Evidence map›Paper›PMID 29857559›Full record

ArticleCancers2018

The Cellular p53 Inhibitor MDM2 and the Growth Factor Receptor FLT3 as Biomarkers for Treatment Responses to the MDM2-Inhibitor Idasanutlin and the MEK1 Inhibitor Cobimetinib in Acute Myeloid Leukemia.

Katja Seipel, Miguel A T Marques, Corinne Sidler, Beatrice U Mueller, Thomas Pabst

Open access · goldAbstract read
In one paragraph

Article in Cancers, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
1.9field-weighted citation impact, top 14% 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

21 citing papers in PubMed, 30 citations in OpenAlex.

  1. Review
  2. Article
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  4. Synergistic Activity of Combined FLT3-ITD and MDM2 Inhibition with Quizartinib and Milademetan in FLT3-ITD Mutant/TP53 Wild-type Acute Myeloid Leukemias.Clinical cancer research : an official journal of the American Association for Cancer Research · 2025
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  7. miR-16-5p enhances sensitivity to RG7388 through targetingCancer drug resistance (Alhambra, Calif.) · 2023
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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

5 authors at 2 institutions in 1 country.

Katja SeipelDepartment for Biomedical Research (DBMR), University of Bern, 3008 Bern, Switzerland. katja.seipel@dbmr.unibe.ch.
Miguel A T MarquesDepartment for Biomedical Research (DBMR), University of Bern, 3008 Bern, Switzerland. Miguel.Teixeiramarques@students.unibe.ch.
Corinne SidlerDepartment for Biomedical Research (DBMR), University of Bern, 3008 Bern, Switzerland. Corinne.Sidler@dbmr.unibe.ch.
Beatrice U MuellerDepartment of Medical Oncology, University Hospital Bern, 3010 Bern, Switzerland. Beatrice.Mueller@insel.ch.
Thomas PabstDepartment of Medical Oncology, University Hospital Bern, 3010 Bern, Switzerland. thomas.pabst@insel.ch.
University Hospital of Bern · CHUniversity of Bern · CH

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The tumor suppressor protein p53 is inactivated in a large variety of cancer cells. Cellular p53 inhibitors like the mouse double minute 2 homolog (MDM2) commonly suppress the p53 function in acute myeloid leukemia (AML). Moreover, fms like tyrosine kinase 3 (FLT3) growth factor signaling pathways including the mitogen-activated kinase (MAPK) cascade (RAS-RAF-MEK-ERK) are highly active in AML cells. Consequently, the combined administration of MDM2 and MEK inhibitors may present a promising anti-leukemic treatment strategy. Here we assessed the MDM2 antagonist idasanutlin and the MEK1 inhibitor cobimetinib as single agents and in combination in a variety of AML cell lines and primary AML blast cells for their ability to induce apoptosis and cell death. AML cell lines and blast cells comprised all major AML subtypes based on the mutational status of

Indexed as

acute myeloid leukemia (AML)FMS like tyrosine kinase 3 (FLT3)MAP2KMAPKK)mitogen-activated protein kinase kinase (MEKmouse double minute 2 homolog (MDM2)tumor suppressor p53 (TP53)

Identifiers

PMID29857559
PMCPMC6025168
OpenAlexW2807521243

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.