Evidence map›Paper›PMID 25801978›Full record

ReviewCancer biology & therapy2015

Targeting mTOR signaling pathways and related negative feedback loops for the treatment of acute myeloid leukemia.

Benedito A Carneiro, Jason B Kaplan, Jessica K Altman, Francis J Giles, Leonidas C Platanias

Open access · bronzeAbstract readReview
In one paragraph

Review in Cancer biology & therapy, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
2.3field-weighted citation impact, top 12% 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

26 citing papers in PubMed, 40 citations in OpenAlex.

  1. Article
  2. Article
  3. The Importance of Phosphoinositide 3-Kinase in Neuroinflammation.International journal of molecular sciences · 2024
    Review
  4. Article
  5. Review
  6. CPT1B, a metabolic molecule, is also an independent risk factor in CN-AML.Cancer biomarkers : section A of Disease markers · 2023
    Article
  7. Article
  8. Article
  9. Article
  10. Lysosome-mediated chemoresistance in acute myeloid leukemia.Cancer drug resistance (Alhambra, Calif.) · 2022
    Review
  11. Review
  12. Article
  13. New insights into the important roles of tumor cell-intrinsic PD-1.International journal of biological sciences · 2021
    Review
  14. Review
  15. Review
  16. Deeping in the Role of the MAP-Kinases Interacting Kinases (MNKs) in Cancer.International journal of molecular sciences · 2020
    Review
  17. Review
  18. Review
  19. Article
  20. 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

5 authors at 3 institutions in 1 country.

Benedito A Carneiroa Robert H Lurie Comprehensive Cancer Center of Northwestern University ; Chicago , IL , USA.
Jason B Kaplan
Jessica K Altman
Francis J Giles
Leonidas C Platanias
Northwestern Medicine · USRobert H. Lurie Comprehensive Cancer Center of Northwestern UniversityJesse Brown VA Medical Center · 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
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 I01CX000916NCI NIH HHS CA121192NCI NIH HHS CA155566NCI NIH HHS CA161196NCI NIH HHS CA77816NCI NIH HHS P30 CA060553NCI NIH HHS R01 CA077816NCI NIH HHS R01 CA121192NCI NIH HHS R01 CA155566
6 · The paper itself

Abstract

An accumulating understanding of the complex pathogenesis of acute myeloid leukemia (AML) continues to lead to promising therapeutic approaches. Among the key aberrant intracellular signaling pathways involved in AML, the phosphatidylinositol 3-kinase/AKT/mammalian target of rapamycin (PI3K/AKT/mTOR) axis is of major interest. This axis modulates a wide array of critical cellular functions, including proliferation, metabolism, and survival. Pharmacologic inhibitors of components of this pathway have been developed over the past decade, but none has an established role in the treatment of AML. This review will discuss the preclinical data and clinical results driving ongoing attempts to exploit the PI3K/AKT/mTOR pathway in patients with AML and address issues related to negative feedback loops that account for leukemic cell survival. Targeting the PI3K/AKT/mTOR pathway is of high interest for the treatment of AML, but combination therapies with other targeted agents may be needed to block negative feedback loops in leukemia cells.

Indexed as

HumansLeukemia, Myeloid, AcutePhosphatidylinositol 3-KinasesSignal TransductionTOR Serine-Threonine KinasesMTOR protein, humanPhosphatidylinositol 3-KinasesTOR Serine-Threonine KinasesAcute myeloid leukemiaAktAMLAML, acute myeloid leukemiaHDAC, histone deacetylaseMAPKMNK, MAPK-interacting kinasemTORmTOR, mammalian target of rapamycinPDK1, phosphoinositide-dependent protein kinase-1PI3KPI3K, phosphatidylinositol 3-kinasetargeted therapy

Identifiers

PMID25801978
PMCPMC4622839
OpenAlexW1573108393

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.