Evidence map›Paper›PMID 22751129›Full record

ArticleOncogene2013

Overexpression of the anti-apoptotic protein AVEN contributes to increased malignancy in hematopoietic neoplasms.

M Eißmann, I M Melzer, S B M Fernández, G Michel, M Hrabě de Angelis, G Hoefler, P Finkenwirth, A Jauch, B Schoell, M Grez and 8 more

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In one paragraph

Article in Oncogene, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
0.5field-weighted citation impact, top 35% 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

15 citing papers in PubMed, 20 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Downregulation of apoptotic repressorProceedings of the National Academy of Sciences of the United States of America · 2023
    Article
  5. Review
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  13. Heritability of in vitro phenotypes exhibited by murine adipose-derived stromal cells.Mammalian genome : official journal of the International Mammalian Genome Society · 2016
    Article
  14. Article
  15. Article
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

18 authors at 8 institutions in 2 countries.

M EißmannChemotherapeutisches Forschungsinstitut Georg-Speyer-Haus, Frankfurt, Germany.
I M Melzer
S B M Fernández
G Michel
M Hrabě de Angelis
G Hoefler
P Finkenwirth
A Jauch
B Schoell
M Grez
M Schmidt
C C Bartholomae
S Newrzela
N Haetscher
M A Rieger
C Zachskorn
M Mittelbronn
M Zörnig
Georg Speyer Haus · DEUniversity Hospital Heidelberg · DEHeidelberg University · DEHelmholtz Zentrum München · DEMedical University of Graz · ATNational Center for Tumor Diseases · DETechnical University of Munich · DEUniversity Hospital Frankfurt · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

AVEN has been identified as an inhibitor of apoptosis, which binds to the adaptor protein, APAF-1, and thereby prevents apoptosome formation and mitochondrial apoptosis. Recent data have demonstrated high expression levels of AVEN messenger RNA in acute leukemias as well as a positive correlation between AVEN mRNA overexpression and poor prognosis in childhood acute lymphoblastic leukemia. On the basis of these data, we investigated the potential involvement of AVEN in tumorigenesis. First, we confirmed the overexpression of AVEN in T-cell acute lymphoblastic leukemia/lymphoma (T-ALL) patient samples. We then established a transgenic mouse model with T-cell-specific overexpression of AVEN, with which we demonstrated the oncogenic cooperation of AVEN with heterozygous loss of p53. Finally, we used a subcutaneous xenograft mouse model to show that AVEN knockdown in the T-ALL cell lines, MOLT-4 and CCRF-CEM, and in the acute myeloblastic leukemia cell line, Kasumi-1, leads to a halt in tumor growth owing to the increased apoptosis and decreased proliferation of tumor cells. Collectively, our data demonstrate that the anti-apoptotic molecule, AVEN, functions as an oncoprotein in hematopoietic neoplasms.

Indexed as

Adaptor Proteins, Signal TransducingAnimalsApoptosis Regulatory ProteinsBase SequenceCell Line, TumorGene Expression Regulation, LeukemicGene Knockdown TechniquesGenes, p53HumansLymphoma, T-CellMembrane ProteinsMiceMice, Inbred C57BLMice, TransgenicMolecular Sequence DataPrecursor Cell Lymphoblastic Leukemia-LymphomaAdaptor Proteins, Signal TransducingApoptosis Regulatory ProteinsAVEN protein, humanMembrane Proteins

Identifiers

PMID22751129
OpenAlexW2006245721

What OpenQuestion holds

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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.