1 Citation (Scopus)

Abstract

A variety of xenobiotics such as dioxin, peroxisome proliferators, hormones, and phorbol esters result in tumors without directly damaging DNA. Instead, these compounds are classified as tumor promoters and their mode of action includes affecting cellular proliferation, apoptosis, or differentiation. The manner in which the aforementioned chemicals affect cellular fate is by altering gene expression initiated by interacting with soluble, intracellular receptors. The targets of receptor-mediated carcinogens include nuclear hormone receptors, the aryl hydrocarbon receptor, protein kinase C, and protein phosphatase 2A. In this chapter, the structure, function, and regulation of these proteins, as well as the downstream events that result from tumor promoters interacting with their cognate receptor, are described.

Original languageEnglish (US)
Title of host publicationCarcinogenesis
PublisherElsevier Inc.
Pages349-369
Number of pages21
Volume14
ISBN (Print)9780080468686
DOIs
StatePublished - Aug 12 2010

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Carcinogens
Carcinogenesis
Peroxisome Proliferators
Aryl Hydrocarbon Receptors
Protein Phosphatase 2
Dioxins
Phorbol Esters
Xenobiotics
Cytoplasmic and Nuclear Receptors
Protein Kinase C
Cell Proliferation
Hormones
Apoptosis
Gene Expression
DNA
Neoplasms
Proteins

All Science Journal Classification (ASJC) codes

  • Medicine(all)

Cite this

Vanden Heuvel, J. P. (2010). Receptor-Mediated Carcinogenesis. In Carcinogenesis (Vol. 14, pp. 349-369). Elsevier Inc.. https://doi.org/10.1016/B978-0-08-046884-6.01418-4
Vanden Heuvel, John Patrick. / Receptor-Mediated Carcinogenesis. Carcinogenesis. Vol. 14 Elsevier Inc., 2010. pp. 349-369
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Receptor-Mediated Carcinogenesis. / Vanden Heuvel, John Patrick.

Carcinogenesis. Vol. 14 Elsevier Inc., 2010. p. 349-369.

Research output: Chapter in Book/Report/Conference proceedingChapter

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