Cell proliferation and carcinogenesis

Research output: Contribution to journalReview article

9 Citations (Scopus)

Abstract

Cancer is due to multiple inherited or acquired mutations occurring in a single cell. DNA replication, although incredibly precise, results in spontaneous errors. A chemical can increase the number of errors per DNA replication by increasing damage to DNA, or it can increase the probability for spontaneous errors by increasing the number of DNA replications. A model has been developed which takes into account the role of DNA reactivity and increased DNA replication in the pluripotential cell population of a tissue on the development of cancer. This model can be used to assess the mode of action of chemicals which are carcinogenic in animal models and to access the relevance of that mode of action to human risk. By using this mode of action-based model, it may then be possible to replace the 2-year cancer bioassay with shorter-term assays which assess DNA reactivity, immunosuppression and estrogenic activity of the chemical and the effects of the chemical on toxicity and cell proliferation.

Original languageEnglish (US)
Pages (from-to)1-7
Number of pages7
JournalJournal of Toxicologic Pathology
Volume21
Issue number1
DOIs
StatePublished - Apr 8 2008

Fingerprint

Cell proliferation
DNA Replication
Carcinogenesis
Cell Proliferation
DNA
Pharmacologic Actions
Neoplasms
Biological Assay
Immunosuppression
DNA Damage
Animal Models
Bioassay
Mutation
Toxicity
Assays
Animals
Population
Cells
Tissue

Keywords

  • Cell proliferation
  • Chemical carcinogen
  • Cytotoxicity
  • Genotoxicity
  • Modeling
  • Risk assessment

ASJC Scopus subject areas

  • Pathology and Forensic Medicine
  • Toxicology

Cite this

Cell proliferation and carcinogenesis. / Cohen, Samuel Monroe; Arnold, Lora L.

In: Journal of Toxicologic Pathology, Vol. 21, No. 1, 08.04.2008, p. 1-7.

Research output: Contribution to journalReview article

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