Skip Navigation
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

National Institute of Environmental Health Sciences

Use this QR code to view the newest version of this document
Use this QR code to view the newest version of this document

Your Environment. Your Health.

Publication Detail

Title: Commentary: is the concept of "tumor promotion" a useful paradigm?

Authors: Trosko, J E

Published In Mol Carcinog, (2001 Mar)

Abstract: Since the demonstration of the multistage nature of carcinogenesis in experimental work on mouse skin carcinogenesis (and subsequently on various other organ systems in other organisms), the concepts of "initiation", "promotion", and "progression" were operationally generated from empiric data. Because these early observations and concepts had no mechanistic explanations, various hypotheses have been generated to explain the unique characteristics of each phase (e.g., initiation, being irreversible, was ascribed as the result of DNA damage leading to mutagenesis; promotion, being interruptible or reversible, was believed to be caused by epigenetic mechanisms; progression, also being irreversible, was believed to be caused by genetic instability that led to mutagenic and epigenetic changes). In addition, many of the molecular, biochemical, and cellular experiments designed to investigate the mechanistic bases of these phases used technologies that did not always lead to unequivocal interpretations, and because "real-life" carcinogenesis does not mimic controlled experimental conditions of the initiation/promotion/progression experiments, many investigators believe that these concepts have lost their usefulness. In this commentary, I explain some of the confusion concerning the concept of promotion and suggest that, by understanding the limitations of many in vitro assays used to characterize mutagens, by integrating other theories of carcinogenesis (i.e., stem cell theory), and by recognizing the role of epigenetic agents, specifically, modulated gap-junctional intercellular communication, the concept of promotion can provide valuable insights into the carcinogenic process. Mol. Carcinog. 30:131--137, 2001.

PubMed ID: 11301473 Exiting the NIEHS site

MeSH Terms: Animals; Carcinogens/pharmacology*; Cell Communication; Cell Transformation, Neoplastic*; Clone Cells; Drug Screening Assays, Antitumor; Gap Junctions/physiology; Humans; Models, Biological; Mutagens/pharmacology; Oligonucleotide Array Sequence Analysis; Research Support, U.S. Gov't, P.H.S.; Stem Cells/physiology

Back
to Top