DNA Global Hypomethylation in EBV-Transformed Interphase Nuclei

Habib, M.; Fares, Fouad; Bourgeois, Claire A.; Bella, Chantal; Bernardino, Jacqueline; Hernandez‐Blazquez, Francisco Javier; Capoa, A. de; Niveleau, Alain

doi:10.1006/excr.1999.4434

Cited by 62 publications

(37 citation statements)

References 36 publications

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“…Similar alterations in DNA methylation have been reported in human cells and cell lines following viral or helminth infection (146)(147)(148)(149)(150)(151)(152). Methylation may be increased or decreased depending on the infectious agent (142,153). Change in epigenetic profile in response to infection may play a role in the development of immunerelated disorders and many cancers previously associated with infectious agents (e.g., gastric cancer).…”

Section: Infective Agents and The Epigenomesupporting

confidence: 55%

Prospects for Epigenetic Epidemiology

Foley¹,

Craig²,

Morley³

et al. 2008

American Journal of Epidemiology

220

162

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Section: Infective Agents and The Epigenomesupporting

confidence: 55%

Prospects for Epigenetic Epidemiology

Foley¹,

Craig²,

Morley³

et al. 2008

American Journal of Epidemiology

220

162

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“…12,13 Both patterns of global hypomethylation and gene-specific hypermethylation have been reported in the host genome following EBV transformation. [14][15][16][17][18][19] It has also been suggested that epigenetic modifications in cell lines may result from intrinsic factors associated with cell culturing, 4,20 including altered methylation maintenance in response to the availability of methyl donors in the culturing media, 21 and altered methylation over time with increasing passage number. 22 The observed differences in methylation between PBLs and LCLs may also be explained by cell-type specific methylation.…”

Section: Resultsmentioning

confidence: 99%

Comparative analysis of DNA methylation profiles in peripheral blood leukocytes versus lymphoblastoid cell lines

Brennan¹,

Ehrich²,

Brazil

et al. 2009

Epigenetics

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Previous reports have shown that DNA methylation profiles within primary human malignant tissues are altered when these cells are transformed into cancer cell lines. However, it is unclear if similar differences in DNA methylation profiles exist between DNA derived from peripheral blood leukocytes (PBLs) and corresponding Epstein-Barr Virus transformed lymphoblastoid cell lines (LCLs). To assess the utility of LCLs as a resource for methylation studies we have compared DNA methylation profiles in promoter and 5' regions of 318 genes in PBL and LCL sample pairs from patients with type 1 diabetes with or without nephropathy. We identified a total of 27 (~8%) genes that revealed different DNA methylation profiles in PBL compared with LCL-derived DNA samples. In conclusion, although the profiles for most promoter regions were similar between PBL-LCL pairs, our results indicate that LCL-derived DNA may not be suitable for DNA methylation studies at least in diabetic nephropathy.

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“…Cells grown on coverslips were stained with mouse monoclonal antibodies against 5mC (kindly provided by Alain Niveleau, Universite Claude Bernard, Lyon, France) as described previously (17). Images of the nuclear immunolocalization of 5 mC were obtained in a Leica DMRA fluorescence microscope coupled to a Leica DC200 digital camera and captured with the Adobe Photoshop software.…”

Section: Methodsmentioning

confidence: 99%

“…We reverse-transcribed total RNA (2 g) treated with DNase I (Ambion) using oligo(dT) [12][13][14][15][16][17][18] primer with Superscript II reverse transcriptase (Life Technologies, Inc.). We used 100 ng of cDNA for PCR amplification, and we amplified all of the genes with multiple cycle numbers (20 -35 cycles) to determine the appropriate conditions for obtaining semiquantitative differences in their expression levels.…”

Section: Methodsmentioning

confidence: 99%

A Mouse Skin Multistage Carcinogenesis Model Reflects the Aberrant DNA Methylation Patterns of Human Tumors

et al. 2004

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Whereas accepted models of tumorigenesis exist for genetic lesions, the timing of epigenetic alterations in cancer is not clearly understood. We have analyzed the profile of aberrations in DNA methylation occurring in cells lines and primary tumors of one of the best-characterized mouse carcinogenesis systems, the multistage skin cancer progression model. Initial analysis using high-performance capillary electrophoresis and immunolocalization revealed a loss of genomic 5-methylcytosine associated with the degree of tumor aggressiveness. Paradoxically, this occurs in the context of a growing number of hypermethylated CpG islands of tumor suppressor genes at the most malignant stages of carcinogenesis. We have observed this last phenomenon using two approaches, a candidate gene approach, studying genes with well-known methylation-associated silencing in human tumors, and a mouse cDNA microarray expression analysis after treatment with DNA demethylating drugs. The transition from epithelial to spindle cell morphology is particularly associated with major epigenetic alterations, such as E-cadherin methylation, demethylation of the Snail promoter, and a decrease of the global DNA methylation. Analysis of data obtained from the cDNA microarray strategy led to the identification of new genes that undergo methylation-associated silencing and have growth-inhibitory effects, such as the insulin-like growth factor binding protein-3. Most importantly, all of the above genes were also hypermethylated in human cancer cell lines and primary tumors, underlining the value of the mouse skin carcinogenesis model for the study of aberrant DNA methylation events in cancer cells.

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DNA Global Hypomethylation in EBV-Transformed Interphase Nuclei

Cited by 62 publications

References 36 publications

Prospects for Epigenetic Epidemiology

Prospects for Epigenetic Epidemiology

Comparative analysis of DNA methylation profiles in peripheral blood leukocytes versus lymphoblastoid cell lines

A Mouse Skin Multistage Carcinogenesis Model Reflects the Aberrant DNA Methylation Patterns of Human Tumors

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