Evidence map›Paper›PMID 24658082›Full record

ReviewCancer discovery2014

Contribution of p53 to metastasis.

Emily Powell, David Piwnica-Worms, Helen Piwnica-Worms

Open access · bronzeAbstract readReview
In one paragraph

Review in Cancer discovery, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 216 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
216citing papers in PubMed, 2 pooled it
12.5field-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

216 citing papers in PubMed, 2 syntheses or guidelines pooled it, 365 citations in OpenAlex.

  1. Pooled it
  2. Targeting p53 pathways: mechanisms, structures, and advances in therapy.Signal transduction and targeted therapy · 2023
    Pooled it
  3. Trial
  4. Review
  5. Multi-omic Profiling of Recurrence Risk Across Breast Cancer Subtypes.medRxiv : the preprint server for health sciences · 2026
    Article
  6. Article
  7. Article
  8. Article
  9. Review
  10. Article
  11. Chemoresistance: The hidden barrier in cancer treatment.Cancer pathogenesis and therapy · 2026
    Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Elucidating the Role ofCurrent issues in molecular biology · 2025
    Review
  18. Review
  19. Review
  20. Review

156 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

3 authors at 1 institution in 1 country.

Emily PowellDepartments of 1Cancer Biology and 2Cancer Systems Imaging, The University of Texas MD Anderson Cancer Center, Houston, Texas.
David Piwnica-Worms
Helen Piwnica-Worms
The University of Texas MD Anderson Cancer Center · US

Funding

WU-MDACC Inter-Institutional Molecular Imaging CenterP50CA094056 · NCI · WASHINGTON UNIVERSITY · PI KOPAN, RAPHAEL · 2002 to 2016
$26.3M
MOLECULAR ONCOLOGY TRAINING GRANTT32CA113275 · NCI · WASHINGTON UNIVERSITY · PI Matthew J Walter · 2006 to 2026
$5.7M
NCI NIH HHS P50 CA094056NCI NIH HHS P50 CA94056NCI NIH HHS T32 CA113275
6 · The paper itself

Abstract

unlabelledThe tumor suppressor p53 is lost or mutated in about half of all human cancers, and in those tumors in which it is wild-type, mechanisms exist to prevent its activation. p53 loss not only prevents incipient tumor cells from undergoing oncogene-induced senescence and apoptosis, but also perturbs cell-cycle checkpoints. This enables p53-deficient tumor cells with DNA damage to continue cycling, creating a permissive environment for the acquisition of additional mutations. Theoretically, this could contribute to the evolution of a cancer genome that is conducive to metastasis. Importantly, p53 loss also results in the disruption of pathways that inhibit metastasis, and transcriptionally defective TP53 mutants are known to gain additional functions that promote metastasis. Here, we review the evidence supporting a role for p53 loss or mutation in tumor metastasis, with an emphasis on breast cancer. SIGNIFICANCE: The metastatic potential of tumor cells can be positively infl uenced by loss of p53 or expression of p53 gain-of-function mutants. Understanding the mechanisms by which p53 loss and mutation promote tumor metastasis is crucial to understanding the biology of tumor progression and how to appropriately apply targeted therapies.

Indexed as

Breast NeoplasmsCell CommunicationFemaleHumansMutationNeoplasm MetastasisPrognosisSignal TransductionTumor Suppressor Protein p53Tumor Suppressor Protein p53

Identifiers

PMID24658082
PMCPMC4063123
OpenAlexW2169385603

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.