Evidence map›Paper›PMID 15630097›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2005

tp53 mutant zebrafish develop malignant peripheral nerve sheath tumors.

Stéphane Berghmans, Ryan D Murphey, Erno Wienholds, Donna Neuberg, Jeffery L Kutok, Christopher D M Fletcher, John P Morris, Ting Xi Liu, Stefan Schulte-Merker, John P Kanki and 3 more

Abstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 351 papers.

0numbers the graph read from it
0cells of the map it votes in
351citing 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

351 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Early ultraviolet exposure disrupts late dorsal fin skeletal development in zebrafish.Developmental dynamics : an official publication of the American Association of Anatomists · 2026
    Article
  6. Review
  7. Article
  8. Article
  9. Choosing the right animal model for sarcoma research.Cellular and molecular life sciences : CMLS · 2026
    Review
  10. Review
  11. Unusual inheritance of a functionalScience advances · 2025
    Article
  12. Beyond Rodents: Alternative Animal Models in Colorectal Cancer Research.International journal of molecular sciences · 2025
    Review
  13. Article
  14. Splicing Defects and Cell Death CauseJournal of dental research · 2025
    Article
  15. Article
  16. Article
  17. iScience · 2025
    Article
  18. Article
  19. Article
  20. Article

291 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

13 authors.

Stéphane BerghmansDepartment of Pediatric Oncology, Dana-Farber Cancer Institute, and Division of Hematology/Oncology, Children's Hospital, Harvard Medical School, Boston, MA 02115, USA.
Ryan D Murphey
Erno Wienholds
Donna Neuberg
Jeffery L Kutok
Christopher D M Fletcher
John P Morris
Ting Xi Liu
Stefan Schulte-Merker
John P Kanki
Ronald Plasterk
Leonard I Zon
A Thomas Look

Funding

VectorP30CA006516 · NCI · DANA-FARBER CANCER INSTITUTE · PI Deborah J Goff · 1985 to 2026
$330.6M
Zebrafish Screens for Genetic Modifiers and Human Application in T-ALLP01CA068484 · NCI · DANA-FARBER CANCER INSTITUTE · PI SALLAN, STEPHEN E · 1995 to 2010
$31.9M
NCI NIH HHS CA-68484NCI NIH HHS P01 CA068484NCI NIH HHS P30 CA006516NCI NIH HHS P30CA6516
6 · The paper itself

Abstract

TP53 is the most frequently mutated tumor suppressor gene in human cancer, with nearly 50% of all tumors exhibiting a loss-of-function mutation. To further elucidate the genetic pathways involving TP53 and cancer, we have exploited the zebrafish, a powerful vertebrate model system that is amenable to whole-genome forward-genetic analysis and synthetic-lethal screens. Zebrafish lines harboring missense mutations in the tp53 DNA-binding domain were identified by using a target-selected mutagenesis strategy. Homozygous mutant fish from two of these lines were viable and exhibited mutations similar to those found in human cancers (tp53(N168K) and tp53(M214K)). Although homozygous tp53(N168K) mutants were temperature-sensitive and suppressed radiation-induced apoptosis only at 37 degrees C, cells in the tp53(M214K) embryos failed to undergo apoptosis in response to gamma radiation at both 28 and 37 degrees C. Unlike wild-type control embryos, irradiated tp53(M214K) embryos also failed to up-regulate p21 and did not arrest at the G(1)/S checkpoint. Beginning at 8.5 months of age, 28% of tp53(M214K) mutant fish developed malignant peripheral nerve sheath tumors. In addition to providing a model for studying the molecular pathogenic pathways of malignant peripheral nerve sheath tumors, these mutant zebrafish lines provide a unique platform for modifier screens to identify genetic mutations or small molecules that affect tp53-related pathways, including apoptosis, cell-cycle delay, and tumor suppression.

Indexed as

AllelesAnimalsApoptosisGenes, p53MutationNerve Sheath NeoplasmsZebrafish

Identifiers

PMID15630097
PMCPMC544293

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.