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Biological Chemistry

Editor-in-Chief: Brüne, Bernhard

Editorial Board: Buchner, Johannes / Lei, Ming / Ludwig, Stephan / Thomas, Douglas D. / Turk, Boris / Wittinghofer, Alfred


IMPACT FACTOR 2018: 3.014
5-year IMPACT FACTOR: 3.162

CiteScore 2018: 3.09

SCImago Journal Rank (SJR) 2018: 1.482
Source Normalized Impact per Paper (SNIP) 2018: 0.820

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1437-4315
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Volume 387, Issue 9

Issues

A role for the aryl hydrocarbon receptor in mammary gland tumorigenesis

Jennifer J. Schlezinger
  • Department of Environmental Health, Boston University School of Public Health, Boston, MA 02118, USA
  • Other articles by this author:
  • De Gruyter OnlineGoogle Scholar
/ Donghui Liu
  • Department of Environmental Health, Boston University School of Public Health, Boston, MA 02118, USA
  • Other articles by this author:
  • De Gruyter OnlineGoogle Scholar
/ Marganit Farago / David C. Seldin / Karine Belguise / Gail E. Sonenshein / David H. Sherr
  • Department of Environmental Health, Boston University School of Public Health, Boston, MA 02118, USA
  • Other articles by this author:
  • De Gruyter OnlineGoogle Scholar
Published Online: 2006-09-14 | DOI: https://doi.org/10.1515/BC.2006.145

Abstract

The aryl hydrocarbon receptor (AhR) is an evolutionarily conserved transcription factor bound and activated by ubiquitous environmental pollutants. Historically, the AhR has been studied for its transcriptional regulation of genes encoding cytochrome P450 enzymes, which metabolize many of these chemicals into mutagenic and toxic intermediates. However, recent studies demonstrate that the AhR plays an important role in the biology of several cell types in the absence of environmental chemicals. Here, this paradigm shift is discussed in the context of a putative role for the AhR in mammary gland tumorigenesis. Data demonstrating high levels of constitutively active AhR in mammary tumors are summarized. Particular focus is placed on the likelihood that the AhR contributes to ongoing mammary tumor cell growth and on the possibility that the AhR inhibits apoptosis while promoting transition to an invasive, metastatic phenotype. A working model is proposed that may help explain the sometimes contradictory outcomes observed after AhR manipulation and that serves as a blueprint for the design of therapeutics which target the AhR in breast cancer. The theme that malignant cells reveal the functions for which the AhR has been evolutionarily conserved is presented throughout this discussion.

Keywords: aryl hydrocarbon receptor; breast cancer; polycyclic aromatic hydrocarbons

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About the article

Corresponding author


Published Online: 2006-09-14

Published in Print: 2006-09-01


Citation Information: Biological Chemistry, Volume 387, Issue 9, Pages 1175–1187, ISSN (Online) 1437-4315, ISSN (Print) 1431-6730, DOI: https://doi.org/10.1515/BC.2006.145.

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