Evidence map›Paper›PMID 22247744›Full record

ArticleClinical epigenetics2011

Dietary phytochemicals, HDAC inhibition, and DNA damage/repair defects in cancer cells.

Praveen Rajendran, Emily Ho, David E Williams, Roderick H Dashwood

Open access · goldAbstract read
In one paragraph

Article in Clinical epigenetics, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 98 papers.

0numbers the graph read from it
0cells of the map it votes in
98citing papers in PubMed
5.9field-weighted citation impact, top 3% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

98 citing papers in PubMed, 209 citations in OpenAlex.

  1. Review
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  15. Current Status of Obesity: Protective Role of Catechins.Antioxidants (Basel, Switzerland) · 2023
    Review
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  18. Article
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38 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors at 1 institution in 1 country.

Praveen RajendranCancer Chemoprotection Program, Linus Pauling Institute, 307 Linus Pauling Science Center, Oregon State University, Corvallis OR 97331, USA.
Emily Ho
David E Williams
Roderick H Dashwood
Oregon State University · US

Funding

Transplacental Chemoprevention of Lung Tumors and LymphomasP01CA090890 · NCI · TEXAS A&M UNIVERSITY HEALTH SCIENCE CTR · PI DASHWOOD, RODERICK H · 2003 to 2014
$14.2M
Dietary HDAC Inhibitors in Colon Cancer PreventionR01CA122959 · NCI · TEXAS A&M UNIVERSITY HEALTH SCIENCE CTR · PI DASHWOOD, RODERICK H · 2008 to 2023
$4.3M
Modulation of Colon Carcinogenesis by ChlorophyllinR01CA065525 · NCI · OREGON STATE UNIVERSITY · PI DASHWOOD, RODERICK H · 2004 to 2008
$1.5M
NCI NIH HHS P01 CA090890NCI NIH HHS R01 CA065525NCI NIH HHS R01 CA122959
6 · The paper itself

Abstract

Genomic instability is a common feature of cancer etiology. This provides an avenue for therapeutic intervention, since cancer cells are more susceptible than normal cells to DNA damaging agents. However, there is growing evidence that the epigenetic mechanisms that impact DNA methylation and histone status also contribute to genomic instability. The DNA damage response, for example, is modulated by the acetylation status of histone and non-histone proteins, and by the opposing activities of histone acetyltransferase and histone deacetylase (HDAC) enzymes. Many HDACs overexpressed in cancer cells have been implicated in protecting such cells from genotoxic insults. Thus, HDAC inhibitors, in addition to unsilencing tumor suppressor genes, also can silence DNA repair pathways, inactivate non-histone proteins that are required for DNA stability, and induce reactive oxygen species and DNA double-strand breaks. This review summarizes how dietary phytochemicals that affect the epigenome also can trigger DNA damage and repair mechanisms. Where such data is available, examples are cited from studies in vitro and in vivo of polyphenols, organosulfur/organoselenium compounds, indoles, sesquiterpene lactones, and miscellaneous agents such as anacardic acid. Finally, by virtue of their genetic and epigenetic mechanisms, cancer chemopreventive agents are being redefined as chemo- or radio-sensitizers. A sustained DNA damage response coupled with insufficient repair may be a pivotal mechanism for apoptosis induction in cancer cells exposed to dietary phytochemicals. Future research, including appropriate clinical investigation, should clarify these emerging concepts in the context of both genetic and epigenetic mechanisms dysregulated in cancer, and the pros and cons of specific dietary intervention strategies.

Indexed as

cancerDNA damageDNA repairEpigeneticsHDAChistonephytochemical

Identifiers

PMID22247744
PMCPMC3255482
OpenAlexW2165717337

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.