Evidence map›Paper›PMID 32999426›Full record

ArticleCommunications biology2020

Comprehensive genetic analysis of pediatric germ cell tumors identifies potential drug targets.

Yasuo Kubota, Masafumi Seki, Tomoko Kawai, Tomoya Isobe, Misa Yoshida, Masahiro Sekiguchi, Shunsuke Kimura, Kentaro Watanabe, Aiko Sato-Otsubo, Kenichi Yoshida and 14 more

Open access · goldAbstract read
In one paragraph

Article in Communications biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
2.0field-weighted citation impact, top 13% 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

12 citing papers in PubMed, 17 citations in OpenAlex.

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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

24 authors at 7 institutions in 2 countries.

Yasuo KubotaDepartment of Pediatrics, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.ORCID http://orcid.org/0000-0002-7909-5422
Masafumi SekiDepartment of Pediatrics, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.ORCID http://orcid.org/0000-0003-4671-7026
Tomoko KawaiDepartment of Maternal-Fetal Biology, National Research Institute for Child Health and Development, Tokyo, Japan.ORCID http://orcid.org/0000-0001-8137-0334
Tomoya IsobeDepartment of Pediatrics, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.ORCID http://orcid.org/0000-0002-3487-3307
Misa YoshidaDepartment of Pediatrics, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.
Masahiro SekiguchiDepartment of Pediatrics, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.
Shunsuke KimuraDepartment of Pediatrics, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.ORCID http://orcid.org/0000-0002-2158-467X
Kentaro WatanabeDepartment of Pediatrics, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.
Aiko Sato-OtsuboDepartment of Pediatrics, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.
Kenichi YoshidaDepartment of Pathology and Tumor Biology, Graduate School of Medicine, Kyoto University, Kyoto, Japan.
Hiromichi SuzukiDepartment of Pathology and Tumor Biology, Graduate School of Medicine, Kyoto University, Kyoto, Japan.
Keisuke KataokaDepartment of Pathology and Tumor Biology, Graduate School of Medicine, Kyoto University, Kyoto, Japan.ORCID http://orcid.org/0000-0002-8263-9902
Yoichi FujiiDepartment of Pathology and Tumor Biology, Graduate School of Medicine, Kyoto University, Kyoto, Japan.
Yuichi ShiraishiSection of Genome Analysis Platform, Center for Cancer Genomic and Advanced Therapeutics, National Cancer Center, Tokyo, Japan.
Kenichi ChibaSection of Genome Analysis Platform, Center for Cancer Genomic and Advanced Therapeutics, National Cancer Center, Tokyo, Japan.
Hiroko TanakaLaboratory of DNA Information Analysis, Human Genome Center, Institute of Medical Science, The University of Tokyo, Tokyo, Japan.ORCID http://orcid.org/0000-0001-9634-8922
Mitsuteru HiwatariDepartment of Pediatrics, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.
Akira OkaDepartment of Pediatrics, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.
Yasuhide HayashiInstitute of Physiology and Medicine, Jobu University, Takasaki, Japan.
Satoru MiyanoLaboratory of DNA Information Analysis, Human Genome Center, Institute of Medical Science, The University of Tokyo, Tokyo, Japan.
Seishi OgawaDepartment of Pathology and Tumor Biology, Graduate School of Medicine, Kyoto University, Kyoto, Japan.
Kenichiro HataDepartment of Maternal-Fetal Biology, National Research Institute for Child Health and Development, Tokyo, Japan.
Yukichi TanakaClinical Research Institute and Department of Pathology, Kanagawa Children's Medical Center, Yokohama, Japan.
Junko TakitaDepartment of Pediatrics, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan. jtakita@kuhp.kyoto-u.ac.jp.ORCID http://orcid.org/0000-0002-2452-6520
The University of Tokyo · JPKyoto University · JPKanagawa Children's Medical Center · JPNational Center For Child Health and Development · JPHiroshima University · JPJobu University · JPUniversity of Tokyo Hospital · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

To elucidate the molecular pathogenesis of pediatric germ cell tumors (GCTs), we performed DNA methylation array analysis, whole transcriptome sequencing, targeted capture sequencing, and single-nucleotide polymorphism array analysis using 51 GCT samples (25 female, 26 male), including 6 germinomas, 2 embryonal carcinomas, 4 immature teratomas, 3 mature teratomas, 30 yolk sac tumors, and 6 mixed germ cell tumors. Among the 51 samples, 11 were from infants, 23 were from young children, and 17 were from those aged ≥10 years. Sixteen of the 51 samples developed in the extragonadal regions. Germinomas showed upregulation of pluripotent genes and global hypomethylation. Pluripotent genes were also highly expressed in embryonal carcinomas. These genes may play essential roles in embryonal carcinomas given that their binding sites are hypomethylated. Yolk sac tumors exhibited overexpression of endodermal genes, such as GATA6 and FOXA2, the binding sites of which were hypomethylated. Interestingly, infant yolk sac tumors had different DNA methylation patterns from those observed in older children. Teratomas had higher expression of ectodermal genes, suggesting a tridermal nature. Based on our results, we suggest that KIT, TNFRSF8, and ERBB4 may be suitable targets for the treatment of germinoma, embryonal carcinomas, and yolk sac tumors, respectively.

Indexed as

Carcinoma, EmbryonalChildChild, PreschoolDNA Copy Number VariationsDNA MethylationEndodermal Sinus TumorExome SequencingFemaleGerminomaHumansInfantMaleNeoplasms, Germ Cell and EmbryonalOligonucleotide Array Sequence AnalysisPolymorphism, Single NucleotideTeratoma

Identifiers

PMID32999426
PMCPMC7528104
OpenAlexW3090805013

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.