scholarly journals Characterization of DNA methylation and its association with other biological systems in lymphoblastoid cell lines

Genomics ◽  
2012 ◽  
Vol 99 (4) ◽  
pp. 209-219 ◽  
Author(s):  
Zhe Zhang ◽  
Jinglan Liu ◽  
Maninder Kaur ◽  
Ian D. Krantz
Keyword(s):  
Dna Methylation ◽  
Cell Lines ◽  
Biological Systems ◽  
Lymphoblastoid Cell Lines

Serologic Characterization of the Reference Panel of B-Lymphoblastoid Cell Lines for Factors of the HLA System

1989 ◽  
pp. 19-38 ◽  
Author(s):  
E. L. Milford ◽  
L. J. Kennedy ◽  
S. Y. Yang ◽  
B. Dupont ◽  
J.-M. Lalouel ◽  
...  
Keyword(s):  
Cell Lines ◽  
Reference Panel ◽  
Lymphoblastoid Cell Lines ◽  
Hla System

Characterization of two newly established EBV-containing lymphoblastoid cell lines from patients with myeloid leukemias

1990 ◽  
Vol 14 (4) ◽  
pp. 309-320 ◽  
Author(s):  
Yu-Sun Chang ◽  
Lee-Yung Shih ◽  
Chen-Lee Peng ◽  
Shih-Hsiung Chen ◽  
Shih-Tung Liu
Keyword(s):  
Cell Lines ◽  
Lymphoblastoid Cell Lines ◽  
Myeloid Leukemias

Cloning and Characterization of EphA3 (Hek) Gene Promoter: DNA Methylation Regulates Expression in Hematopoietic Tumor Cells

Blood ◽  
1999 ◽  
Vol 94 (7) ◽  
pp. 2477-2486 ◽  
Author(s):  
Mirella Dottori ◽  
Michelle Down ◽  
Andreas Hüttmann ◽  
David R. Fitzpatrick ◽  
Andrew W. Boyd
Keyword(s):  
Dna Methylation ◽  
Cell Lines ◽  
Tyrosine Kinases ◽  
Expression Patterns ◽  
Gene Promoter ◽  
Restriction Enzymes ◽  
Clinical Samples ◽  
Cpg Dinucleotides ◽  
Normal Tissues

The Eph family of receptor tyrosine kinases (RTK) has restricted temporal and spatial expression patterns during development, and several members are also found to be upregulated in tumors. Very little is known of the promoter elements or regulatory factors required for expression of Eph RTK genes. In this report we describe the identification and characterization of the EphA3 gene promoter region. A region of 86 bp located at −348 bp to −262 bp upstream from the transcription start site was identified as the basal promoter. This region was shown to be active in both EphA3-expressing and -nonexpressing cell lines, contrasting with the widely different levels of EphA3 expression. We noted a region rich in CpG dinucleotides downstream of the basal promoter. Using Southern blot analyses with methylation-sensitive restriction enzymes and bisulfite sequencing of genomic DNA, sites of DNA methylation were identified in hematopoietic cell lines which correlated with their levels of EphA3 gene expression. We showed that EphA3 was not methylated in normal tissues but that a subset of clinical samples from leukemia patients showed extensive methylation, similar to that observed in cell lines. These results suggest that DNA methylation may be an important mechanism regulating EphA3 transcription in hematopoietic tumors.

Genome Wide DNA Methylation Profiling In Patients with Multiple Myeloma.

Blood ◽  
2010 ◽  
Vol 116 (21) ◽  
pp. 3622-3622
Author(s):  
Yang Liu ◽  
Shenghua Duan ◽  
Xavier Leleu ◽  
Yong Zhang ◽  
Abdel Kareem A. Azab ◽  
...  
Keyword(s):  
Dna Methylation ◽  
Bone Marrow ◽  
Cell Lines ◽  
Promoter Region ◽  
Genomic Dna ◽  
Research Funding ◽  
Plasma Cells ◽  
Genome Wide

