Evidence map›Paper›PMID 24413737›Full record

ArticleNature genetics2014

Somatic RHOA mutation in angioimmunoblastic T cell lymphoma.

Mamiko Sakata-Yanagimoto, Terukazu Enami, Kenichi Yoshida, Yuichi Shiraishi, Ryohei Ishii, Yasuyuki Miyake, Hideharu Muto, Naoko Tsuyama, Aiko Sato-Otsubo, Yusuke Okuno and 26 more

Abstract read
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In one paragraph

Article in Nature genetics, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 364 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
364citing papers in PubMed, 1 pooled it
41.6field-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

364 citing papers in PubMed, 1 synthesis or guideline pooled it, 635 citations in OpenAlex.

  1. Pooled it
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  15. Novel agents and therapeutic advances in T cell lymphoma.International journal of hematology · 2026
    Review
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  20. RHOA controls oncogenic B cell receptor signaling in aggressive lymphoma.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article

304 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

36 authors at 11 institutions in 1 country.

Mamiko Sakata-Yanagimoto1] Department of Hematology, Faculty of Medicine, University of Tsukuba, Tsukuba, Japan. [2].
Terukazu Enami1] Department of Hematology, Faculty of Medicine, University of Tsukuba, Tsukuba, Japan. [2].
Kenichi Yoshida1] Cancer Genomics Project, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan. [2] Department of Pathology and Tumor Biology, Graduate School of Medicine, Kyoto University, Kyoto, Japan. [3].
Yuichi ShiraishiLaboratory of DNA Information Analysis, Human Genome Center, Institute of Medical Science, The University of Tokyo, Tokyo, Japan.
Ryohei IshiiDepartment of Biophysics and Biochemistry, Graduate School of Science, The University of Tokyo, Tokyo, Japan.
Yasuyuki MiyakeDepartment of Hematology, Faculty of Medicine, University of Tsukuba, Tsukuba, Japan.
Hideharu MutoDepartment of Hematology, Faculty of Medicine, University of Tsukuba, Tsukuba, Japan.
Naoko TsuyamaDivision of Pathology, Cancer Institute, Japanese Foundation for Cancer Research, Tokyo, Japan.
Aiko Sato-Otsubo1] Cancer Genomics Project, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan. [2] Department of Pathology and Tumor Biology, Graduate School of Medicine, Kyoto University, Kyoto, Japan.
Yusuke OkunoCancer Genomics Project, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.
Seiji SakataPathology Project for Molecular Targets, Cancer Institute, Japanese Foundation for Cancer Research, Tokyo, Japan.
Yuhei KamadaDepartment of Hematology, Faculty of Medicine, University of Tsukuba, Tsukuba, Japan.
Rie Nakamoto-MatsubaraDepartment of Hematology, Faculty of Medicine, University of Tsukuba, Tsukuba, Japan.
Nguyen Bich TranDepartment of Hematology, Faculty of Medicine, University of Tsukuba, Tsukuba, Japan.
Koji Izutsu1] Department of Hematology, Toranomon Hospital, Tokyo, Japan. [2] Okinaka Memorial Institute for Medical Research, Tokyo, Japan.
Yusuke Sato1] Cancer Genomics Project, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan. [2] Department of Pathology and Tumor Biology, Graduate School of Medicine, Kyoto University, Kyoto, Japan.
Yasunori OhtaDepartment of Pathology, Toranomon Hospital, Tokyo, Japan.
Junichi FurutaDepartment of Dermatology, Faculty of Medicine, University of Tsukuba, Tsukuba, Japan.
Seiichi ShimizuDepartment of Hematology, Tsuchiura Kyodo General Hospital, Tsuchiura, Japan.
Takuya KomenoDepartment of Hematology, Mito Medical Center, National Hospital Organization, Mito, Japan.
Yuji SatoDepartment of Hematology, Tsukuba Memorial Hospital, Tsukuba, Japan.
Takayoshi ItoDepartment of Hematology, JA Toride Medical Center, Toride, Japan.
Masayuki NoguchiDepartment of Pathology, Faculty of Medicine, University of Tsukuba, Tsukuba, Japan.
Emiko NoguchiDepartment of Medical Genetics, Faculty of Medicine, University of Tsukuba, Tsukuba, Japan.
