Evidence map›Paper›PMID 24584070›Full record

ArticleNature genetics2014

A recurrent inactivating mutation in RHOA GTPase in angioimmunoblastic T cell lymphoma.

Hae Yong Yoo, Min Kyung Sung, Seung Ho Lee, Sangok Kim, Haeseung Lee, Seongjin Park, Sang Cheol Kim, Byungwook Lee, Kyoohyoung Rho, Jong-Eun Lee and 8 more

Abstract read
PubMed Publisher
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 224 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
224citing papers in PubMed, 2 pooled it
26.6field-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

224 citing papers in PubMed, 2 syntheses or guidelines pooled it, 381 citations in OpenAlex.

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

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

18 authors at 7 institutions in 1 country.

Hae Yong Yoo1] Department of Health Sciences and Technology, Samsung Advanced Institute for Health Sciences and Technology, Sungkyunkwan University, Seoul, Korea. [2] Samsung Biomedical Research Institute, Research Institute for Future Medicine, Samsung Medical Center, Seoul, Korea. [3].
Min Kyung Sung1] Korean Bioinformation Center (KOBIC), Korea Research Institute of Bioscience and Biotechnology, Daejeon, Korea. [2].
Seung Ho LeeDepartment of Health Sciences and Technology, Samsung Advanced Institute for Health Sciences and Technology, Sungkyunkwan University, Seoul, Korea.
Sangok Kim1] Ewha Research Center for Systems Biology (ERCSB), Ewha Womans University, Seoul, Korea. [2] Department of Life Science, Ewha Womans University, Seoul, Korea.
Haeseung Lee1] Ewha Research Center for Systems Biology (ERCSB), Ewha Womans University, Seoul, Korea. [2] Department of Life Science, Ewha Womans University, Seoul, Korea.
Seongjin ParkKorean Bioinformation Center (KOBIC), Korea Research Institute of Bioscience and Biotechnology, Daejeon, Korea.
Sang Cheol KimKorean Bioinformation Center (KOBIC), Korea Research Institute of Bioscience and Biotechnology, Daejeon, Korea.
Byungwook LeeKorean Bioinformation Center (KOBIC), Korea Research Institute of Bioscience and Biotechnology, Daejeon, Korea.
Kyoohyoung RhoDNA Link, Inc., Seoul, Korea.
Jong-Eun LeeDNA Link, Inc., Seoul, Korea.
Kwang-Hwi ChoSchool of Systems Biomedical Science, Soongsil University, Seoul, Korea.
Wankyu Kim1] Ewha Research Center for Systems Biology (ERCSB), Ewha Womans University, Seoul, Korea. [2] Department of Life Science, Ewha Womans University, Seoul, Korea.
Hyunjung JuSamsung Biomedical Research Institute, Research Institute for Future Medicine, Samsung Medical Center, Seoul, Korea.
Jaesang Kim1] Ewha Research Center for Systems Biology (ERCSB), Ewha Womans University, Seoul, Korea. [2] Department of Life Science, Ewha Womans University, Seoul, Korea.
Seok Jin Kim1] Samsung Biomedical Research Institute, Research Institute for Future Medicine, Samsung Medical Center, Seoul, Korea. [2] Division of Hematology and Oncology, Department of Medicine, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul, Korea.
Won Seog Kim1] Samsung Biomedical Research Institute, Research Institute for Future Medicine, Samsung Medical Center, Seoul, Korea. [2] Division of Hematology and Oncology, Department of Medicine, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul, Korea.
Sanghyuk Lee1] Ewha Research Center for Systems Biology (ERCSB), Ewha Womans University, Seoul, Korea. [2] Department of Life Science, Ewha Womans University, Seoul, Korea.
Young Hyeh Ko1] Samsung Biomedical Research Institute, Research Institute for Future Medicine, Samsung Medical Center, Seoul, Korea. [2] Department of Pathology, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul, Korea.
Korea Research Institute of Bioscience and Biotechnology · KREwha Womans University · KRDNA Link (South Korea) · KRSamsung Medical Center · KRSamsung (South Korea) · KRSungkyunkwan University · KRSoongsil University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The molecular mechanisms underlying angioimmunoblastic T cell lymphoma (AITL), a common type of mature T cell lymphoma of poor prognosis, are largely unknown. Here we report a frequent somatic mutation in RHOA (encoding p.Gly17Val) using exome and transcriptome sequencing of samples from individuals with AITL. Further examination of the RHOA mutation encoding p.Gly17Val in 239 lymphoma samples showed that the mutation was specific to T cell lymphoma and was absent from B cell lymphoma. We demonstrate that the RHOA mutation encoding p.Gly17Val, which was found in 53.3% (24 of 45) of the AITL cases examined, is oncogenic in nature using multiple molecular assays. Molecular modeling and docking simulations provided a structural basis for the loss of GTPase activity in the RHOA Gly17Val mutant. Our experimental data and modeling results suggest that the RHOA mutation encoding p.Gly17Val is a driver mutation in AITL. On the basis of these data and through integrated pathway analysis, we build a comprehensive signaling network for AITL oncogenesis.

Indexed as

Gene SilencingModels, MolecularBase SequenceComparative Genomic HybridizationExomeHigh-Throughput Nucleotide SequencingHumansLymphoma, T-CellModels, BiologicalMolecular Sequence DataMutation, MissensePolymorphism, Single NucleotideProtein BindingrhoA GTP-Binding ProteinSequence Analysis, RNASignal TransductionrhoA GTP-Binding ProteinRHOA protein, human

Identifiers

PMID24584070
OpenAlexW2069271377

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.