Abstract Abstract 3622 Introduction: Epigenetic factors such as DNA methylation have been shown to play a crucial role in the pathogenesis and progression of multiple myeloma (MM), yet studies of DNA methylation in MM are still limited. Therefore, in order to better understand the role of DNA methylation and identify specific genes that may be affected by differential methylation in MM patients, we conducted genome-wide DNA methylation profiling in cd138+ plasma cells purified from bone marrow of the patients with MM and normal donors. Methods: Genomic DNA of CD138+ Plasma cell selected from both MM patients and normal primary bone marrow was extracted using QIAGEN genome isolation kit. Following extraction, methylated DNA was isolated by Chip and hybridized to Affymetrix Human 2.0 tiling arrays. Chip assay and array hybridization was performed by Genepathway Inc. CEL files were processed and normalized using the MAT program, and methylation peaks were called from the resulting MAT scores using a custom segmentation method. Peak annotation and characterization of different genomic regions was done with custom tools and using genome annotation files from the UCSC genome database. All peaks were visualized by IGB online software. Medip-PCR was done in human MM cell lines to validate the methylation status. Methylated gene expression was determined by both Semi-quantitative PCR and real-time PCR. 5′aza was used for demethylation in human MM cell lines. Methylated gene expression with or without 5′aza treatment was determined by both Semi-quantitative PCR and real-time PCR. Results: Genomic DNA from CD138+ plasma cells from bone marrow of MM patients showed a significant increase in methylation levels compared to normal controls. We demonstrated that the hypermethylated sites were distributed across the genome in the following proportions: 3.2% in the promoter region; 45.6% in the intragenic region; 5.4 % in the 3′ end region; and 46.8 % in the intergenic region. Furthermore, around 9 % promoter CpG islands (CGIs); 11% intragenic CGIs; 15 % CGIs in 3′end region; and 14.3 % intergenic CGIs of patients genomic DNA were methylated. Moreover 2.1% promoter CGIs; 2.3 % intragenic CGIs; 2.5% CGIs in 3′end region; and 4.7% intergenic CGIs were methylated for the normal control. Medip-PCR showed that the identified methylation pattern in MM patients showed similar results in MM cell lines. Expectedly, we also observed that suppressor of cytokine signaling 1 (SOCS1) was hypermethylated at the promoter region (MAT score=19.986) as has been reported in human cell lines. Importantly, another member of SOCS family SOCS3 showed much stronger signal in the promoter region with CpG island (MAT score=31.707) in MM patients compared to normal control. Notably, the expression of two members of TNFR superfamily TNFRSF18 and TNFRSF4 which play an important role in development and programmed cell death of lymphocyte significantly have increased 283 and 141-fold after treatment with 5′aza in MM cell lines. Conclusion: These findings enhance our understanding of the role of DNA methylation in MM, as one of the epigenetic changes that may contribute to the pathogenesis of this disease. The identification and functional characterization of novel key molecules affected by DNA methylation will provide deeper insight into the molecular basis of MM disease. Disclosures: Leleu: Celgene: Consultancy, Research Funding; Janssen Cilag: Consultancy, Research Funding; Leo Pharma: Consultancy; Amgen: Consultancy; Chugai: Research Funding; Roche: Consultancy, Research Funding; Novartis: Consultancy, Research Funding. Anderson:Millennium Pharmaceuticals: Honoraria, Membership on an entity's Board of Directors or advisory committees, Research Funding, Speakers Bureau.

scholarly journals ESTABLISHMENT AND CHARACTERIZATION OF LYMPHOBLASTOID CELL LINES (LCL) DERIVED FROM PATIENTS WITH IMMUNE DEFICIENCY SYNDROMES (IDS)

1977 ◽  
Vol 11 (4) ◽  
pp. 495-495 ◽  
Author(s):  
John L Sullivan ◽  
Hans D Ochs ◽  
Carol L Dunsmoor ◽  
Ralph J Wedgwood
Keyword(s):  
Immune Deficiency ◽  
Cell Lines ◽  
Lymphoblastoid Cell Lines

scholarly journals Characterization of the microDNA through the response to chemotherapeutics in lymphoblastoid cell lines

PLoS ONE ◽  
2017 ◽  
Vol 12 (9) ◽  
pp. e0184365 ◽  
Author(s):  
Pamela Mehanna ◽  
Vincent Gagné ◽  
Mathieu Lajoie ◽  
Jean-François Spinella ◽  
Pascal St-Onge ◽  
...  
Keyword(s):  
Cell Lines ◽  
Lymphoblastoid Cell Lines
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