Evidence map›Paper›PMID 31310659›Full record

ReviewJournal of molecular cell biology2019

Inhibition of p53 inhibitors: progress, challenges and perspectives.

Gema Sanz, Madhurendra Singh, Sylvain Peuget, Galina Selivanova

Open access · goldAbstract readReview
In one paragraph

Review in Journal of molecular cell biology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 92 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
92citing papers in PubMed, 1 pooled it
9.7field-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

92 citing papers in PubMed, 1 synthesis or guideline pooled it, 135 citations in OpenAlex.

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32 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

4 authors at 1 institution in 1 country.

Gema SanzDepartment of Microbiology, Tumor and Cell Biology, Biomedicum 8C, Karolinska Institute, Sweden.
Madhurendra SinghDepartment of Microbiology, Tumor and Cell Biology, Biomedicum 8C, Karolinska Institute, Sweden.
Sylvain PeugetDepartment of Microbiology, Tumor and Cell Biology, Biomedicum 8C, Karolinska Institute, Sweden.
Galina SelivanovaDepartment of Microbiology, Tumor and Cell Biology, Biomedicum 8C, Karolinska Institute, Sweden.
Karolinska Institutet · SE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

p53 is the major tumor suppressor and the most frequently inactivated gene in cancer. p53 could be disabled either by mutations or by upstream negative regulators, including, but not limited to MDM2 and MDMX. p53 activity is required for the prevention as well as for the eradication of cancers. Restoration of p53 activity in mouse models leads to the suppression of established tumors of different origin. These findings provide a strong support to the anti-cancer strategy aimed for p53 reactivation. In this review, we summarize recent progress in the development of small molecules, which restore the tumor suppressor function of wild-type p53 and discuss their clinical advance. We discuss different aspects of p53-mediated response, which contribute to suppression of tumors, including non-canonical p53 activities, such as regulation of immune response. While targeting p53 inhibitors is a very promising approach, there are certain limitations and concerns that the intensive research and clinical evaluation of compounds will hopefully help to overcome.

Indexed as

NeoplasmsTumor Suppressor Protein p53AnimalsAntineoplastic AgentsCell Cycle ProteinsHumansMiceProto-Oncogene ProteinsProto-Oncogene Proteins c-mdm2Antineoplastic AgentsCell Cycle ProteinsMDM2 protein, humanMdm2 protein, mouseMDM4 protein, humanMdm4 protein, mouseProto-Oncogene ProteinsProto-Oncogene Proteins c-mdm2TP53 protein, humanTrp53 protein, mouseTumor Suppressor Protein p53anti-cancer therapyimmune responsep53targeted drugstranscription factortumor suppression

Identifiers

PMID31310659
PMCPMC6735775
OpenAlexW2958197380

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.