Evidence map›Paper›PMID 10393850›Full record

ArticleThe American journal of pathology1999

Transgene expression and repression in transgenic rats bearing the phosphoenolpyruvate carboxykinase-simian virus 40 T antigen or the phosphoenolpyruvate carboxykinase-transforming growth factor-alpha constructs.

M J Haas, Y P Dragan, H Hikita, R Shimel, K Takimoto, S Heath, J Vaughan, H C Pitot

Open access · greenAbstract read
In one paragraph

Article in The American journal of pathology, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
0.6field-weighted citation impact, top 29% 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

5 citing papers in PubMed, 14 citations in OpenAlex.

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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

8 authors at 1 institution in 1 country.

M J HaasMcArdle Laboratory for Cancer Research, Departments of Oncology and Pathology, The Medical School, University of Wisconsin, Madison, Wisconsin, USA.
Y P Dragan
H Hikita
R Shimel
K Takimoto
S Heath
J Vaughan
H C Pitot
University of Wisconsin–Madison · US

Funding

TRANSGENIC MODELS OF DIOXIN CARCINOGENICITY AND AH RECEPTOR FUNCTIONP01CA022484 · NCI · UNIVERSITY OF WISCONSIN-MADISON · PI BRADFIELD, CHRISTOPHER A · 1985 to 2011
$9.2M
STOREROOM AND MATERIALS ACQUISITION LABORATORYP30CA007175 · NCI · UNIVERSITY OF WISCONSIN MADISON · PI PITOT, JR., HENRY C · 1985 to 2000
$2.4M
INSTABILITY OF TUMOR PROMOTION IN HEPATOCARCINOGENESISR01CA045700 · NCI · UNIVERSITY OF WISCONSIN-MADISON · PI PITOT, JR., HENRY C · 1987 to 2006
$2.1M
NCI NIH HHS CA-07175NCI NIH HHS CA-22484NCI NIH HHS CA-45700NCI NIH HHS P01 CA022484NCI NIH HHS R01 CA045700
6 · The paper itself

Abstract

Transgenic Sprague-Dawley rats expressing either human transforming growth factor-alpha (TGFalpha) or simian virus 40 large and small T antigen (TAg), each under the control of the phosphoenolpyruvate carboxykinase (PEPCK) promoter, were developed as an approach to the study of the promotion of hepatocarcinogenesis in the presence of a transgene regulatable by diet and/or hormones. Five lines of PEPCK-TGFalpha transgenic rats were established, each genetic line containing from one to several copies of the transgene per haploid genome. Two PEPCK-TAg transgenic founder rats were obtained, each with multiple copies of the transgene. Expression of the transgene was undetectable in the TGFalpha transgenic rats and could not be induced when the animals were placed on a high-protein, low-carbohydrate diet. The transgene was found to be highly methylated in all of these lines. No pathological alterations in the liver and intestine were observed at any time (up to 2 years) during the lives of these rats. One line of transgenic rats expressing the PEPCK-TAg transgene developed pancreatic islet cell hyperplasias and carcinomas, with few normal islets evident in the pancreas. This transgene is integrated as a hypomethylated tandem array of 10 to 12 copies on chromosome 8q11. Expression of large T antigen is highest in pancreatic neoplasms, but is also detectable in the normal brain, kidney, and liver. Mortality is most rapid in males, starting at 5 months of age and reaching 100% by 8 months. Morphologically, islet cell differentiation in the tumors ranges from poor to well differentiated, with regions of necrosis and fibrosis. Spontaneous metastasis of TAg-positive tumor cells to regional lymph nodes was observed. These studies indicate the importance of DNA methylation in the repression of specific transgenes in the rat. However, the expression of the PEPCK-TAg induces neoplastic transformation in islet cells, probably late in neuroendocrine cell differentiation. T antigen expression during neoplastic development may result in a pervasive change in the islet cell growth properties with selection of a transformed phenotype as a possible requirement for cell viability.

Indexed as

AnimalsAnimals, Genetically ModifiedAntigens, Polyomavirus TransformingCell Transformation, NeoplasticFemaleGene ExpressionHyperplasiaIslets of LangerhansMalePancreatic NeoplasmsPhosphoenolpyruvate Carboxykinase (GTP)RatsRats, Sprague-DawleyRecombinant Fusion ProteinsSurvival AnalysisTransforming Growth Factor alphaAntigens, Polyomavirus TransformingPhosphoenolpyruvate Carboxykinase (GTP)Recombinant Fusion ProteinsTransforming Growth Factor alpha

Identifiers

PMID10393850
PMCPMC1866666
OpenAlexW2072462863

What OpenQuestion holds

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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.