutive activation of STAT5 suffices to drive PTCL and whether inhibition of the JAK/STAT pathway offers a novel therapeutic opportunity in this disease. We found pronounced STAT5 expression and activity in patients from different PTCL subsets. To mimic high STAT5 activity we expressed a hyperactive STAT5A variant (termed vcS5) in the hematopoietic lineage in transgenic mice. vcS5-transgenic animals developed a lethal PTCL-like disease with full penetrance, characterized by massive expansion of CD8+ T-cells and destructive organ-infiltration. Adoptive transfer of vcS5-expressing CD8+ T-cell rapidly induced the disease in immunocompetent recipient mice. Neoplastic vcS5-T-cells displayed cytokine-hypersensitivity and showed activated, memory CD8+ T-lymphocyte characteristics. Histo-pathological analysis as well as mRNA expression profiles of vcS5 mice was closely correlated with distinct human lymphoma subtypes, including PTCL. Treatment of murine and human PTCL cell lines with the clinical JAK inhibitor Ruxolitinib or a selective STAT5 SH2 domain inhibitor induced cell death. Thus, our results demonstrate that enhanced STAT5 signaling drives PTCL development and suggest inhibition of the JAK/STAT5 pathway as a valuable therapeutic option for patients suffering from these aggressive lymphomas.

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Lymph nodes with follicular lymphoma or reactive hyperplasia

Project description:Comparison of gene expression profiles of follicular lymphoma vs. reactive lymph nodes. 8 cases of follicular lymphoma; 5 cases of reactive lymph nodes.

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Project description:EBV positive PTCL-U is a very rare but aggressive disease entity. To investigate gene expression profile, we performed gene expression analysis using two different types of microarray kits (Agilent chip 4x44K and 8x60K) We compared gene expression between in 3 EBV positive PTCL-Us and in 6 normal reactive lymph nodes.

2012-02-01 | E-GEOD-34143 | biostudies-arrayexpress

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