B. C. Lewis, S. Hudgins, A. Lewis, K. Schorr, R. Sommer, R. E. Peterson, et al., “In Utero and Lactational Treatment with 2,3,7,8-Tetrachlorodibenzo-P-Dioxin Impairs Mammary Gland Differentiation but Does Not Block the Response to Exogenous Estrogen in the Postpubertal Female Rat,” Toxicological Sciences, Vol. 62, No. 1, 2001, pp. 46-53. doi:10.1093/toxsci/62.1.46

has been cited by the following article:

• TITLE: The Aryl Hydrocarbon Receptor: A Target for Breast Cancer Therapy

  AUTHORS: Joann B. Powell, Gennifer D. Goode, Sakina E. Eltom

  KEYWORDS: Aryl Hydrocarbon Receptor; Therapeutic Targeting; Breast Cancer Progression; Chemosensitization

  JOURNAL NAME: Journal of Cancer Therapy, Vol.4 No.7, August 22, 2013

  ABSTRACT: The aryl hydrocarbon receptor (AhR) is a ligand-activated transcription factor that regulates a battery of genes in response to exposure to a broad class of environmental poly aromatic hydrocarbons (PAH). AhR is historically characterized for its role in mediating the toxicity and adaptive responses to these chemicals, however mounting evidence has established a role for it in ligand-independent physiological processes and pathological conditions, including cancer. The AhR is overexpressed and constitutively activated in advanced breast cancer cases and was shown to drive the progression of breast cancer. In this article we will review the current state of knowledge on the possible role of AhR in breast cancer and how it will be exploited in targeting AhR for breast cancer therapy.