Evidence map›Paper›PMID 21795762›Full record

ReviewOncotarget2011

Evi1 forms a bridge between the epigenetic machinery and signaling pathways.

Akihide Yoshimi, Mineo Kurokawa

Open access · hybridAbstract readReview
In one paragraph

Review in Oncotarget, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.9field-weighted citation impact, top 15% 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

16 citing papers in PubMed, 39 citations in OpenAlex.

  1. Article
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  4. Multifaceted Role of PRDM Proteins in Human Cancer.International journal of molecular sciences · 2020
    Review
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  7. Pleiotropic Contribution ofFrontiers in behavioral neuroscience · 2018
    Article
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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

2 authors at 2 institutions in 1 country.

Akihide YoshimiDepartment of Hematology and Oncology, Graduate School of Medicine, University of Tokyo, Tokyo, Japan.
Mineo Kurokawa
The University of Tokyo · JPUniversity hospital Medical Information Network · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Recent studies have demonstrated the significance of the leukemia oncogene Evi1 as the regulator of hematopoietic stem cells and marker of poor clinical outcomes in myeloid malignancies. Evi1-mediated leukemogenic activities include a wide array of functions such as the induction of epigenetic modifications, transcriptional control, and regulation of signaling pathways. We have recently succeeded in comprehensively elucidating the oncogenic function of Evi1 in a model of the polycomb-Evi1-PTEN/AKT/mTOR axis. These results may provide us with novel therapeutic approaches to conquer the poor prognosis associated with Evi1-activated leukemia or other solid tumors with high Evi1 expression. Here, we review the current understanding of the role of Evi1 in controlling the development of leukemia and highlight potential modalities for targeting factors involved in Evi1-regulated signaling.

Indexed as

Epigenesis, GeneticSignal TransductionAnimalsDNA-Binding ProteinsHematopoietic Stem CellsHumansLeukemia, MyeloidMDS1 and EVI1 Complex Locus ProteinMiceMolecular Targeted TherapyPhosphatidylinositol 3-KinasesPrognosisProto-Oncogene Proteins c-aktProto-OncogenesTOR Serine-Threonine KinasesTranscription FactorsDNA-Binding ProteinsMDS1 and EVI1 Complex Locus ProteinMECOM protein, humanMTOR protein, humanPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktTOR Serine-Threonine KinasesTranscription Factors

Identifiers

PMID21795762
PMCPMC3248179
OpenAlexW1953928363

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.