Evidence map›Paper›PMID 26138366›Full record

ArticleNature communications2015

Integrated genetic and epigenetic analysis defines novel molecular subgroups in rhabdomyosarcoma.

Masafumi Seki, Riki Nishimura, Kenichi Yoshida, Teppei Shimamura, Yuichi Shiraishi, Yusuke Sato, Motohiro Kato, Kenichi Chiba, Hiroko Tanaka, Noriko Hoshino and 21 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Nature communications, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 119 papers.

0numbers the graph read from it
0cells of the map it votes in
119citing papers in PubMed
10.3field-weighted citation impact, top 1% 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

119 citing papers in PubMed, 177 citations in OpenAlex.

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  13. Rhabdomyosarcoma in children and young adults.Virchows Archiv : an international journal of pathology · 2025
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  18. JCO precision oncology · 2024
    Article
  19. Review
  20. Complete loss ofHGG advances · 2023
    Article

59 more citing papers are in PubMed but not listed here.

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

31 authors at 13 institutions in 1 country.

Masafumi SekiDepartment of Pediatrics, Graduate School of Medicine, The University of Tokyo, Tokyo 113-8655, Japan.
Riki NishimuraDepartment of Pediatrics, Graduate School of Medicine, The University of Tokyo, Tokyo 113-8655, Japan.
Kenichi Yoshida1] Department of Pathology and Tumor Biology, Graduate School of Medicine, Kyoto University, Kyoto 606-8501, Japan [2] Cancer Genomics Project, Graduate School of Medicine, The University of Tokyo, Tokyo, 113-8655, Japan.
Teppei Shimamura1] Laboratory of DNA Information Analysis, Human Genome Center, Institute of Medical Science, The University of Tokyo, Tokyo 108-8639, Japan [2] Division of Systems Biology, Nagoya University Graduate School of Medicine, Nagoya 466-8550, Japan.
Yuichi ShiraishiLaboratory of DNA Information Analysis, Human Genome Center, Institute of Medical Science, The University of Tokyo, Tokyo 108-8639, Japan.
Yusuke Sato1] Department of Pathology and Tumor Biology, Graduate School of Medicine, Kyoto University, Kyoto 606-8501, Japan [2] Cancer Genomics Project, Graduate School of Medicine, The University of Tokyo, Tokyo, 113-8655, Japan.
Motohiro Kato1] Department of Pediatrics, Graduate School of Medicine, The University of Tokyo, Tokyo 113-8655, Japan [2] Department of Cell Therapy and Transplantation Medicine, The University of Tokyo, Tokyo 113-8655, Japan [3] Department of Hematology/Oncology, Saitama Children's Medical Center, Saitama 339-8551, Japan.
Kenichi ChibaLaboratory of DNA Information Analysis, Human Genome Center, Institute of Medical Science, The University of Tokyo, Tokyo 108-8639, Japan.
Hiroko TanakaLaboratory of Sequence Data Analysis, Human Genome Center, Institute of Medical Science, The University of Tokyo, Tokyo 108-8639, Japan.
Noriko HoshinoDepartment of Pediatric Surgery, Graduate School of Medicine, The University of Tokyo, Tokyo, 113-8655, Japan.
Genta NagaeGenome Science Division, Research Center for Advanced Science and Technology, The University of Tokyo, Tokyo 153-8904, Japan.
Yusuke Shiozawa1] Department of Pathology and Tumor Biology, Graduate School of Medicine, Kyoto University, Kyoto 606-8501, Japan [2] Cancer Genomics Project, Graduate School of Medicine, The University of Tokyo, Tokyo, 113-8655, Japan.
Yusuke Okuno1] Cancer Genomics Project, Graduate School of Medicine, The University of Tokyo, Tokyo, 113-8655, Japan [2] Department of Pediatrics, Nagoya University Graduate School of Medicine, Nagoya 466-8550, Japan.ORCID 0000000331399272
Hajime HosoiDepartment of Pediatrics, Kyoto Prefectural University of Medicine, Graduate School of Medical Science, Kyoto 602-8566, Japan.
Yukichi TanakaDepartment of Pathology, Kanagawa Children's Medical Center, Yokohama 232-8555, Japan.
Hajime OkitaMolecular Pathology Laboratory, Department of Pediatric Hematology and Oncology Research, National Research Institute for Child Health and Development, Tokyo 157-8535, Japan.
Mitsuru MiyachiDepartment of Pediatrics, Kyoto Prefectural University of Medicine, Graduate School of Medical Science, Kyoto 602-8566, Japan.
Ryota SouzakiDepartment of Pediatric Surgery, Reproductive and Developmental Medicine, Faculty of Medical Sciences, Kyushu University, Fukuoka 812-8582, Japan.
