Evidence map›Paper›PMID 25352953›Full record

ArticleGenes & cancer2014

The apoptosis associated tyrosine kinase gene is frequently hypermethylated in human cancer and is regulated by epigenetic mechanisms.

Tanja Haag, Christina E Herkt, Sara K Walesch, Antje M Richter, Reinhard H Dammann

Open access · diamondAbstract read
In one paragraph

Article in Genes & cancer, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
1.7field-weighted citation impact, top 16% 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

22 citing papers in PubMed, 31 citations in OpenAlex.

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  12. Kinases and Cancer.Cancers · 2018
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  16. Changes in 30K protein synthesis during delayed degeneration of the silk gland by a caspase-dependent pathway in a Bombyx (silkworm) mutant.Journal of comparative physiology. B, Biochemical, systemic, and environmental physiology · 2016
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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

5 authors at 2 institutions in 1 country.

Tanja HaagInstitute for Genetics; Justus-Liebig-University; Universities of Giessen and Marburg Lung Center, Member of the German Center for Lung Research; Giessen, Germany.
Christina E HerktInstitute for Genetics; Justus-Liebig-University; Universities of Giessen and Marburg Lung Center, Member of the German Center for Lung Research; Giessen, Germany.
Sara K WaleschInstitute for Genetics; Justus-Liebig-University; Universities of Giessen and Marburg Lung Center, Member of the German Center for Lung Research; Giessen, Germany.
Antje M RichterInstitute for Genetics; Justus-Liebig-University; Universities of Giessen and Marburg Lung Center, Member of the German Center for Lung Research; Giessen, Germany.
Reinhard H DammannInstitute for Genetics; Justus-Liebig-University; Universities of Giessen and Marburg Lung Center, Member of the German Center for Lung Research; Giessen, Germany.
German Center for Lung Research · DEUniversities of Giessen and Marburg Lung Center · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Epigenetic gene inactivation through promoter hypermethylation is an important aberration involved in the silencing of tumor-associated genes in cancer. Here we identified the apoptosis associated tyrosine kinase (AATK) as an epigenetically downregulated tumor related gene. We analyzed the epigenetic regulation of AATK in several human cancer cell lines and normal tissues by methylation and expression analysis. Hypermethylation of AATK was also analyzed in 25 primary lung tumors, 30 breast cancers and 24 matching breast tissues. In normal tissues the AATK CpG island promoter was unmethylated and AATK was expressed. Hypermethylation of AATK occurred frequently in 13 out of 14 (93%) human cancer cell lines. Methylation was reversed by 5-aza-2'-deoxycytidine treatment leading to re-expression of AATK in cancer cell lines. Aberrant methylation of AATK was also revealed in primary lung (40%) and breast (53%) cancers, but was found to be significantly less methylated in matching normal breast tissues (17%; p<0.01). In addition, we observed that AATK is epigenetically reactivated through the chromatin regulator CTCF. We further show that overexpression of Aatk significantly suppresses colony formation in cancer cell lines. Our findings suggest that the apoptosis associated tyrosine kinase is frequently inactivated in human cancers and acts as a tumor suppressive gene.

Indexed as

AATKCTCFDNA methylationepigenetic regulationhuman cancertumor suppressor

Identifiers

PMID25352953
PMCPMC4209602
OpenAlexW2147056827

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.