Center for Reproductive Biology

Participating Faculty


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Name: Beth Vorderstresse
Department: Pharmaceutical Sciences
Credentials: 2000~Ph.D., Toxicology, Oregon State University
Office: Wegner Hall 340B
Phone: 509-335-8812
Fax: 509-335-5902
Mailing Address: Pharmaceutical Sciences
PO Box 646534
Pullman, WA 99164
E-mail: vordersb@wsu.edu

Research Interests

Reproductive Toxicology (mammary gland and breast cancer)
Immunotoxicology (Infectious disease)

Research Summary

Our laboratory is interested in understanding the mechanisms of toxicity caused by activation of an orphan nuclear receptor known as the aryl hydrocarbon receptor (AhR). Numerous environmental pollutants activate the AhR, and we study the highest affinity ligand, TCDD (2,3,7,8-tetrachlorodibenzo-p-dioxin, or “dioxin”). We have found that activation of the AhR during pregnancy impairs normal differentiation of the mammary gland, and are currently investigating a possible link between this impaired differentiation and breast cancer development. Another research interest is understanding how AhR activation alters the immune response to infectious disease. Currently we are examining the effects of TCDD on host resistance to Streptococcus pneumoniae infection.

Research Publications

2005-2009

Petty, A.P., S.E. Wright, K.A. Rewers-Felkins, M.A. Yenderrozos, B.A. Vorderstrasse, and J.S. Lindsey, Targeting migration inducting gene-7 inhibits carcinoma cell invasion, early primary tumor growth, and stimulates monocyte oncolytic activity. Mol Cancer Ther, 2009. 8(8): p. 2412-23.

Lawrence, B.P., M.S. Denison, H. Novak, B.A. Vorderstrasse, N. Harrer, W. Neruda, C. Reichel, and M. Woisetschlager, Activation of the aryl hydrocarbon receptor is essential for mediating the anti-inflammatory effects of a novel low-molecular-weight compound. Blood, 2008. 112(4): p. 1158-65.

Vorderstrasse, B.A., J.A. Cundiff, and B.P. Lawrence, A dose-response study of the effects of prenatal and lactational exposure to TCDD on the immune response to influenza a virus. J Toxicol Environ Health A, 2006. 69(6): p. 445-63

Vorderstrasse, BA and BP Lawrence. (2006) Protection against lethal challenge  with Streptococcus pneumoniae is conferred by activation of the aryl hydrocarbon receptor, but is not associated with an enhanced inflammatory response. Infection and Immunity. 74(10): 5679-86.

Vorderstrasse, BA, JA Cundiff, and BP Lawrence. (2004) Developmental exposure to the potent aryl hydrocarbon receptor agonist 2,3,7,8-Tetrachlorodibenzo-p-dioxin impaires the cell-mediated immune response to infection with influenza A virus, but enhances elements of innate immunity. J. Immunotox. 1:103-112.


Center for Reproductive Biology, PO Box 647521, Washington State University, Pullman WA 99164-7521, 509-335-2473, Contact Us