Evidence map›Paper›PMID 27094611›Full record

ReviewCytokine2017

Dual targeting of eIF4E by blocking MNK and mTOR pathways in leukemia.

Ewa M Kosciuczuk, Diana Saleiro, Leonidas C Platanias

Open access · greenAbstract readReview
In one paragraph

Review in Cytokine, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
2.1field-weighted citation impact, top 13% 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

24 citing papers in PubMed, 42 citations in OpenAlex.

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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

3 authors at 2 institutions in 1 country.

Ewa M KosciuczukRobert H. Lurie Comprehensive Cancer Center and Division of Hematology-Oncology, Feinberg School of Medicine, Northwestern University, Chicago, IL 60611, USA; Department of Medicine, Jesse Brown Veterans Affairs Medical Center, Chicago, IL 60612, USA. Electronic address: ewa.kosciuczuk@northwestern.edu.
Diana SaleiroRobert H. Lurie Comprehensive Cancer Center and Division of Hematology-Oncology, Feinberg School of Medicine, Northwestern University, Chicago, IL 60611, USA.
Leonidas C PlataniasRobert H. Lurie Comprehensive Cancer Center and Division of Hematology-Oncology, Feinberg School of Medicine, Northwestern University, Chicago, IL 60611, USA; Department of Medicine, Jesse Brown Veterans Affairs Medical Center, Chicago, IL 60612, USA.
Jesse Brown VA Medical Center · USNorthwestern University · US

Funding

Tumor Environment and Metastasis (TEAM) Research ProgramP30CA060553 · NCI · NORTHWESTERN UNIVERSITY AT CHICAGO · PI Daniela E Matei · 1993 to 2026
$153.9M
Signal Transduction of Type I Interferons in Malignant CellsR01CA077816 · NCI · UNIVERSITY OF ILLINOIS AT CHICAGO · PI PLATANIAS, LEONIDAS C. · 1998 to 2024
$6.6M
Targeting Novel Protein Complexes for the Treatment of Acute Myeloid LeukemiaR01CA121192 · NCI · NORTHWESTERN UNIVERSITY AT CHICAGO · PI PLATANIAS, LEONIDAS C. · 2006 to 2023
$4.1M
TRAINING PROGRAM IN ONCOGENESIS &DEVELOPMENT BIOLOGYT32CA080621 · NCI · NORTHWESTERN UNIVERSITY AT CHICAGO · PI EKLUND, ELIZABETH ANN · 2001 to 2018
$4.1M
Mnk Pathways and IFN-responses in Malignant CellsR01CA155566 · NCI · NORTHWESTERN UNIVERSITY AT CHICAGO · PI PLATANIAS, LEONIDAS C. · 2011 to 2015
$1.6M
Signaling Pathways and Therapeutic Targeting of Leukemic CellsI01CX000916 · VA · JESSE BROWN VA MEDICAL CENTER · PI PLATANIAS, LEONIDAS C. · 2013 to 2025
–
CSRD VA I01 CX000916NCI NIH HHS P30 CA060553NCI NIH HHS R01 CA077816NCI NIH HHS R01 CA121192NCI NIH HHS R01 CA155566NCI NIH HHS T32 CA080621
6 · The paper itself

Abstract

Dysregulation of mRNA translation leads to aberrant activation of cellular pathways that promote expansion and survival of leukemic clones. A key element of the initiation translation complex is eIF4E (eukaryotic translation initiation factor 4E). The mitogen-activated protein kinase (MAPK) and mammalian target of rapamycin (mTOR) pathways play important roles in the regulation of eIF4E expression and downstream functional outcomes. Mitogen-activated protein kinase interacting protein kinases (Mnks) control translation by phosphorylation of eIF4E, whereas the mTOR kinase phosphorylates/de-activates the eIF4E inhibitor, 4E-BP1, to release translational repression. Both pathways are often abnormally activated in leukemia cells and promote cell survival events by controlling expression of oncogenic proteins. Targeting these pathways may provide approaches to avoid aberrant proliferation and neoplastic transformation.

Indexed as

Signal TransductionAnimalsEukaryotic Initiation Factor-4EHumansLeukemia, Myeloid, AcuteMiceNeoplasm ProteinsProtein Kinase InhibitorsTOR Serine-Threonine KinaseseIF4E protein, mouseEukaryotic Initiation Factor-4EMTOR protein, humanmTOR protein, mouseNeoplasm ProteinsProtein Kinase InhibitorsTOR Serine-Threonine KinasesAcute myeloid leukemiaeIF4EMNKmTORTranslation initiation

Identifiers

PMID27094611
PMCPMC5065931
OpenAlexW2339057360

What OpenQuestion holds

Textmetadata
LicenceTDM
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.