Tomoaki TaguchiDepartment of Pediatric Surgery, Reproductive and Developmental Medicine, Faculty of Medical Sciences, Kyushu University, Fukuoka 812-8582, Japan.
Katsuyoshi KohDepartment of Hematology/Oncology, Saitama Children's Medical Center, Saitama 339-8551, Japan.
Ryoji HanadaDepartment of Hematology/Oncology, Saitama Children's Medical Center, Saitama 339-8551, Japan.
Keisuke KatoDivision of Pediatric Hematology and Oncology, Ibaraki Children's Hospital, Mito 311-4145, Japan.
Yuko NomuraDepartment of Pediatrics, School of Medicine, Fukuoka University, Fukuoka 814-0180, Japan.
Masaharu AkiyamaDepartment of Pediatrics, The Jikei University School of Medicine, Tokyo 105-8471, Japan.
Akira OkaDepartment of Pediatrics, Graduate School of Medicine, The University of Tokyo, Tokyo 113-8655, Japan.
Takashi Igarashi1] Department of Pediatrics, Graduate School of Medicine, The University of Tokyo, Tokyo 113-8655, Japan [2] National Center for Child Health and Development, Tokyo 157-8535, Japan.
Satoru Miyano1] Laboratory of DNA Information Analysis, Human Genome Center, Institute of Medical Science, The University of Tokyo, Tokyo 108-8639, Japan [2] Laboratory of Sequence Data Analysis, Human Genome Center, Institute of Medical Science, The University of Tokyo, Tokyo 108-8639, Japan.
Hiroyuki AburataniGenome Science Division, Research Center for Advanced Science and Technology, The University of Tokyo, Tokyo 153-8904, Japan.
Yasuhide HayashiDepartment of Hematology/Oncology, Gunma Children's Medical Center, Shibukawa, Gunma, 377-8577, Japan.
Seishi Ogawa1] Department of Pathology and Tumor Biology, Graduate School of Medicine, Kyoto University, Kyoto 606-8501, Japan [2] Cancer Genomics Project, Graduate School of Medicine, The University of Tokyo, Tokyo, 113-8655, Japan.
Junko TakitaDepartment of Pediatrics, Graduate School of Medicine, The University of Tokyo, Tokyo 113-8655, Japan.
The University of Tokyo · JPKyoto University · JPKyoto Prefectural University of Medicine · JPKyushu University · JPNagoya University · JPNational Center For Child Health and Development · JPSaitama Children's Medical Center · JPTokyo Medical University · JPFukuoka University · JPGunma Children's Medical Center · JPIbaraki Children's Hospital · JPJikei University School of Medicine · JPKanagawa Children's Medical Center · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Rhabdomyosarcoma (RMS) is the most common soft-tissue sarcoma in childhood. Here we studied 60 RMSs using whole-exome/-transcriptome sequencing, copy number (CN) and DNA methylome analyses to unravel the genetic/epigenetic basis of RMS. On the basis of methylation patterns, RMS is clustered into four distinct subtypes, which exhibits remarkable correlation with mutation/CN profiles, histological phenotypes and clinical behaviours. A1 and A2 subtypes, especially A1, largely correspond to alveolar histology with frequent PAX3/7 fusions and alterations in cell cycle regulators. In contrast, mostly showing embryonal histology, both E1 and E2 subtypes are characterized by high frequency of CN alterations and/or allelic imbalances, FGFR4/RAS/AKT pathway mutations and PTEN mutations/methylation and in E2, also by p53 inactivation. Despite the better prognosis of embryonal RMS, patients in the E2 are likely to have a poor prognosis. Our results highlight the close relationships of the methylation status and gene mutations with the biological behaviour in RMS.

Indexed as

Adolescentbeta CateninCell Cycle ProteinsChildChild, PreschoolDNA MethylationEpigenesis, GeneticExomeF-Box ProteinsF-Box-WD Repeat-Containing Protein 7FemaleForkhead Box Protein O1Forkhead Transcription FactorsGene Expression Regulation, NeoplasticHumansInfantBCOR protein, humanbeta CateninCell Cycle ProteinsCTNNB1 protein, humanF-Box ProteinsF-Box-WD Repeat-Containing Protein 7FBXW7 protein, humanFGFR4 protein, humanForkhead Box Protein O1Forkhead Transcription FactorsFOXO1 protein, humanPaired Box Transcription FactorsPAX3 protein, humanPAX3 Transcription FactorPAX7 protein, humanPAX7 Transcription FactorProto-Oncogene ProteinsProto-Oncogene Proteins c-aktPTEN PhosphohydrolasePTEN protein, humanras ProteinsReceptor, Fibroblast Growth Factor, Type 4Repressor ProteinsRNA, MessengerTP53 protein, humanTumor Suppressor Protein p53Ubiquitin-Protein Ligases

Identifiers

PMID26138366
PMCPMC4506514
OpenAlexW848101669

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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.