Evidence map›Paper›PMID 20824434›Full record

ArticleDer Pathologe2010

[DNA methylation. From basic research to routine diagnostics].

U Lehmann

Abstract read
PubMed Publisher
In one paragraph

Article in Der Pathologe, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing 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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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.

U LehmannInstitut für Pathologie, Medizinische Hochschule Hannover, Carl-Neuberg-Str. 1, 30625 Hannover. Lehmann.Ulrich@MH-Hannover.de

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

On a molecular level cancer is characterized not only by genetic defects, such as deletions, mutations or translocations, but also by epigenetic lesions. The most important epigenetic mechanisms are DNA methylation, Polycomb/trithorax complexes, histon modifications, non-coding RNAs, and chromosomal territories. These epigenetic mechanisms contribute to a stable modification of gene expression without changes in primary DNA sequence. During the development and progression of human tumours a gene-specific hypermethylation with resulting repression of transcription can occur. At the same time, global hypomethylation can very often be observed which contributes to an increase in chromosomal instability. In tumour pathology, the detection of somatic hMLH1 hypermethylation is important for molecular diagnostics of Lynch syndrome. The detection of MGMT gene methylation is a good prognostic and predictive factor for glioblastoma patients. Performing DNA methylation assays for routine diagnostics requires technical as well as theoretical expertise.

Indexed as

Molecular Diagnostic TechniquesAdaptor Proteins, Signal TransducingBiomarkers, TumorChromosomal InstabilityDNA MethylationDNA Modification MethylasesDNA Repair EnzymesEpigenesis, GeneticGene Expression Regulation, NeoplasticHumansMutL Protein Homolog 1NeoplasmsNuclear ProteinsTumor Suppressor ProteinsAdaptor Proteins, Signal TransducingBiomarkers, TumorDNA Modification MethylasesDNA Repair EnzymesMGMT protein, humanMLH1 protein, humanMutL Protein Homolog 1Nuclear ProteinsTumor Suppressor Proteins

Identifiers

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.