Evidence map›Paper›PMID 20935488›Full record

ArticleEpigenetics2011

DNA methyltransferase inhibition may limit cancer cell growth by disrupting ribosome biogenesis.

Tom Moss

Abstract read
In one paragraph

Article in Epigenetics, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
–field-weighted citation impact
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

6 citing papers in PubMed.

  1. Article
  2. Article
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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

1 author.

Tom MossCancer Research Centre and Dept. of Molecular Biology, Medical Biochemistry and Pathology, Laval University, Quebec, Canada. Tom.Moss@crhdq.ulaval.ca

Funding

Canadian Institutes of Health Research MOP-12205
6 · The paper itself

Abstract

"Mutations" in the pattern of CpG methylation imprinting of the human genome have been correlated with a number of diseases including cancer. In particular, aberrant imprinting of tumor suppressor genes by gain of CpG methylation has been observed in many cancers and thus represents an important alternative pathway to gene "mutation" and tumor progression. Inhibitors of DNA methylation display therapeutic effects in the treatment of certain cancers, and it has been assumed these effects are due to the reversal of "mutant" gene imprinting. However, significant reactivation of imprinted tumor suppressor genes is rarely observed in vivo following treatment with DNA methylation inhibitors. A recent study revealed an unexpected requirement for CpG methylation in the synthesis and assembly of the ribosome, an essential function for cell growth and proliferation. As such, the data provide an unforeseen explanation of the action of DNA methylation inhibitors in restricting cancer cell growth.

Indexed as

Gene SilencingAzacitidineCell ProliferationCpG IslandsDecitabineDNA (Cytosine-5-)-MethyltransferasesDNA MethylationEnzyme InhibitorsGenes, rRNAGenes, Tumor SuppressorGenomic ImprintingHCT116 CellsHumansNeoplasmsRepetitive Sequences, Nucleic AcidRibosomesAzacitidineDecitabineDNA (Cytosine-5-)-MethyltransferasesEnzyme Inhibitors

Identifiers

PMID20935488
PMCPMC3278780

What OpenQuestion holds

Textmetadata
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.