Evidence map›Paper›PMID 28062691›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2017

Activating mutations and translocations in the guanine exchange factor VAV1 in peripheral T-cell lymphomas.

Francesco Abate, Ana C da Silva-Almeida, Sakellarios Zairis, Javier Robles-Valero, Lucile Couronne, Hossein Khiabanian, S Aidan Quinn, Mi-Yeon Kim, Maria Antonella Laginestra, Christine Kim and 12 more

Open access · bronzeAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 70 papers.

0numbers the graph read from it
0cells of the map it votes in
70citing papers in PubMed
5.8field-weighted citation impact, top 3% 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

70 citing papers in PubMed, 118 citations in OpenAlex.

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  11. Prognostic Significance ofBiomedicines · 2024
    Article
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  15. TCR Pathway Mutations in Mature T Cell Lymphomas.Journal of immunology (Baltimore, Md. : 1950) · 2023
    Review
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10 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 12 institutions in 5 countries.

Francesco AbateDepartment of Systems Biology, Columbia University Medical Center, New York, NY 10032.
Ana C da Silva-AlmeidaInstitute for Cancer Genetics, Columbia University, New York, NY 10032.
Sakellarios ZairisDepartment of Systems Biology, Columbia University Medical Center, New York, NY 10032.
Javier Robles-ValeroCentro de Investigación del Cáncer, Consejo Superior de Investigaciones Científicas-University of Salamanca, 37007 Salamanca, Spain.
Lucile CouronneDepartment of Adult Hematology, Necker Hospital, 75015 Paris, France.
Hossein KhiabanianDepartment of Systems Biology, Columbia University Medical Center, New York, NY 10032.
S Aidan QuinnInstitute for Cancer Genetics, Columbia University, New York, NY 10032.
Mi-Yeon KimInstitute for Cancer Genetics, Columbia University, New York, NY 10032.
Maria Antonella LaginestraHemopathology Unit, European Institute of Oncology, 20139 Milan, Italy.
Christine KimInstitute for Cancer Genetics, Columbia University, New York, NY 10032.
Danilo FioreDepartment of Pathology and Laboratory Medicine, Weill Cornell Medical College, New York, NY 10065.
Govind BhagatDepartment of Pathology and Cell Biology, Columbia University Medical Center, New York, NY 10032.
Miguel Angel PirisInstituto de Formación e Investigación, Hospital Universitario Marqués de Valdecilla, 39008 Santander, Spain.
Elias CampoDepartment of Pathology, Hospital Clinic, 08036 Barcelona, Spain.
Izidore S LossosDivision of Hematology-Oncology, Sylvester Comprehensive Cancer Center, Miami, FL 33136.
Olivier A BernardINSERM U1170, 94805 Villejuif, France.
Giorgio InghiramiDepartment of Pathology and Laboratory Medicine, Weill Cornell Medical College, New York, NY 10065.
Stefano PileriHemopathology Unit, European Institute of Oncology, 20139 Milan, Italy.
Xosé R BusteloCentro de Investigación del Cáncer, Consejo Superior de Investigaciones Científicas-University of Salamanca, 37007 Salamanca, Spain.
Raul RabadanDepartment of Systems Biology, Columbia University Medical Center, New York, NY 10032; rr2579@cumc.columbia.edu af2196@columbia.edu tp2151@columbia.edu.
Adolfo A FerrandoInstitute for Cancer Genetics, Columbia University, New York, NY 10032; rr2579@cumc.columbia.edu af2196@columbia.edu tp2151@columbia.edu.
Teresa PalomeroInstitute for Cancer Genetics, Columbia University, New York, NY 10032; rr2579@cumc.columbia.edu af2196@columbia.edu tp2151@columbia.edu.
Columbia University Irving Medical Center · USCancer Genetics (United States) · USCornell University · USEuropean Institute of Oncology · ITCentro de Investigación del Cáncer · ESColumbia University · USConsejo Superior de Investigaciones Científicas · ESHospital Clínic de Barcelona · ESInstituto de Investigación Marqués de Valdecilla · ESUniversité Paris Cité · FRUniversité Paris-Sud · FRUniversity of Miami · US

Funding

MEDICAL SCIENTIST TRAINING PROGRAMT32GM007367 · NIGMS · COLUMBIA UNIV NEW YORK MORNINGSIDE · PI REINER, STEVEN L · 1985 to 2021
$25.1M
The role of RHOA G17V mutation in peripheral t-cell lymphomasR01CA197945 · NCI · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI PALOMERO, TERESA · 2015 to 2019
$1.8M
Clinical and Translational Science AwardTL1TR000082 · NCATS · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI GINSBERG, HENRY N · 2012 to 2015
$732k
NCATS NIH HHS TL1 TR000082NCI NIH HHS R01 CA197945NIGMS NIH HHS T32 GM007367Worldwide Cancer Research 14-1248
6 · The paper itself

Abstract

Peripheral T-cell lymphomas (PTCLs) are a heterogeneous group of non-Hodgkin lymphomas frequently associated with poor prognosis and for which genetic mechanisms of transformation remain incompletely understood. Using RNA sequencing and targeted sequencing, here we identify a recurrent in-frame deletion (VAV1 Δ778-786) generated by a focal deletion-driven alternative splicing mechanism as well as novel VAV1 gene fusions (VAV1-THAP4, VAV1-MYO1F, and VAV1-S100A7) in PTCL. Mechanistically these genetic lesions result in increased activation of VAV1 catalytic-dependent (MAPK, JNK) and non-catalytic-dependent (nuclear factor of activated T cells, NFAT) VAV1 effector pathways. These results support a driver oncogenic role for VAV1 signaling in the pathogenesis of PTCL.

Indexed as

Alternative SplicingAmino Acid SequenceBase SequenceCell Line, TumorGuanineGuanine Nucleotide Exchange FactorsHumansJurkat CellsLymphoma, T-Cell, PeripheralMutationProto-Oncogene Proteins c-vavSequence DeletionTranslocation, GeneticGuanineGuanine Nucleotide Exchange FactorsProto-Oncogene Proteins c-vavVAV1 protein, humangene fusionmutationperipheral T-cell lymphomaVAV1

Identifiers

PMID28062691
PMCPMC5278460
OpenAlexW2569137528

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.