Evidence map›Paper›PMID 28832024›Full record

ArticleLeukemia2018

Activation of RHOA-VAV1 signaling in angioimmunoblastic T-cell lymphoma.

M Fujisawa, M Sakata-Yanagimoto, S Nishizawa, D Komori, P Gershon, M Kiryu, S Tanzima, K Fukumoto, T Enami, M Muratani and 12 more

Open access · hybridAbstract read
In one paragraph

Article in Leukemia, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 77 papers.

0numbers the graph read from it
0cells of the map it votes in
77citing papers in PubMed
7.0field-weighted citation impact, top 2% 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

77 citing papers in PubMed, 127 citations in OpenAlex.

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  6. RHOA controls oncogenic B cell receptor signaling in aggressive lymphoma.Proceedings of the National Academy of Sciences of the United States of America · 2026
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17 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

22 authors at 10 institutions in 3 countries.

M FujisawaDepartment of Hematology, Graduate School of Comprehensive Human Sciences, University of Tsukuba, Tsukuba, Japan.
M Sakata-YanagimotoDepartment of Hematology, Graduate School of Comprehensive Human Sciences, University of Tsukuba, Tsukuba, Japan.
S NishizawaDepartment of Hematology, Graduate School of Comprehensive Human Sciences, University of Tsukuba, Tsukuba, Japan.
D KomoriDepartment of Hematology, Graduate School of Comprehensive Human Sciences, University of Tsukuba, Tsukuba, Japan.
P GershonDepartment of Molecular Biology and Biochemistry, UC-Irvine, Irvine, CA, USA.
M KiryuDepartment of Hematology, Graduate School of Comprehensive Human Sciences, University of Tsukuba, Tsukuba, Japan.
S TanzimaDepartment of Hematology, Graduate School of Comprehensive Human Sciences, University of Tsukuba, Tsukuba, Japan.
K FukumotoDepartment of Hematology, Graduate School of Comprehensive Human Sciences, University of Tsukuba, Tsukuba, Japan.
T EnamiDepartment of Hematology, Graduate School of Comprehensive Human Sciences, University of Tsukuba, Tsukuba, Japan.
M MurataniDepartment of Genome Biology, Faculty of Medicine, University of Tsukuba, Tsukuba, Japan.ORCID 0000-0002-0276-8000
K YoshidaDepartment of Pathology and Tumor Biology, Graduate School of Medicine, Kyoto University, Kyoto, Japan.
S OgawaDepartment of Pathology and Tumor Biology, Graduate School of Medicine, Kyoto University, Kyoto, Japan.
K MatsueDivision of Hematology/Oncology, Department of Medicine, Kameda Medical Center, Kamogawa, Japan.
N NakamuraDepartment of Pathology, Tokai University School of Medicine, Isehara, Japan.
K TakeuchiDivision of Pathology, Cancer Institute, Japanese Foundation for Cancer Research, Tokyo, Japan.ORCID 0000-0002-1599-5800
K IzutsuDepartment of Hematology, Toranomon Hospital, Tokyo, Japan.
K FujimotoDepartment of Hematology, Hokkaido University Graduate School of Medicine, Sapporo, Japan.
T TeshimaDepartment of Hematology, Hokkaido University Graduate School of Medicine, Sapporo, Japan.ORCID 0000-0002-0941-271X
H MiyoshiDepartment of Pathology, Kurume University School of Medicine, Kurume, Japan.
P GaulardInserm U955, Université Paris Est and Département de Pathologie, Hôpital Henri Mondor, Assistance Publique-Hôpitaux de Paris, Créteil, France.
K OhshimaDepartment of Pathology, Kurume University School of Medicine, Kurume, Japan.
S ChibaDepartment of Hematology, Graduate School of Comprehensive Human Sciences, University of Tsukuba, Tsukuba, Japan.
University of Tsukuba · JPHokkaido University · JPKurume University · JPKyoto University · JPInserm · FRJapanese Foundation For Cancer Research · JPKameda Medical Center · JPTokai University · JPToranomon Hospital · JPUniversity of California, Irvine · US

Funding

LTQ Velos Pro mass spectrometer with ETD and other optionsS10OD016328 · OD · UNIVERSITY OF CALIFORNIA-IRVINE · PI GERSHON, PAUL D · 2013 to 2013
$374k
NIH HHS S10 OD016328
6 · The paper itself

Abstract

Somatic G17V RHOA mutations were found in 50-70% of angioimmunoblastic T-cell lymphoma (AITL). The mutant RHOA lacks GTP binding capacity, suggesting defects in the classical RHOA signaling. Here, we discovered the novel function of the G17V RHOA: VAV1 was identified as a G17V RHOA-specific binding partner via high-throughput screening. We found that binding of G17V RHOA to VAV1 augmented its adaptor function through phosphorylation of 174Tyr, resulting in acceleration of T-cell receptor (TCR) signaling. Enrichment of cytokine and chemokine-related pathways was also evident by the expression of G17V RHOA. We further identified VAV1 mutations and a new translocation, VAV1-STAP2, in seven of the 85 RHOA mutation-negative samples (8.2%), whereas none of the 41 RHOA mutation-positive samples exhibited VAV1 mutations. Augmentation of 174Tyr phosphorylation was also demonstrated in VAV1-STAP2. Dasatinib, a multikinase inhibitor, efficiently blocked the accelerated VAV1 phosphorylation and the associating TCR signaling by both G17V RHOA and VAV1-STAP2 expression. Phospho-VAV1 staining was demonstrated in the clinical specimens harboring G17V RHOA and VAV1 mutations at a higher frequency than those without. Our findings indicate that the G17V RHOA-VAV1 axis may provide a new therapeutic target in AITL.

Indexed as

Signal TransductionBiomarkers, TumorCell Line, TumorCytokinesDNA Mutational AnalysisHumansImmunoblastic LymphadenopathyLymphoma, T-CellMutationNFATC Transcription FactorsPhosphorylationProtein BindingProto-Oncogene Proteins c-vavReceptors, Antigen, T-CellrhoA GTP-Binding ProteinBiomarkers, TumorCytokinesNFATC Transcription FactorsProto-Oncogene Proteins c-vavReceptors, Antigen, T-CellrhoA GTP-Binding ProteinVAV1 protein, human

Identifiers

PMID28832024
PMCPMC5843900
OpenAlexW2624092568

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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.