DNA methylation profile of Korean CLL patients and normal controls
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ABSTRACT:
PROVIDER: PRJNA564224 | ENA |
REPOSITORIES: ENA
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Project description:We performed genome-wide methylation profiling of CLL in an Asian cohort for the first time. Eight Korean patients without somatic immunoglobulin heavy chain gene hypermutations underwent methyl-CpG binding domain sequencing (MBD-seq), as did five control subjects. Gene Ontology, pathway analysis, and network-based prioritization of differentially methylated genes were also performed. We found more hypomethylated regions (2,062 windows) than hypermethylated regions (777 windows). Promoters contained the highest proportion of differentially methylated regions (DMRs; approximately 0.08%), while distal intergenic and intron regions contained the largest number of DMRs. Protein-coding genes were the most abundant, followed by long noncoding and short noncoding genes. The most significantly dysregulated signaling pathways included immune/cancer-related pathways and B-cell receptor signaling. Among the top 10 hub genes identified via network-based prioritization, four novel candidate genes (UBC, GRB2, CREBBP, and GAB2) had no known relevance to CLL while the other six (STAT3, PTPN6, SYK, STAT5B, XPO1, and ABL1) have previously been linked to CLL in Caucasians. As such, our analysis identified four novel candidate genes of potential significance to Asian patients with CLL.
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Project description:We collected monocytes from peripheral blood of 5 chronic lymphocytic leukemia (CLL) patients and 5 healthy donors and we performed gene expression analysis by microarray. Comparison of gene expression profiles (GEPs) between CLL-derived and normal monocytes was used to discover molecular abnormalities in this nonmalignant immune cellular population in leukemia-bearing patients. Although analysed cells were not part of the malignant clone, in unsupervised hierarchical clustering analysis, GEPs of normal monocytes were clearly distinguishable from those of monocytes obtained from CLL patients. Supervised analysis identified 65 genes significantly up-regulated and 48 genes down-regulated in CLL monocytes compared with monocytes from normal controls (FC=2, p<0.05). Modification of gene expression profile would imply impairment of phagocytosis and production of immunosuppressive mediators in CLL-derived monocytes. The alterations described in our study further contribute to characterize the complexity of factors potentially involved in acquired immune deficiency of CLL patients.
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Project description:We collected monocytes from peripheral blood of 5 chronic lymphocytic leukemia (CLL) patients and 5 healthy donors and we performed gene expression analysis by microarray. Comparison of gene expression profiles (GEPs) between CLL-derived and normal monocytes was used to discover molecular abnormalities in this nonmalignant immune cellular population in leukemia-bearing patients. Although analysed cells were not part of the malignant clone, in unsupervised hierarchical clustering analysis, GEPs of normal monocytes were clearly distinguishable from those of monocytes obtained from CLL patients. Supervised analysis identified 65 genes significantly up-regulated and 48 genes down-regulated in CLL monocytes compared with monocytes from normal controls (FC=2, p<0.05). Modification of gene expression profile would imply impairment of phagocytosis and production of immunosuppressive mediators in CLL-derived monocytes. The alterations described in our study further contribute to characterize the complexity of factors potentially involved in acquired immune deficiency of CLL patients. Large-scale gene expression profiling (GEP) was performed on total RNA extracted from purified CD14+ monocytes (RNeasy Mini kit Plus, QIAGEN, Valencia, CA, USA) isolated from 5 individual CLL patients and 5 healthy controls by hybridization on 4X44K Whole Human Genome Microarray (Agilent Technologies, Palo alto, CA). Fluorescence data were analysed with Feature Extraction Software v.10.5 (Agilent Technologies) an QC Chart tool v.1.3. Agglomerative two-dimensional clustering analysis and supervised analyses based on t-test were performed using Gene Spring GX (Agilent) software. Genes were defined as differentially expressed between groups at a significant level of p<0.05 and with a fold change cut off ± 2 in all the pair wise comparisons.
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Project description:In the present study, the methylation profiling (MeDIP) was carried out in 14 treatment-naive, early stage (Rai stage 0-2) CLL patients and pooled 19+ normal controls. To find an association of methylation with IGHV mutation status, CLL patients were further segregated into IGHV unmutated (n=9) and IGHV mutated (n=5) subgroups. The methylation signature obtained for CLL versus nornal controls and; unmutated versus mutated CLL was integrated with gene expression profile of these patients and the results were correlated with clinical outcome.
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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.
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