Evidence map›Paper›PMID 9343166›Full record

ArticleJournal of virology1997

A simian virus 40 large T-antigen segment containing amino acids 1 to 127 and expressed under the control of the rat elastase-1 promoter produces pancreatic acinar carcinomas in transgenic mice.

M J Tevethia, R H Bonneau, J W Griffith, L Mylin

Open access · bronzeAbstract read
In one paragraph

Article in Journal of virology, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
1.0field-weighted citation impact, top 22% 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

27 citing papers in PubMed, 56 citations in OpenAlex.

  1. Trial
  2. Altered glycosylation in cancer: A promising target for biomarkers and therapeutics.Biochimica et biophysica acta. Reviews on cancer · 2021
    Review
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  12. T antigen transgenic mouse models.Seminars in cancer biology · 2009
    Review
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  15. Article
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  17. Review
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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

4 authors at 1 institution in 1 country.

M J TevethiaDepartment of Microbiology and Immunology, Pennsylvania State University College of Medicine, Hershey 17033, USA.
R H Bonneau
J W Griffith
L Mylin
Penn State Milton S. Hershey Medical Center · US

Funding

MUTAGENESIS OF SPECIFIC REGIONS OF THE SV40 GENOMER01CA024694 · NCI · PENNSYLVANIA STATE UNIV HERSHEY MED CTR · PI TEVETHIA, MARY J · 1985 to 2006
$2.0M
MUTAGENESIS OF SPECIFIC REGIONS OF THE SV40 GENOMER55CA024694 · NCI · PENNSYLVANIA STATE UNIV HERSHEY MED CTR · PI TEVETHIA, MARY J · 1991 to 1991
–
NCI NIH HHS CA24694
6 · The paper itself

Abstract

The simian virus 40 large T antigen induces tumors in a wide variety of tissues in transgenic mice, the precise tissues depending on the tissue specificity of the upstream region controlling T-antigen expression. Expression of mutant T antigens that contain a subset of the protein's activities restricts the spectrum of tumors induced. Others showed previously that expression of a mutant large T antigen containing the N-terminal 121 amino acids (T1-121) under control of the lymphotropic papovavirus promoter resulted in slow-growing choroid plexus tumors, whereas full-length T antigen under the same promoter induced rapidly growing CPR tumors, T-cell lymphomas, and B-cell lymphomas. In those instances, the alteration in tumor induction or progression correlated with inability of the mutant large T antigen to bind the tumor suppressor p53. In the study reported here, we investigated the capacity of an N-terminal T antigen segment (T1-127) expressed in conjunction with small t antigen under control of the rat elastase-1 (E1) promoter to induce pancreatic tumors. The results show that pancreases of transgenic mice expressing T1-127 and small t antigen display acinar cell dysplasia at birth that progresses to neoplasia. The average age to death in these mice is within the range reported for transgenic mice expressing full-length T antigen under control of the E1 promoter. These results indicate that sequestering p53 by binding is not required for the development of rapidly growing acinar cell carcinomas. In addition, we provide evidence that small t antigen is unlikely to be required. Finally, we show that the p53 protein in acinar cell carcinomas is wild type in conformation.

Indexed as

AnimalsAntigens, Polyomavirus TransformingCarcinoma, Acinar CellGenes, p53MiceMice, Inbred C57BLMice, TransgenicPancreatic ElastasePancreatic NeoplasmsPromoter Regions, GeneticAntigens, Polyomavirus TransformingPancreatic Elastase

Identifiers

PMID9343166
PMCPMC192272
OpenAlexW2108160743

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.