Evidence map›Paper›PMID 19538162›Full record

ReviewAnti-cancer agents in medicinal chemistry2009

Recent advances in validating MDM2 as a cancer target.

Elizabeth R Rayburn, Scharri J Ezell, Ruiwen Zhang

Abstract readReviewValidation Study
In one paragraph

Review in Anti-cancer agents in medicinal chemistry, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing 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

26 citing papers in PubMed.

  1. Review
  2. Article
  3. Review
  4. Three-Dimensional Gene Regulation Network in Glioblastoma Ferroptosis.International journal of molecular sciences · 2023
    Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. A quantitative LC-MS/MS method for determination of SP-141, a novel pyrido[b]indole anticancer agent, and its application to a mouse PK study.Journal of chromatography. B, Analytical technologies in the biomedical and life sciences · 2014
    Article
  19. Article
  20. 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

3 authors.

Elizabeth R RayburnDepartment of Pharmacology and Toxicology, Division of Clinical Pharmacology, University of Alabama at Birmingham, Birmingham, AL 35294-0019, USA.
Scharri J Ezell
Ruiwen Zhang

Funding

Dietary Chemopreventive Components/Oncogene Interaction and CancerR01CA121211 · NCI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI ZHANG, RUIWEN · 2007 to 2011
$1.4M
MDM2 AS A NEGATIVE REGULATOR OF P21 WAF1/CIP1R01CA112029 · NCI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI ZHANG, RUIWEN · 2005 to 2009
$1.3M
CANCER GENE THERAPY TRAINING PROGRAMT32CA075930 · NCI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI CURIEL, DAVID TERRY · 1998 to 2008
$1.1M
NCI NIH HHS R01 CA112029NCI NIH HHS R01 CA121211NCI NIH HHS T32 CA075930
6 · The paper itself

Abstract

The MDM2 oncogene is overexpressed in various human cancers. Its expression correlates with the phenotypes of high-grade, late-stage, and more resistant tumors. The auto-regulatory loop between MDM2 and the tumor suppressor p53 has long been considered the epitome of a rational target for cancer therapy. As such, many novel agents have been generated to interfere with the interaction of the two proteins, which results in the activation of p53. Among these agents are several small molecule inhibitors synthesized based upon the crystal structures of the MDM2-p53 complex. With use of high-throughput screening, several specific and effective agents for inhibition of the protein-protein interaction were discovered. Recent investigations, however, have demonstrated that many proteins regulate the MDM2-p53 interaction, and that MDM2 may have p53-independent oncogenic functions. In order for novel MDM2 inhibitors to be translated to the clinic, it is necessary to obtain a better understanding of the regulation of MDM2 and of the MDM2-p53 interaction. In particular, the implications of various interactions between certain regulator(s) and MDM2/p53 under different circumstances need to be elucidated to determine which pathway(s) represent the best targets for therapy. Targeting both MDM2 itself and regulators of MDM2 and the MDM2-p53 interaction, or use of MDM2 inhibitors in combination with conventional treatments, may improve prospects for tumor eradication.

Indexed as

Antineoplastic AgentsCell CycleHumansNeoplasmsOncogenesProto-Oncogene Proteins c-mdm2Tumor Suppressor Protein p53Antineoplastic AgentsMDM2 protein, humanProto-Oncogene Proteins c-mdm2Tumor Suppressor Protein p53

Identifiers

PMID19538162
PMCPMC6728151

What OpenQuestion holds

Textmetadata
LicenceTDM
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.