Research Description

Steroid hormones signal throughout the body to regulate various physiological processes.  These steroids interact with proteins called nuclear receptors that act as transcription factors to bind DNA and initiate a cascade of events leading to the activation or repression of target genes.  The process of turning on nuclear steroid receptors is tightly controlled through a variety of molecular mechanisms.  These mechanisms of control are frequently deregulated in cancer.  The Burd laboratory is specifically interested in the estrogen receptor class of nuclear receptors.   Mammals express two different forms of the estrogen receptor (ER): alpha (α) and beta (β).  Both of these receptors have the ability to bind estrogen hormones and regulate gene targets, however their role in cancer is very disparate.  In general, the α isoform is typically associated with promoting cancer, most notably breast cancer.  Conversely, the β isoform is mostly known to repress cancer progression.  The current focus of the lab is investigating various aspects of these signaling pathways in three broad projects: 1) The role of environmental endocrine disruptors in promoting breast cancer risk ; 2) The role of an estrogen-dependent gene, GREB1, in regulating breast cancer proliferation;  3) The protective function of ERβ in melanoma.