Evidence map›Paper›PMID 26625317›Full record

ArticleOncotarget2016

Synergistic cooperation between ABT-263 and MEK1/2 inhibitor: effect on apoptosis and proliferation of acute myeloid leukemia cells.

Kelly Airiau, Valérie Prouzet-Mauléon, Benoit Rousseau, Arnaud Pigneux, Marie Jeanneteau, Manon Giraudon, Kaoutar Allou, Pierre Dubus, Francis Belloc, François-Xavier Mahon

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.4field-weighted citation impact, top 19% 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

13 citing papers in PubMed, 21 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. Oncotarget · 2019
    Article
  9. Pharmacology of Pimasertib, A Selective MEK1/2 Inhibitor.European journal of drug metabolism and pharmacokinetics · 2018
    Review
  10. Article
  11. Inducing Apoptosis and Decreasing Cell Proliferation in Human Acute Promyelocytic Leukemia Through Regulation Expression ofIndian journal of hematology & blood transfusion : an official journal of Indian Society of Hematology and Blood Transfusion · 2018
    Article
  12. Review
  13. 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

10 authors at 3 institutions in 1 country.

Kelly AiriauLaboratoire d'Hématopoïèse Leucémique et Cibles Thérapeutiques, INSERM 1035, Université Bordeaux, Bordeaux, France.
Valérie Prouzet-MauléonLaboratoire d'Hématopoïèse Leucémique et Cibles Thérapeutiques, INSERM 1035, Université Bordeaux, Bordeaux, France.
Benoit RousseauAnimalerie A2, Université Bordeaux Segalen, Bordeaux, France.
Arnaud PigneuxLaboratoire d'Hématopoïèse Leucémique et Cibles Thérapeutiques, INSERM 1035, Université Bordeaux, Bordeaux, France.
Marie JeanneteauCHU Bordeaux, Hôpital Haut-Lévêque, Laboratoire d'Hématologie, Pessac, France.
Manon GiraudonCHU Bordeaux, Hôpital Haut-Lévêque, Laboratoire d'Hématologie, Pessac, France.
Kaoutar AllouLaboratoire d'Hématopoïèse Leucémique et Cibles Thérapeutiques, INSERM 1035, Université Bordeaux, Bordeaux, France.
Pierre DubusEA 2406 Histologie et Pathologie, Université Bordeaux, Bordeaux, France.
Francis BellocLaboratoire d'Hématopoïèse Leucémique et Cibles Thérapeutiques, INSERM 1035, Université Bordeaux, Bordeaux, France.
François-Xavier MahonLaboratoire d'Hématopoïèse Leucémique et Cibles Thérapeutiques, INSERM 1035, Université Bordeaux, Bordeaux, France.
Université de Bordeaux · FRHôpital Cardiologique du Haut-Lévêque · FRInserm · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In spite of intensive research to improve treatment of acute myeloid leukemia (AML) more than half of all patients continue to develop a refractory disease. Therefore there is need to improve AML treatment. The overexpression of the BCL-2 family anti-apoptotic members, like BCL-2 or BCL-xL has been largely reported in lymphoid tumors but also in AML and other tumors. To counteract the anti-apoptotic effect of BCL-2, BH3 mimetics have been developed to target cancer cells. An increase in activity of ERK1/2 mitogen activated protein (MAP) kinase has also been reported in AML and might be targeted by MEK1/2 inhibitors. Hence, in the current work, we investigated whether the association of a BH3 mimetic such ABT-263 and the MEK1/2 inhibitor pimasertib (MEKI), was efficient to target AML cells. A synergistic increasing of apoptosis was observed in AML cell lines and in primary cells without affecting normal bone marrow cells. Such cooperation was confirmed on tumor growth in a mouse xenograft model of AML. In addition we demonstrated that MEKI sensitized the cells to apoptosis through its ability to promote a G1 cell cycle arrest. So, this combination of a MAP Kinase pathway inhibitor and a BH3 mimetic could be a promising strategy to improve the treatment of AML.

Indexed as

Acute DiseaseAniline CompoundsAnimalsAntineoplastic AgentsAntineoplastic Combined Chemotherapy ProtocolsApoptosisCell Line, TumorCell ProliferationCell SurvivalDrug SynergismG1 Phase Cell Cycle CheckpointsHL-60 CellsHumansImmunohistochemistryLeukemia, MyeloidMAP Kinase Kinase 1Aniline CompoundsAntineoplastic AgentsMAP2K1 protein, humanMAP2K2 protein, humanMAP Kinase Kinase 1MAP Kinase Kinase 2N-(2,3-dihydroxypropyl)-1-((2-fluoro-4-iodophenyl)amino)isonicotinamidenavitoclaxNiacinamideProtein Kinase InhibitorsSulfonamidesacute myeloid leukemiaBH3 mimetic drugsMEK inhibitors

Identifiers

PMID26625317
PMCPMC4808037
OpenAlexW2186148426

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.