Cancer Prevention: Epigenetics Steps Up to the Plate

Issa, Jean–Pierre J.

doi:10.1158/1940-6207.capr-08-0029

Cited by 57 publications

(51 citation statements)

References 32 publications

(38 reference statements)

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…15,16 Given that epigenetic alterations are often present in the earliest stages of cancer, even in the normal-appearing mucosa, there is a growing enthusiasm that demethylating agents could be more beneficial for cancer prevention instead for their use in chemotherapy for advanced cancers. 17,18 Indeed, DAC and zebularine, an oral DNA methylation inhibitor, have been shown to prevent tumor formation in the Apc Min/+ mouse model. 19,20 In spite of its promise, DAC AKBA treatment increased the number of active caspase-3 positive cells, as evidenced by a greater number of bright yellow cells, in all three cell lines, in a dose-dependent manner.…”

Section: Boswellic Acid Induces Epigenetic Alterationsmentioning

confidence: 99%

Boswellic acid induces epigenetic alterations by modulating DNA methylation in colorectal cancer cells

Yan

Takahashi

Byun

et al. 2012

Cancer Biology & Therapy

View full text Add to dashboard Cite

Section: Boswellic Acid Induces Epigenetic Alterationsmentioning

confidence: 99%

Boswellic acid induces epigenetic alterations by modulating DNA methylation in colorectal cancer cells

Yan

Takahashi

Byun

et al. 2012

Cancer Biology & Therapy

View full text Add to dashboard Cite

“…The importance of epimutation in cancer is increasingly being recognised. Indeed, some consider cancer to be as much an epigenetic disease as it is a genetic disease [18]. Many imprinted genes play roles in cellular growth and proliferation and consequently there may be selective pressure for their deregulation in cancer cells.…”

Section: Perturbation Of Imprinted Gene Dosage Is Associated With Neomentioning

confidence: 99%

Genomic imprinting as an adaptative model of developmental plasticity

2011

View full text Add to dashboard Cite

Developmental plasticity can be defined as the ability of one genotype to produce a range of phenotypes in response to environmental conditions. Such plasticity can be manifest at the level of individual cells, an organ, or a whole organism. Imprinted genes are a group of approximately 100 genes with functionally monoallelic, parental‐origin specific expression. As imprinted genes are critical for prenatal growth and metabolic axis development and function, modulation of imprinted gene dosage has been proposed to play a key role in the plastic development of the unborn foetus in response to environmental conditions. Evidence is accumulating that imprinted dosage may also be involved in controlling the plastic potential of individual cells or stem cell populations. Imprinted gene dosage can be modulated through canonical, transcription factor mediated mechanisms, or through the relaxation of imprinting itself, reactivating the normally silent allele.

show abstract

“…Suppression of aberrant methylation is considered as one of the novel targets for cancer chemoprevention (15,16). Traditionally, chemoprevention has used substances based on 2 strategies: the anti-initiation and anti-promotion/progression strategies (17)(18)(19).…”

Section: Introductionmentioning

confidence: 99%

Prevention of Helicobacter pylori–Induced Gastric Cancers in Gerbils by a DNA Demethylating Agent

Niwa

Toyoda

Tsukamoto

et al. 2013

Cancer Prevention Research

View full text Add to dashboard Cite

Suppression of aberrant DNA methylation is a novel approach to cancer prevention, but, so far, the efficacy of the strategy has not been evaluated in cancers associated with chronic inflammation. Gastric cancers induced by Helicobacter pylori infection are known to involve aberrant DNA methylation and associated with severe chronic inflammation in their early stages. Here, we aimed to clarify whether suppression of aberrant DNA methylation can prevent H. pylori-induced gastric cancers using a Mongolian gerbil model. Administration of a DNA demethylating agent, 5-aza-2 0 -deoxycytidine (5-aza-dC), to gerbils (0.125 mg/kg for 50-55 weeks) decreased the incidence of gastric cancers induced by H. pylori infection and N-methyl-N-nitrosourea (MNU) treatment from 55.2% to 23.3% (P < 0.05). In gastric epithelial cells, DNA methylation levels of six CpG islands (HE6, HG2, SB1, SB5, SF12, and SH6) decreased to 46% to 68% (P < 0.05) of gerbils without 5-aza-dC treatment. Also, the global DNA methylation level decreased from 83.0% AE 4.5% to 80.3% AE 4.4% (mean AE SD) by 5-aza-dC treatment (P < 0.05). By 5-aza-dC treatment, Il1b and Nos2 were downregulated (42% and 58% of gerbils without, respectively) but Tnf was upregulated (187%), suggesting that 5-aza-dC treatment induced dysregulation of inflammatory responses.No obvious adverse effect of 5-aza-dC treatment was observed, besides testicular atrophy. These results showed that 5-aza-dC treatment can prevent H. pylori-induced gastric cancers and suggested that removal of induced DNA methylation and/or suppression of DNA methylation induction can become a target for prevention of chronic inflammation-associated cancers. Cancer Prev Res; 6(4); 263-70. Ó2013 AACR.

show abstract

Cancer Prevention: Epigenetics Steps Up to the Plate

Cited by 57 publications

References 32 publications

Boswellic acid induces epigenetic alterations by modulating DNA methylation in colorectal cancer cells

Boswellic acid induces epigenetic alterations by modulating DNA methylation in colorectal cancer cells

Genomic imprinting as an adaptative model of developmental plasticity

Prevention of Helicobacter pylori–Induced Gastric Cancers in Gerbils by a DNA Demethylating Agent

Contact Info

Product

Resources

About