Evidence map›Paper›PMID 38994976›Full record

ReviewCells2024

Targeting Hdm2 and Hdm4 in Anticancer Drug Discovery: Implications for Checkpoint Inhibitor Immunotherapy.

Monde Ntwasa

Abstract readReview
In one paragraph

Review in Cells, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
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

1 citing paper in PubMed.

  1. 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

1 author.

Monde NtwasaDepartment of Life and Consumer Sciences, University of South Africa, Cnr Pioneer Road and Christiaan de Wet Road, Florida, Johannesburg 1710, South Africa.ORCID 0000-0002-6400-8867

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hdm2 and Hdm4 are structural homologs that regulate the tumor suppressor protein, p53. Since some tumors express wild-type p53, Hdm2 and Hdm4 are plausible targets for anticancer drugs, especially in tumors that express wild-type p53. Hdm4 can enhance and antagonize the activity of Tp53, thereby playing a critical role in the regulation of p53's activity and stability. Moreover, Hdm2 and Hdm4 are overexpressed in many cancers, some expressing wild-type Tp53. Due to experimental evidence suggesting that the activation of wild-type Tp53 can augment the antitumor activity by some checkpoint inhibitors, drugs targeting Hdm2 and Hdm4 may be strong candidates for combining with checkpoint inhibitor immunotherapy. However, other evidence suggests that the overexpression of Hdm2 and Hdm4 may indicate poor response to immune checkpoint inhibitors. These findings require careful examination and scrutiny. In this article, a comprehensive analysis of the Hdm2/Hdm4 partnership will be conducted. Furthermore, this article will address the current progress of drug development regarding molecules that target the Hdm2/Hdm4/Tp53 partnership.

Indexed as

Antineoplastic AgentsDrug DiscoveryImmune Checkpoint InhibitorsImmunotherapyProto-Oncogene Proteins c-mdm2AnimalsCell Cycle ProteinsHumansNeoplasmsProto-Oncogene ProteinsTumor Suppressor Protein p53Antineoplastic AgentsCell Cycle ProteinsImmune Checkpoint InhibitorsMDM2 protein, humanMDM4 protein, humanProto-Oncogene ProteinsProto-Oncogene Proteins c-mdm2Tumor Suppressor Protein p53anticancer drugscancerHdm2Hdm4immune checkpoint inhibitorsoncology

Identifiers

PMID38994976
PMCPMC11240505

What Socratic 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 Socratic graph.