Masashi Sanada1] Cancer Genomics Project, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan. [2] Department of Pathology and Tumor Biology, Graduate School of Medicine, Kyoto University, Kyoto, Japan.
Kenichi ChibaLaboratory of DNA Information Analysis, Human Genome Center, Institute of Medical Science, The University of Tokyo, Tokyo, Japan.
Hiroko TanakaLaboratory of Sequence Analysis, Human Genome Center, Institute of Medical Science, The University of Tokyo, Tokyo, Japan.
Kazumi Suzukawa1] Department of Hematology, Faculty of Medicine, University of Tsukuba, Tsukuba, Japan. [2] Department of Clinical Laboratory, University of Tsukuba Hospital, Tsukuba, Japan.
Toru NanmokuDepartment of Clinical Laboratory, University of Tsukuba Hospital, Tsukuba, Japan.
Yuichi HasegawaDepartment of Hematology, Faculty of Medicine, University of Tsukuba, Tsukuba, Japan.
Osamu NurekiDepartment of Biophysics and Biochemistry, Graduate School of Science, The University of Tokyo, Tokyo, Japan.
Satoru Miyano1] Laboratory of DNA Information Analysis, Human Genome Center, Institute of Medical Science, The University of Tokyo, Tokyo, Japan. [2] Laboratory of Sequence Analysis, Human Genome Center, Institute of Medical Science, The University of Tokyo, Tokyo, Japan.
Naoya NakamuraDepartment of Pathology, Tokai University School of Medicine, Isehara, Japan.
Kengo Takeuchi1] Division of Pathology, Cancer Institute, Japanese Foundation for Cancer Research, Tokyo, Japan. [2] Pathology Project for Molecular Targets, Cancer Institute, Japanese Foundation for Cancer Research, Tokyo, Japan.
Seishi Ogawa1] Cancer Genomics Project, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan. [2] Department of Pathology and Tumor Biology, Graduate School of Medicine, Kyoto University, Kyoto, Japan. [3].
Shigeru Chiba1] Department of Hematology, Faculty of Medicine, University of Tsukuba, Tsukuba, Japan. [2] Life Science Center, Tsukuba Advanced Research Alliance, University of Tsukuba, Tsukuba, Japan. [3].
University of Tsukuba · JPThe University of Tokyo · JPJapanese Foundation For Cancer Research · JPKyoto University · JPToranomon Hospital · JPTsukuba Memorial Hospital · JPUniversity of Tsukuba Hospital · JPJA Toride Medical Center · JPNational Hospital Organization Mito Medical Center · JPTokai University · JPTsuchiura Kyodo General Hospital · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Angioimmunoblastic T cell lymphoma (AITL) is a distinct subtype of peripheral T cell lymphoma characterized by generalized lymphadenopathy and frequent autoimmune-like manifestations. Although frequent mutations in TET2, IDH2 and DNMT3A, which are common to various hematologic malignancies, have been identified in AITL, the molecular pathogenesis specific to this lymphoma subtype is unknown. Here we report somatic RHOA mutations encoding a p.Gly17Val alteration in 68% of AITL samples. Remarkably, all cases with the mutation encoding p.Gly17Val also had TET2 mutations. The RHOA mutation encoding p.Gly17Val was specifically identified in tumor cells, whereas TET2 mutations were found in both tumor cells and non-tumor hematopoietic cells. RHOA encodes a small GTPase that regulates diverse biological processes. We demonstrated that the Gly17Val RHOA mutant did not bind GTP and also inhibited wild-type RHOA function. Our findings suggest that impaired RHOA function in cooperation with preceding loss of TET2 function contributes to AITL-specific pathogenesis.

Indexed as

AnimalsBase SequenceBromodeoxyuridineDioxygenasesDNA-Binding ProteinsDNA (Cytosine-5-)-MethyltransferasesDNA Methyltransferase 3AExomeHumansImmunoblastic LymphadenopathyIsocitrate DehydrogenaseJurkat CellsLymphoma, T-Cell, PeripheralMiceMolecular Sequence DataMutation, MissenseBromodeoxyuridineDioxygenasesDNA-Binding ProteinsDNA (Cytosine-5-)-MethyltransferasesDNA Methyltransferase 3ADNMT3A protein, humanDnmt3a protein, mouseIDH1 protein, humanIDH2 protein, humanIsocitrate DehydrogenaseProto-Oncogene ProteinsrhoA GTP-Binding ProteinRHOA protein, humanTET2 protein, human

Identifiers

PMID24413737
OpenAlexW2146146853

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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.