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Array comparative genomic hybridization data from 313 CLL specimens to study outcome associations

ABSTRACT: This study investigates genomic imbalance in chronic lymphocytic leukemia (CLL) and aims to identify genomic gains and losses with prognostic significance. Two-condition experiment, Test CLL specimens vs. Reference human genome DNA equimixture of normal male and normal female.

ORGANISM(S): Homo sapiens

SUBMITTER: Jane Houldsworth

PROVIDER: E-GEOD-40834 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Array comparative genomic hybridization data from 313 CLL specimens to study outcome associations

Project description:This study investigates genomic imbalance in chronic lymphocytic leukemia (CLL) and aims to identify genomic gains and losses with prognostic significance.

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Project description:Genome-wide profiling of histone 3 lysine 4 trimethylation is used for identification of microRNA transcriptional start sites. Various cell types allow a broad range detection of putative promoters rather independent of tissue specific expression patterns. These data are used for identification of aberrant epigenetic regulation at the respective regions. 5 samples total: 1 primary CLL sample, 1 CLL related cell line -/+ 5-aza-2M-bM-^@M-^Y-deoxycytidine (DAC) treatment (Granta-519), myeloid cell line Kasumi-1 (-/+ 5-aza-2M-bM-^@M-^Y-deoxycytidine treatment); H3K4me3 enriched vs. Input

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Project description:Genome-wide profiling of histone 3 lysine 4 trimethylation is used for identification of microRNA transcriptional start sites. Various cell types allow a broad range detection of putative promoters rather independent of tissue specific expression patterns. These data are used for identification of aberrant epigenetic regulation at the respective regions. 11 samples total: 3 primary B-cell samples (1 chronic lymphocytic leukemia [CLL] and 2 healthy controls), 2 CLL related cell lines -/+ 5-aza-2M-bM-^@M-^Y-deoxycytidine (DAC) treatment (Mec-1, EHEB), T-lymphoid cell line JURKAT, myeloid cell line HL-60, colon cancer cell line HCT-116 wild type and double knock out; H3K4me3 enriched vs. input

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T-Cells from CLL patients

Project description:T cells may have a role in sustaining the leukemic clone in chronic lymphocytic leukemia (CLL). In this study, we have examined the ability of T cells from CLL patients to support the survival of the leukemic B cells in vitro. Additionally, we compared global gene expression of T cells from indolent CLL patients with healthy individuals and multiple myeloma (MM) patients. Apoptosis of purified CLL cells was inhibited in vitro when cocultured with increasing numbers of autologous T cells (p<0.01) but not with normal donors. The anti-apoptotic effect exceeded that of the antiapoptotic cytokine IL-4 (p=0.02) and was greater with CD8+ T cells than with CD4+ cells (p<0.05). The effect depended mainly on cell-cell contact although a significant effect was observed in transwell experiments (p<0.05). Additionally, about 356 genes involved in different cellular pathways were deregulated in T cells of CLL patients compared to healthy individuals and MM patients. The results of gene expression profiling was verified for 7 genes (KLF6, TRAF1, CCL4, CCL5, RANTES, XCL1 and XCL2) using qRT-PCR and immunoblotting. Our results demonstrate that CLL-derived T cells can prevent apoptosis of leukemic cells and have altered expression of genes that may facilitate survival of the leukemic clone. Peripheral blood was collected by venipuncture from CLL patients, multiple myeloma (MM) patients and age-matched healthy individuals with informed consent and approval of the local Ethics Committee in keeping with the Helsinki declaration on the use of human subjects for research.

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The proto-oncogene TCL1A deregulates mitotic checkpoint transition and genomic stability in CLL

Project description:Upregulation of the proto-oncogene TCL1A is causally implicated in various B- and T-cell malignancies. High-level TCL1A correlates with aggressive disease features and inferior clinical outcomes. However, molecular and cell-biological consequences of TCL1A dysregulation are not fully elucidated. Here, we identify CDC20 and other molecules of the safeguarding cell cycle checkpoints as novel TCL1A-interactors. In different model systems of B-cell leukemia/lymphoma, TCL1A overexpression accelerated cell cycle transition, impaired apoptotic damage responses in association with pronounced chromosome mis-segregation and caused cellular aneuploidy. In primary CLL samples, low CDC20 expression correlated with high expression of TCL1A and more aggressive disease characteristics. In line, a low CDC20 expression was a marker for reduced progression-free survival in CLL patients. Finally, knockdown of CDC20 in TCL1A-initiated murine lymphomas promoted chromosome disbalances and leukemia outgrowth. Overall, we discovered a cell-cycle associated effect of TCL1A by interfering with a proficient cell cycle transition. This adds to our concept of TCL1A’s transforming impact by targeting genome stability.

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