Evidence map›Paper›PMID 23494221›Full record

ArticleInternational journal of clinical oncology2014

Promoter methylation of DAPK1, FHIT, MGMT, and CDKN2A genes in cervical carcinoma.

Chiaki Banzai, Koji Nishino, Jinhua Quan, Kosuke Yoshihara, Masayuki Sekine, Tetsuro Yahata, Kenichi Tanaka, Gynecological Cancer Registry of Niigata

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Article in International journal of clinical oncology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers, 7 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed, 7 pooled it
2.7field-weighted citation impact, top 10% 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

29 citing papers in PubMed, 7 syntheses or guidelines pooled it, 50 citations in OpenAlex.

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  19. Identification ofFrontiers in genetics · 2018
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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

8 authors at 1 institution in 1 country.

Chiaki BanzaiDivision of Obstetrics and Gynecology, Graduate School of Medical and Dental Sciences, Niigata University, 1-757 Asahimachi-dori, Chuo Ward, Niigata, 951-8510, Japan, chiaki-b@med.niigata-u.ac.jp.
Koji Nishino
Jinhua Quan
Kosuke Yoshihara
Masayuki Sekine
Tetsuro Yahata
Kenichi Tanaka
Gynecological Cancer Registry of Niigata
Niigata University Medical and Dental Hospital · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

BACKGROUND AND

objectivesAberrant DNA methylation contributes to the malignant phenotype in virtually all types of human cancer. This study explored the relationship between promoter methylation and inactivation of the DAPK1, FHIT, MGMT, and CDKN2A genes in cervical cancer.

methodsThe promoter methylation of DAPK1, FHIT, MGMT, and CDKN2A was investigated by using a methylation-specific polymerase chain reaction in 53 specimens of cervical cancer (42 squamous cell carcinoma, 11 adenocarcinoma), 22 specimens of intraepithelial neoplasia tissues, and 24 control normal cervical tissue specimens. The correlation of promoter methylation with the clinicopathological features of cervical cancer was analyzed. The expressions of DAPK1, FHIT, MGMT, and CDKN2A were detected by measuring relative mRNA levels.

resultsThe promoter methylation of DAPK1, FHIT, MGMT, and CDKN2A in cervical cancer vs. intraepithelial neoplasia vs. normal cervical tissue was 75.5 vs. 31.8 vs. 4.2 % (p < 0.0001), 66.0 vs. 59.1 vs. 25.0 % (p = 0.0033), 34.0 vs. 27.3 vs. 20.8 % (p = 0.76), and 17.0 vs. 31.8 vs. 8.3 % (p = 0.11), respectively. The methylation of the promoter region significantly decreased the expression of only DAPK1 (p = 0.03). The methylation rate of the DAPK1 gene promoter was significantly higher in cervical cancer tissues than in cervical intraepithelial neoplasia and normal cervical tissues.

conclusionPromoter methylation may therefore lead to the inactivation of the DAPK1 gene, and may be related to the progression of cervical oncogenesis.

Indexed as

Acid Anhydride HydrolasesAdultBis(5'-adenosyl)triphosphataseCarcinoma in SituCarcinoma, Squamous CellCyclin-Dependent Kinase Inhibitor p16Death-Associated Protein KinasesDNA MethylationDNA Modification MethylasesDNA Repair EnzymesFemaleGene Expression Regulation, NeoplasticHumansMiddle AgedNeoplasm ProteinsPromoter Regions, GeneticAcid Anhydride HydrolasesBis(5'-adenosyl)triphosphataseCyclin-Dependent Kinase Inhibitor p16DAPK1 protein, humanDeath-Associated Protein KinasesDNA Modification MethylasesDNA Repair EnzymesMGMT protein, humanNeoplasm ProteinsTumor Suppressor Proteins

Identifiers

PMID23494221
OpenAlexW2008937722

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.