Evidence map›Paper›PMID 24319589›Full record

ArticleInternational journal of hematologic oncology2013

Acute myeloid leukemia: potential for new therapeutic approaches targeting mRNA translation pathways.

Jessica K Altman, Leonidas C Platanias

Open access · greenAbstract read
In one paragraph

Article in International journal of hematologic oncology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.6field-weighted citation impact, top 30% 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

3 citing papers in PubMed, 5 citations in OpenAlex.

  1. Review
  2. Review
  3. Autophagy is a survival mechanism of acute myelogenous leukemia precursors during dual mTORC2/mTORC1 targeting.Clinical cancer research : an official journal of the American Association for Cancer Research · 2014
    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

2 authors at 2 institutions in 1 country.

Jessica K AltmanRobert H Lurie Comprehensive Cancer Center & Division of Hematology-Oncology, Lurie 3-107, 303 East Superior Street, Chicago, IL 60611, USA ; Feinberg School of Medicine, Northwestern University, Chicago, IL 60611, USA ; Department of Medicine, Jesse Brown VA Medical Center, Chicago, IL 60612, USA.
Leonidas C Platanias
Northwestern University · USRobert H. Lurie Comprehensive Cancer Center of Northwestern University

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
Mnk Pathways and IFN-responses in Malignant CellsR01CA155566 · NCI · NORTHWESTERN UNIVERSITY AT CHICAGO · PI PLATANIAS, LEONIDAS C. · 2011 to 2015
$1.6M
NCI NIH HHS P30 CA060553NCI NIH HHS R01 CA077816NCI NIH HHS R01 CA121192NCI NIH HHS R01 CA155566
6 · The paper itself

Abstract

Despite advances in molecular research related to acute myeloid leukemia (AML) and a better understanding of the mechanisms of leukemogenesis and pathophysiology of the disease, the pharmacological agents used in the treatment of AML have remained essentially unchanged for the last three decades. Advances in the clinical management of AML patients have been achieved by defining better molecular prognostic markers, but there remains a need for new targeted drugs that disrupt non-overlapping pathways in leukemia cells. The mTOR cellular cascade is critical for cell metabolism, growth, proliferation and survival. Extensive preclinical work suggests that targeting mTOR may provide a powerful approach to block AML precursor cells, while other findings suggest enhanced antileukemic effects by combining mTOR inhibitors with traditional chemotherapy. Such combinations may increase antileukemic responses further, offering unique ways to overcome leukemic cell resistance and to eliminate primitive leukemic precursors.

Identifiers

PMID24319589
PMCPMC3851308
OpenAlexW2163540029

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.