Evidence map›Paper›PMID 19245437›Full record

ArticleCancer science2009

Yolk sac tumor but not seminoma or teratoma is associated with abnormal epigenetic reprogramming pathway and shows frequent hypermethylation of various tumor suppressor genes.

Shinsuke Furukawa, Masayuki Haruta, Yasuhito Arai, Shohei Honda, Junjiro Ohshima, Waka Sugawara, Yukio Kageyama, Yotsuo Higashi, Kazunori Nishida, Yukiko Tsunematsu and 3 more

Open access · greenAbstract read
In one paragraph

Article in Cancer science, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
2.7field-weighted citation impact, top 11% 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

14 citing papers in PubMed, 34 citations in OpenAlex.

  1. Trial
  2. Review
  3. The Enigmatic Role of TP53 in Germ Cell Tumours: Are We Missing Something?International journal of molecular sciences · 2021
    Review
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  14. Pediatric germ cell tumors and maternal vitamin supplementation: a Children's Oncology Group study.Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology · 2009
    Article
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

13 authors at 4 institutions in 2 countries.

Shinsuke FurukawaDepartment of Cancer Diagnosis, Research Institute for Clinical Oncology, Saitama Cancer Center, 818 Komuro, Ina, Saitama 362-0806, Japan.
Masayuki Haruta
Yasuhito Arai
Shohei Honda
Junjiro Ohshima
Waka Sugawara
Yukio Kageyama
Yotsuo Higashi
Kazunori Nishida
Yukiko Tsunematsu
Hisaya Nakadate
Masahiro Ishii
Yasuhiko Kaneko
Kitasato University · JPNational Cancer Research Institute · GBNational Center For Child Health and Development · JPSaitama Cancer Center · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Germ cell tumors (GCTs) are thought to arise from primordial germ cells (PGCs) that undergo epigenetic reprogramming: erasure of the somatic imprint in the genital ridge, and re-establishment of the sex-specific imprint at gametogenesis in the developing gonad. Previous studies suggested that GCTs show epigenetic patterns reflecting the reprogramming process of PGCs; however, epigenetic alterations of imprinted genes and their relationship with the methylation status of tumor suppressor genes (TSGs) have not been comprehensively studied. We analyzed the methylation status of the H19 and SNRPN differential methylated regions (DMRs) and the promoter region of 17 TSGs, and the expression status of H19, IGF2 and SNRPN in 45 GCTs, and found that 25 and 20 were in the normal and abnormal reprogramming pathways, respectively, defined on the basis of the methylation status of the two DMRs and the anatomical tumor site. The methylation pattern of the H19 and SNRPN DMRs was total erasure in seminomas, mostly physiological in teratomas, and various in yolk sac tumors. There were no correlations between the methylation status of the H19 DMR and mono- or biallelic expression of H19 or IGF2. Furthermore, we found that yolk sac tumors had a higher number of methylated TSGs than seminomas (P < 0.001) teratomas (P = 0.004) or other childhood tumors. While TSG methylation was known to have prognostic implications in various cancers, it did not affect the outcomes of patients with yolk sac tumor, suggesting that mechanisms of TSG methylation may be different between yolk sac tumor and other cancers.

Indexed as

DNA MethylationEpigenesis, GeneticGenes, Tumor SuppressorAdolescentAdultChildChild, PreschoolEndodermal Sinus TumorFemaleGenomic ImprintingHumansInfantInfant, NewbornMaleModels, GeneticPromoter Regions, Genetic

Identifiers

PMID19245437
PMCPMC11159010
OpenAlexW1999187444

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

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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.