Evidence map›Paper›PMID 32651541›Full record

ReviewLeukemia2020

MDM2 inhibition: an important step forward in cancer therapy.

Marina Konopleva, Giovanni Martinelli, Naval Daver, Cristina Papayannidis, Andrew Wei, Brian Higgins, Marion Ott, John Mascarenhas, Michael Andreeff

Abstract readReview
PubMed Publisher
In one paragraph

Review in Leukemia, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 227 papers.

0numbers the graph read from it
0cells of the map it votes in
227citing papers in PubMed
18.2field-weighted citation impact, top 1% 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

227 citing papers in PubMed, 370 citations in OpenAlex.

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  16. Hot-Spot-Guided Generative Deep Learning for Drug-Like PPI Inhibitor Design.Interdisciplinary sciences, computational life sciences · 2026
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167 more citing papers are in PubMed but not listed here.

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

9 authors at 6 institutions in 4 countries.

Marina KonoplevaDepartment of Leukemia, The University of Texas MD Anderson Cancer Center, Houston, TX, USA. mkonople@mdanderson.org.ORCID http://orcid.org/0000-0002-9347-2212
Giovanni MartinelliIstituto Scientifico Romagnolo per lo Studio e la Cura dei Tumori, IRST IRCCS, Meldola, FC, Italy.
Naval DaverDepartment of Leukemia, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
Cristina PapayannidisInstitute of Hematology "L. and A". Seràgnoli, University Hospital S. Orsola-Malpighi, Bologna, Italy.
Andrew WeiThe Alfred Hospital, Monash University, Melbourne, VIC, Australia.ORCID http://orcid.org/0000-0002-7514-3298
Brian HigginsGenentech, Inc, South San Francisco, CA, USA.
Marion OttF. Hoffmann-La Roche, Basel, Switzerland.
John MascarenhasTisch Cancer Institute, Icahn School of Medicine at Mount Sinai, New York, NY, USA.ORCID http://orcid.org/0000-0002-8400-0483
Michael AndreeffDepartment of Leukemia, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
The University of Texas MD Anderson Cancer Center · USIcahn School of Medicine at Mount Sinai · USIRCCS Azienda Ospedliero-Universitaria di Bologna Policlinico di Sant'Orsola · ITIstituto Scientifico Romagnolo per lo Studio e la Cura dei Tumori · ITRoche (Switzerland) · CHThe Alfred Hospital · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Targeting the interaction between tumor suppressor p53 and the E3 ligase MDM2 represents an attractive treatment approach for cancers with wild-type or functional TP53. Indeed, several small molecules have been developed and evaluated in various malignancies. We provide an overview of MDM2 inhibitors under preclinical and clinical investigation, with a focus on molecules with ongoing clinical trials, as indicated by ClinicalTrials.gov . Because preclinical and clinical exploration of combination strategies is underway, data supporting these combinations are also described. We identified the following molecules for inclusion in this review: RG7112 (RO5045337), idasanutlin (RG7388), AMG-232 (KRT-232), APG-115, BI-907828, CGM097, siremadlin (HDM201), and milademetan (DS-3032b). Information about each MDM2 inhibitor was collected from major congress records and PubMed using the following search terms: each molecule name, "MDM2"and "HDM2." Only congress records were limited by date (January 1, 2012-March 6, 2020). Special attention was given to available data in hematologic malignancies; however, available safety data in any indication are reported. Overall, targeting MDM2 is a promising treatment strategy, as evidenced by the increasing number of MDM2 inhibitors entering the clinic. Additional clinical investigation is needed to further elucidate the role of MDM2 inhibitors in the treatment of human cancers.

Indexed as

Molecular Targeted TherapyAnimalsAntineoplastic AgentsAntineoplastic Combined Chemotherapy ProtocolsDisease ManagementDisease SusceptibilityDrug DevelopmentEnzyme InhibitorsHumansNeoplasmsProtein BindingProto-Oncogene Proteins c-mdm2Signal TransductionStructure-Activity RelationshipAntineoplastic AgentsEnzyme InhibitorsProto-Oncogene Proteins c-mdm2

Identifiers

PMID32651541
OpenAlexW3041100082

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.