Evidence map›Paper›PMID 15958052›Full record

ArticleCancer science2005

High susceptibility of human c-Ha-ras proto-oncogene transgenic rats to carcinogenesis: a cancer-prone animal model.

Hiroyuki Tsuda, Katsumi Fukamachi, Yutaka Ohshima, Shinobu Ueda, Yoichiro Matsuoka, Tetsuya Hamaguchi, Takamasa Ohnishi, Nobuo Takasuka, Akihiro Naito

Open access · bronzeAbstract read
In one paragraph

Article in Cancer science, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
2.3field-weighted citation impact, top 13% 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

11 citing papers in PubMed, 26 citations in OpenAlex.

  1. Article
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  4. Review
  5. Effect of Nrf2 on rat ovarian tissues against atrazine-induced anti-oxidative response.International journal of clinical and experimental pathology · 2014
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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

9 authors at 6 institutions in 3 countries.

Hiroyuki TsudaDepartment of Molecular Toxicology, Nagoya City University Graduate School of Medical Sciences, 1 Kawasumi, Mizuho-ku, Nagoya 467-8601, Japan. htsuda@med.nagoya-cu.ac.jp
Katsumi Fukamachi
Yutaka Ohshima
Shinobu Ueda
Yoichiro Matsuoka
Tetsuya Hamaguchi
Takamasa Ohnishi
Nobuo Takasuka
Akihiro Naito
Nagoya City University · JPKansai Medical University · JPMie University · JPNational Cancer Research Institute · GBNational Center for Toxicological Research · USTokushima University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Transgenic animals carrying human c-Ha-ras proto-oncogene, v-Ha-ras transgenic mice, pim-1 transgenic mice and several knockout mice deficient of tumor suppressor genes, such as p53, have been shown to exhibit increased carcinogen susceptibility. As a result, studies into practical application and medium-term screening of environmental carcinogens are under way. Given the advantages of rat models characterized by larger organ size, abundant information regarding preneoplasias and virus-free constitution, we have concentrated on the generation of transgenic rats bearing copies of the human c-Ha-ras proto-oncogene and shown the Hras128 strain to be extremely sensitive to the induction of mammary carcinomas, and to a lesser extent, lesions in the urinary bladder, esophagus and skin. In most, if not all, the mammary cancers mutations of the transgene but not the endogenous H-ras gene are present, appearing to occur early in the process of tumorigenesis, which involves proliferation of cells in TEB and intraductal hyperplasia before carcinomas arise. Preliminary findings suggest that this is independent of endogenous ovarian hormones, although inhibited by soy isoflavones and promoted by atrazine and nonylphenols. Although further studies of the mechanisms are clearly necessary, the model appears to have great potential for screening purposes, not only for modifiers active in the breast, but also other organs where tumors characterized by ras gene mutations develop.

Indexed as

Disease Models, AnimalGenetic Predisposition to DiseaseAnimalsAnimals, Genetically ModifiedCarcinogensCell ProliferationCell Transformation, NeoplasticEsophageal NeoplasmsFemaleGenes, rasHumansMaleMammary Neoplasms, AnimalProto-Oncogene MasRatsRats, Sprague-DawleyCarcinogensMAS1 protein, humanProto-Oncogene Mas

Identifiers

PMID15958052
PMCPMC11158793
OpenAlexW2070416576

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.