Evidence map›Paper›PMID 14627978›Full record

ArticleOncogene2003

Genetic interactions between Pten and p53 in radiation-induced lymphoma development.

Jian-Hua Mao, Di Wu, Jesus Perez-Losada, Hiroki Nagase, Reyno DelRosario, Allan Balmain

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
1.8field-weighted citation impact, top 16% 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

24 citing papers in PubMed, 44 citations in OpenAlex.

  1. Article
  2. Article
  3. Nuclear PTEN and p53 suppress stress-induced liver cancer through distinct mechanisms.Biochemical and biophysical research communications · 2021
    Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. Mouse models for efficacy testing of agents against radiation carcinogenesis—a literature review.International journal of environmental research and public health · 2012
    Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Review
  14. Cis lethal genetic interactions attenuate and alter p53 tumorigenesis.Proceedings of the National Academy of Sciences of the United States of America · 2010
    Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Review
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

6 authors at 2 institutions in 1 country.

Jian-Hua MaoCancer Research Institute, University of California at San Francisco, 2340 Sutter Street, San Francisco, CA 94143, USA.
Di Wu
Jesus Perez-Losada
Hiroki Nagase
Reyno DelRosario
Allan Balmain
Cancer Research Institute · USCancer Genetics (United States) · US

Funding

Identification of epithelial tumor susceptiility genesU01CA084244 · NCI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI BALMAIN, ALLAN · 1999 to 2013
$13.3M
NCI NIH HHS U01 CA84244
6 · The paper itself

Abstract

Genetic analysis of radiation-induced lymphomas from p53 heterozygous or null mice has revealed a high frequency of genetic alterations on mouse chromosome 19. Detailed microsatellite analysis of chromosome 19 deletions identified three independent regions of loss of heterozygosity, one of which was refined to a 0.3 Mb interval that contained the Pten tumor suppressor gene. More than 50% of radiation-induced tumors from p53+/- and p53-/- mice showed heterozygous loss of one Pten allele. In most cases, the remaining allele was wild type and expressed, suggesting that Pten is a haploinsufficient tumor suppressor gene for mouse lymphoma development. This conclusion was supported by the detection of specific intragenic deletions in Pten in tumors that retained one wild-type allele. Pten heterozygous mice were just as sensitive as p53+/- mice to induction of tumors by radiation, and surprisingly, the double p53+/-Pten+/-mice were equivalent to p53 null mice in radiation sensitivity. Despite the fact that Pten appears to be a haploinsufficient tumor suppressor gene, most tumors from both the single and double heterozygous mice had lost the remaining wild-type allele. The mechanism of loss in all cases involved the complete chromosome, suggesting that it is driven by other tumor suppressor genes on this chromosome. This sensitized screen therefore identified complementary roles for Pten and p53 pathways in suppression of tumor development induced by radiation exposure.

Indexed as

AnimalsBlotting, WesternLoss of HeterozygosityLymphomaMiceNeoplasms, Radiation-InducedPhosphoric Monoester HydrolasesPTEN PhosphohydrolaseReverse Transcriptase Polymerase Chain ReactionTime FactorsTumor Suppressor Protein p53Tumor Suppressor ProteinsPhosphoric Monoester HydrolasesPTEN PhosphohydrolaseTumor Suppressor Protein p53Tumor Suppressor Proteins

Identifiers

PMID14627978
OpenAlexW2009425130

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.