- BS, Honors Pharmacology, University of Toronto
- MSc, Pharmacology, University of Toronto
- PhD, Department of Pharmacology, University of Toronto
- Postdoctoral Research, University of California/Los Angeles
Dr. Beischlag received his PhD from the University of Toronto in 1996. There he cloned and studied the transcriptional regulation of dopamine receptor genes. Following his PhD, Dr. Beischlag’s post-doctoral research began at the University of California/Los Angeles where he studied and characterized the molecular determinants of aryl hydrocarbon receptor-mediated gene transcription. He continued this work at the University of California/San Diego. In 2004, Dr. Beischlag joined the Center for Molecular Toxicology and Carcinogenesis at Pennsylvania State University as an assistant research professor. Dr. Beischlag joined the Faculty of Health Sciences in 2007.
Dr. Beischlag is actively seeking M.Sc. and Ph.D. level graduate students for his lab. Interested candidates should apply directly to Dr. Beischlag at: firstname.lastname@example.org
More information about the Beischlag Lab.
Dr. Beischlag's lab is interested in the molecular mechanisms underlying an organism’s response environmental stimuli including environmental contaminants and hypoxia. One avenue of research concerns how environmental sensors such as the aryl hydrocarbon receptor and its partner the aryl hydrocarbon receptor nuclear translocator mediate endocrine disruption in response to exposure to ubiquitous environmental contaminants.
A more recent endeavor examines how hypoxia, or low oxygen "promotes" metastasis in cancer. Dr. Beischlag's lab has identified an unrecognized mode of regulation of hypoxia-controlled gene expression and intends to exploit this to develop better therapeutic anti-cancer agents and strategies. Hypoxia-inducible factors (HIF’s) regulate gene expression in response to low oxygen tension. This includes the formation of new vasculature, and the biochemical transformation of cancer cells into more lethal, metastatic forms. Evidence suggests that the retinoblastoma protein, Rb, attenuates the physiological response to hypoxia by HIF’s. Mutations that eliminate Rb function cause uncontrolled HIF activity and promote the formation of new blood vessels and tumour progression. In addition, loss of Rb leads to aggressive cellular behaviour in the human breast and prostate cancer cell lines. The hypothesis that Dr. Beischlag's lab is pursuing is that loss of Rb results in uncontrolled expression of hypoxia-regulated factors. Targeting the factors regulating the growth of vasculature has been an attractive strategy for the development of therapies in cancer. However, these approaches are limited. If therapies that fight cancer progression are to be improved, the multiple factors regulating metastasis including cell invasion must be targeted.
View Dr. Beischlag's publications here.