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Matrix metalloproteinase-9 in chronic lymphocytic leukemia

ABSTRACT: Chronic lymphocytic leukemia (CLL) is characterized by the accumulation of malignant CD5+ B lymphocytes (CLL cells) in the peripheral blood, and their progressive infiltration in lymphoid organs. MMP-9 plays an important role in cell migration and survival, contributes to CLL pathogenesis by proteolytic and non-proteolytic mechanisms and may constitutive a therapeutic target. We used Affimetrix microarray technology to characterize the global gene expression profile of chronic lymphocytic leukemia (CLL) cells upon MMP-9 transfection. The aim was to establish whether MMP-9 regulates gene expression and to identify new therapeutic targets in CLL.

ORGANISM(S): Homo sapiens

PROVIDER: GSE78174 | GEO | 2016/03/21

SECONDARY ACCESSION(S): PRJNA312827

REPOSITORIES: GEO

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Regulation of gene expression in chronic lymphocytic leukemia cells in response to arsenic trioxide.

Project description:Chronic lymphocytic leukemia (CLL) is characterized by the accumulation of malignant CD5+ B lymphocytes (CLL cells) in the peripheral blood, and their progressive infiltration in lymphoid organs. Despite the efforts made, CLL remains an incurable disease. It is therefore crucial to continue searching for new therapeutic agents and targets. Arsenic trioxide (ATO) induces apoptosis in all CLL cases and it could constitute an efficient therapy for this disease. We used Affimetrix microarray technology to characterize the global gene expression profile underlying CLL cell response to ATO, with the aim of identifying the ATO mechanism of action as well as new therapeutic targets in CLL.

2016-03-21 | GSE78207 | GEO

Nanda2013 - B cell chronic lymphocytic leukemia A model with immune response

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2020-01-09 | MODEL2001090002 | BioModels

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2023-05-03 | GSE227678 | GEO

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CLL intraclonal fractions exhibit established and recently-acquired patterns of DNA methylation [GE]

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Cellular Origin and Pathophysiology of Chronic Lymphocytic Leukemia

Project description:The cellular origin of chronic lymphocytic leukemia (CLL) is debated. Transcriptome analysis of CLL and normal peripheral blood and splenic B cell subsets displayed highest similarity of CLL to mature CD5+ B cells. We identified a distinct CD5+CD27+ post-germinal center B cell subset, and revealed that immunoglobulin V gene mutated CLL are more similar to mutated CD5+ B cells, whereas unmutated CLL are more related to unmutated CD5+ B cells. Stereotyped immunoglobulin V gene rearrangements were significantly enriched among CD5+ B cells, providing further genetic evidence for a derivation of CLL from CD5+ B cells. Moreover, we identified deregulated expression patterns providing novel insights into the pathophysiology of CLL, including downregulation of EBF1 and KLF family members. Transcriptome profiling of CLL and healthy human blood and splenic mature B cell subsets. Identification of deregulated transcription patterns with implications on CLL pathobiology. Human mature B cell subsets and CLL with mutated (mCLL) and unmutated V gene status (uCLL) were purified from peripheral blood and spleen. Samples of 5 to 7 donors each were collected and processed in three batches in a two rounded in vitro transcription protocol. Retrieved data were batch corrected and subjected to analysis. Human mature CD5+ B cell subsets and CLL with mutated (mCLL) and unmutated V gene status (uCLL) were purified from peripheral blood.

2012-09-27 | E-GEOD-36907 | biostudies-arrayexpress

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Project description:B cell chronic lymphocytic leukemia (CLL) is often preceded by a benign monoclonal or oligoclonal CD5+ B cell lymphocytosis. We have generated transgenic mice expressing a catalytically inactive, dominant-negative recombination activating gene 1 (dnRAG1 mice) in the periphery. These animals develop an early-onset indolent CD5+ B cell lymphocytosis, caused in part by a defect in secondary V(D)J rearrangements initiated to alter autoreactive B cell receptor specificity. Hypothesizing that the CD5+ B cells accumulating in dnRAG1 mice represent a CLL precursor, we crossed dnRAG1 mice with CLL-prone Eµ-TCL1 mice to determine whether dnRAG1 expression in Eµ-TCL1 mice accelerates the onset of CLL-like disease. We find that CD5+ B cell expansion and CLL progression occurs more rapidly and uniformly in double-transgenic mice (DTG mice) compared to Eµ-TCL1 mice, but with similar phenotypic and leukemogenic features. To gain insight into genes or pathways responsible for CD5+ B cell accumulation in the transgenic mice, we performed comparative gene expression profiling studies using normal and CD5+ B cells isolated from wild-type and transgenic mice at either 12 weeks of age (pre-leukemia) or at CLL onset in DTG mice (using age-matched wild-type and single-transgenic mice as controls). These analyses confirm the upregulation of tolerogenic genes in CD5+ B cells and reveal a possible role for prolactin signaling in the regulation of receptor editing. This study suggests that a failure to remodel B cell antigen receptor genes in response to autoreactivity may promote the benign accumulation of CD5+ B cells, which may then be subjected to secondary genetic lesions that promote CLL progression.

2013-06-04 | GSE44940 | GEO

MiR-181b is a biomarker of disease progression in Chronic Lymphocytic Leukemia

Project description:We studied the value of the microRNAs as a signature for Chronic lymphocytic leukemia (CLL) patients with specific chromosomal abnormalities. We found that MiR-181b is abiomarker of disease progression in Chronic Lymphocytic Leukemia

2011-09-22 | E-MTAB-683 | biostudies-arrayexpress

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2009-12-16 | GSE19458 | GEO

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Project description:In human chronic lymphocytic leukemia (CLL) pathogenesis B cell antigen receptor signaling seems important for leukemia B cell ontogeny, whereas the microenvironment influences B cell activation, tumor cell lodging and provision of antigenic stimuli. Using the murine E?-Tcl1 CLL model, we demonstrate that CXCR5-controlled access to follicular dendritic cells (FDCs) confers proliferative stimuli to leukemia B cells. Intravital imaging revealed a marginal zone B cell-like leukemia cell trafficking route. Murine and human CLL cells reciprocally stimulated resident mesenchymal stromal cells through lymphotoxin-?-receptor activation, resulting in CXCL13 secretion and stromal compartment remodeling. Inhibition of lymphotoxin/lymphotoxin-?-receptor signaling or of CXCR5 signaling retards leukemia progression. Thus, CXCR5 activity links tumor cell homing, shaping a survival niche, and access to localized proliferation stimuli. This GEO dataset is comprised of GEP measurements for EµTCL mouse CD5+CD19+ tumor cells and healthy WT controls, including healthy MZB cells and B1 cells. 6 measurements are for WT EµTCL1 mice, 5 for the CXCR5-KO EµTCL1 genotype. MZB and B1 cells were pooled from 15 animals. WT reference was obtained from 5 WT animals

2014-09-01 | E-GEOD-60925 | biostudies-arrayexpress

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