Evidence map›Paper›PMID 9001226›Full record

ArticleMolecular and cellular biology1997

Increased tumor proliferation and genomic instability without decreased apoptosis in MMTV-ras mice deficient in p53.

J E Hundley, S K Koester, D A Troyer, S G Hilsenbeck, M A Subler, J J Windle

Open access · bronzeAbstract read
In one paragraph

Article in Molecular and cellular biology, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
4.9field-weighted citation impact, top 4% 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

37 citing papers in PubMed, 92 citations in OpenAlex.

  1. Review
  2. Molecular interactions in juvenile nasopharyngeal angiofibroma: preliminary signature and relevant review.European archives of oto-rhino-laryngology : official journal of the European Federation of Oto-Rhino-Laryngological Societies (EUFOS) : affiliated with the German Society for Oto-Rhino-Laryngology - Head and Neck Surgery · 2019
    Review
  3. Article
  4. Genome Stability Requires p53.Cold Spring Harbor perspectives in medicine · 2016
    Review
  5. Review
  6. Review
  7. Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Influence of Hoxa5 on p53 tumorigenic outcome in mice.The American journal of pathology · 2010
    Article
  15. Review
  16. Article
  17. Loss of cryptochrome reduces cancer risk in p53 mutant mice.Proceedings of the National Academy of Sciences of the United States of America · 2009
    Article
  18. Article
  19. p21 delays tumor onset by preservation of chromosomal stability.Proceedings of the National Academy of Sciences of the United States of America · 2006
    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

6 authors at 1 institution in 1 country.

J E HundleyDepartment of Cellular and Structural Biology, The University of Texas Health Science Center at San Antonio, 78284, USA.
S K Koester
D A Troyer
S G Hilsenbeck
M A Subler
J J Windle
The University of Texas Health Science Center at San Antonio · US

Funding

TUMOR SUPPRESSOR GENES IN BREAST CANCER DEVELOPMENTP50CA058183 · NCI · UNIVERSITY OF TEXAS HLTH SCI CTR SAN ANT · PI OSBORNE, C KENT · 1992 to 2012
$30.9M
NCI NIH HHS P30 CA54714NCI NIH HHS P50 CA58183
6 · The paper itself

Abstract

We have used an in vivo tumor model to evaluate the consequences of p53 tumor suppressor protein deficiency in a tissue-specific context. By breeding MMTV-ras transgenic mice, which are highly susceptible to the development of mammary and salivary tumors, with p53(-/-) mice, we generated three classes of animals which contained the MMTV-ras transgene but differed in their p53 functional status (ras/p53(+/+), ras/p53(+/-), or ras/p53(-/-)). ras/p53(-/-) mice developed tumors more rapidly than animals of the other two genotypes; however, the distribution of tumors was unexpectedly altered. Whereas the most frequently observed tumors in ras/p53(+/+) and ras/p53(+/-) mice were of mammary origin, ras/p53(-/-) mice developed primarily salivary tumors. In addition, the mammary and salivary tumors from ras/p53(-/-) mice consistently exhibited a number of unfavorable characteristics, including higher histologic grades, increased growth rates, and extensive genomic instability and heterogeneity, relative to tumors from ras/p53(+/+) mice. Interestingly, the increased growth rates of ras/p53(-/-) tumors appear to be due to impaired cell cycle regulation rather than decreased apoptosis, suggesting that p53-mediated tumor suppression can occur independent of its role in apoptosis.

Indexed as

Mammary Tumor Virus, MouseAneuploidyAnimalsApoptosisCell DivisionCrosses, GeneticFemaleGenes, rasGenetic HeterogeneityGenotypeMammary Neoplasms, ExperimentalMiceMice, KnockoutMice, TransgenicSalivary Gland NeoplasmsTumor Suppressor Protein p53Tumor Suppressor Protein p53

Identifiers

PMID9001226
PMCPMC231798
OpenAlexW2168640139

What OpenQuestion holds

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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.