Evidence map›Paper›PMID 16355251›Full record

ReviewOncogene2005

Biological, cellular, and molecular characteristics of an inducible transgenic skin tumor model: a review.

Michael C Humble, Carol S Trempus, Judson W Spalding, Ronald E Cannon, Raymond W Tennant

Abstract readReview
PubMed Publisher
In one paragraph

Review in Oncogene, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
3.3field-weighted citation impact, top 9% 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

9 citing papers in PubMed, 27 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Arsenic, stem cells, and the developmental basis of adult cancer.Toxicological sciences : an official journal of the Society of Toxicology · 2011
    Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Transplacental arsenic carcinogenesis in mice.Toxicology and applied pharmacology · 2007
    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

5 authors at 2 institutions in 1 country.

Michael C HumbleCurriculum in Toxicology, University of North Carolina at Chapel Hill, Chapel Hill, NC 27514, USA.
Carol S Trempus
Judson W Spalding
Ronald E Cannon
Raymond W Tennant
National Institute of Environmental Health Sciences · USUniversity of North Carolina at Chapel Hill · US

Funding

TOXICOLOGYT32ES007126 · NIEHS · UNIV OF NORTH CAROLINA CHAPEL HILL · PI ILONA JASPERS, Bernard E. Weissman · 1985 to 2026
$13.0M
V-HA-RAS EXPRESSION, PROLIFERATION AND SKIN TUMORIGENESIS IN RAS TRANSGENIC MICEZ01ES021175 · NIEHS · NATIONAL INSTITUTE OF ENVIRONMENTAL HEALTH SCIENCES · PI TENNANT, RAYMOND W · 1992 to 2008
$2.3M
Molecular Mechanisms Of Skin TumorigenesisZ01ES100610 · NIEHS · NATIONAL INSTITUTE OF ENVIRONMENTAL HEALTH SCIENCES · PI PRITCHARD, JOHN · 2002 to 2008
$1.9M
Characterization of epidermal stem cells: biology, carcinogenesis, and functionZIAES021175 · NIEHS · NATIONAL INSTITUTE OF ENVIRONMENTAL HEALTH SCIENCES · PI LANGENBACH, ROBERT · 2009 to 2010
$696k
NIEHS NIH HHS T32 ES07126
6 · The paper itself

Abstract

The genetically initiated Tg.AC transgenic mouse carries a transgene consisting of an oncogenic v-Ha-ras coding region flanked 5' by a mouse zeta-globin promoter and 3' by an SV-40 polyadenylation sequence. Located on chromosome 11, the transgene is transcriptionally silent until activated by chemical carcinogens, UV light, or full-thickness wounding. Expression of the transgene is an early event that drives cellular proliferation resulting in clonal expansion and tumor formation, the unique characteristics now associated with the Tg.AC mouse. This ras-dependent phenotype has resulted in the widespread interest and use of the Tg.AC mouse in experimental skin carcinogenesis and as an alternative carcinogenesis assay. This review examines the general biology of the tumorigenic responses observed in Tg.AC mice, the genetic interactions of the ras transgene, and explores the cellular and molecular regulation of zeta-globin promoted transgene expression. As a prototype alternative model to the current long-term rodent bioassays, the Tg.AC has generated a healthy discussion on the future of transgenic bioassays, and opened the doors for subsequent models for toxicity testing. The further exploration and elucidation of the molecular controls of transgene expression will enhance the usefulness of this mouse and enable a better understanding of the Tg.AC's discriminate response to chemical carcinogens.

Indexed as

Disease Models, AnimalGene Expression Regulation, NeoplasticGenes, rasMice, TransgenicAnimalsHumansMiceSkin Neoplasms

Identifiers

PMID16355251
OpenAlexW2017779792

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.