Dose response and potential thresholds in proliferation and cell survival and death

Raluca Mateuca (born Teodorescu), Ilse Decordier, Micheline Volders

    Research output: Chapter in Book/Report/Conference proceedingChapterpeer-review

    Abstract

    Tumourigenicity is the result of the balance between mutations, epigenetic changes, cell
    proliferation and cell death. Cell proliferation can be a primary effect of the carcinogen or
    a secondary effect consequent to cell toxicity [1]. For cancer risk assessment, the role of
    cell proliferation and cell death (apoptosis and necrosis) is particularly critical for nongenotoxic
    agents because a threshold effect is likely (Fig. 5.1). Whether induction or
    inhibition of apoptosis (or necrosis) is carcinogenic may be dependent on the type and
    concentration of the carcinogen. Apoptosis is considered to be anti-carcinogenic when
    eliminating mutated cells after exposure to genotoxic carcinogens or epigenetically
    modified cells after exposure to non-genotoxic carcinogens. On the other hand, excessive
    elimination of cells can induce compensatory cell proliferation to restore homeostasis.
    This process will contribute to expansion of mutated or modified cells. Moreover, rapid
    proliferation may in itself lead to genomic instability.
    Original languageEnglish
    Title of host publicationMechanisms of chemical carcinogenesis and their impact on dose-response relationshipsthe
    EditorsC. Dietrich, F. Oesch, Oesch-bartlomowicz
    PublisherThe Nofer Institute of Occupational Medicine (publisher), Lodz,
    Pages47-76
    Number of pages30
    Publication statusPublished - 2008

    Bibliographical note

    C. Dietrich ,F. Oesch , Oesch-Bartlomowicz

    Keywords

    • thresholds
    • cell death
    • cel survival

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