Differential methylation of human LINE-1 retrotransposons in malignant cells

Alves, Gilda; Tatro, Alicia; Fanning, Thomas G.

doi:10.1016/0378-1119(96)00205-3

Cited by 95 publications

(57 citation statements)

References 12 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…In all, nine L1 insertions were identified, which when assayed against normal tissues from the same individual, were found to be specific to the tumor. Further analysis suggested that hypomethylation in the tumor cell-lines is at least partially responsible for the increased activity, an observation that is in agreement with numerous studies of L1 regulation (Alves et al 1996;Jurgens et al 1996;Yoder et al 1997;Steinhoff and Schulz 2003;Suter et al 2004;and Coufal et al 2009 are several examples from among many). Is this a general pattern for human tumors?…”

Section: Human Applications: Biomedicalsupporting

confidence: 83%

Reading TE leaves: New approaches to the identification of transposable element insertions

Ray¹,

Batzer²

2011

Genome Res.

View full text Add to dashboard Cite

Transposable elements (TEs) are a tremendous source of genome instability and genetic variation. Of particular interest to investigators of human biology and human evolution are retrotransposon insertions that are recent and/or polymorphic in the human population. As a consequence, the ability to assay large numbers of polymorphic TEs in a given genome is valuable. Five recent manuscripts each propose methods to scan whole human genomes to identify, map, and, in some cases, genotype polymorphic retrotransposon insertions in multiple human genomes simultaneously. These technologies promise to revolutionize our ability to analyze human genomes for TE-based variation important to studies of human variability and human disease. Furthermore, the approaches hold promise for researchers interested in nonhuman genomic variability. Herein, we explore the methods reported in the manuscripts and discuss their applications to aspects of human biology and the biology of other organisms.

show abstract

Section: Human Applications: Biomedicalsupporting

confidence: 83%

Reading TE leaves: New approaches to the identification of transposable element insertions

Ray¹,

Batzer²

2011

Genome Res.

View full text Add to dashboard Cite

show abstract

“…The most abundant retrotransposons in the human genome are LINE elements or long interspersed nuclear elements. Loss of promoter methylation and transcriptional activation of LINE elements have been reported in a variety of cancers (Alves et al, 1996;Thayer et al, 1993). The deleterious effects of hypomethylation of LINE retrotransposons in cancer has been linked with both mutational disruption of genes as well as the potential disruption of nearby gene expression.…”

Section: Methylation Changes In Cancermentioning

confidence: 99%

DNA methylation and gene silencing in cancer: which is the guilty party?

2002

View full text Add to dashboard Cite

The DNA methylation pattern of a cell is exquisitely controlled during early development resulting in distinct methylation patterns. The tight control of DNA methylation is released in the cancer cell characterized by a reversal of methylation states. CpG island associated genes, in particular tumour suppressor or related genes, are often hypermethylated and this is associated with silencing of these genes. Therefore methylation is commonly convicted as a critical causal event in silencing this important class of genes in cancer. In this review, we argue that methylation is not the initial guilty party in triggering gene silencing in cancer, but that methylation of CpG islands is a consequence of prior gene silencing, similar to the role of methylation in maintaining the silencing of CpG island genes on the inactive X chromosome. We propose that gene silencing is the critical precursor in cancer, as it changes the dynamic interplay between de novo methylation and demethylation of the CpG island and tilts the balance to favour hypermethylation and chromatin inactivation.

show abstract

“…DNA methylation also functions to repress repetitive elements, such as Alu and LINE‐1, which are generally highly methylated in the human genome. (Kochanek et al ., 1993; Alves et al ., 1996). …”

Section: Introductionmentioning

confidence: 99%

DNA methylation and healthy human aging

2015

View full text Add to dashboard Cite

SummaryThe process of aging results in a host of changes at the cellular and molecular levels, which include senescence, telomere shortening, and changes in gene expression. Epigenetic patterns also change over the lifespan, suggesting that epigenetic changes may constitute an important component of the aging process. The epigenetic mark that has been most highly studied is DNA methylation, the presence of methyl groups at CpG dinucleotides. These dinucleotides are often located near gene promoters and associate with gene expression levels. Early studies indicated that global levels of DNA methylation increase over the first few years of life and then decrease beginning in late adulthood. Recently, with the advent of microarray and next‐generation sequencing technologies, increases in variability of DNA methylation with age have been observed, and a number of site‐specific patterns have been identified. It has also been shown that certain CpG sites are highly associated with age, to the extent that prediction models using a small number of these sites can accurately predict the chronological age of the donor. Together, these observations point to the existence of two phenomena that both contribute to age‐related DNA methylation changes: epigenetic drift and the epigenetic clock. In this review, we focus on healthy human aging throughout the lifetime and discuss the dynamics of DNA methylation as well as how interactions between the genome, environment, and the epigenome influence aging rates. We also discuss the impact of determining ‘epigenetic age’ for human health and outline some important caveats to existing and future studies.

show abstract

Differential methylation of human LINE-1 retrotransposons in malignant cells

Cited by 95 publications

References 12 publications

Reading TE leaves: New approaches to the identification of transposable element insertions

Reading TE leaves: New approaches to the identification of transposable element insertions

DNA methylation and gene silencing in cancer: which is the guilty party?

DNA methylation and healthy human aging

Contact Info

Product

Resources

About