Veronique Baron, Ph.D., Assistant Professor

Cancer is a proliferative disease that affects about one in three persons at some point in their life. Tailored therapeutic intervention requires diagnostic markers and targeted treatment. Before this can happen, we need an indepth understanding of the molecular mechanisms underlying cancer tumorigenesis. Bringing these mechanisms to light is one of the most essential aspects of cancer research, one with direct consequences for cancer patients.
Cell proliferation in cancer is triggered by genetic alterations that activate oncogenes or inactivate tumor suppressors. Our laboratory currently focuses its efforts on the study of Egr-1 (Early Growth Response-1), a transcription factor that regulates genes implicated in the growth and survival of cancer cells and that acts as an oncogene or as a tumor suppressor depending on the circumstances.

We have been particularly involved in testing the hypothesis, backed by recent evidence from independent laboratories, that Egr-1 promotes the progression of prostate cancer, a prevalent malignancy among men in the United-States. The progression of the disease follows multiple defined steps, from benign hyperplasia to hormone-independent metastatic desease. Current therapies are limited and discovery of a successful treatment is still an important challenge. Our approach is based on the hypothesis that suppression of Egr-1 in cancer cells will impede tumor growth. We have observed that abrogating Egr-1 function in prostate cancer cells causes an almost complete stop of cell division and a delay in the development of prostate tumors in mice. Thus, we have identified Egr-1 as a novel potential target for prostate cancer therapy. Our next step is to design a search for small molecule inhibitors of Egr-1, since none exists as of today. After characterization of the identified inhibitor(s) in cell-based assays, pre-clinical studies in animal models of prostate cancer and eventually phase I clinical trials are our long term goals.