Professor of Pathology
Albert Einstein College of Medicine
Bronx, New York
Cancer stem cells are responsible for indefinitely propagating breast cancer, thus causing recurrence and metastasis. Scientists believe that because cancer stem cells can survive chemotherapy or radiation they are the seeds that give rise to new cancer. To eliminate cancer stem cells, scientists need to discover the factors that drive their growth and survival. Dr. Hazan’s group has shown that inhibiting a molecule known as p21 can kill the cancer stem cells and suppress metastasis in experimental models. They believe that p21 activates a key molecular pathway known as Wnt that fuels cancer stem cell renewal. They will confirm this hypothesis in human breast cancer cells and study ways of targeting p21 in cancer cells while not affecting normal cells. They hope to expand their recent discoveries into targeted therapies to block breast cancer recurrence and metastasis.
Dr. Rachel Hazan received her PhD from George Washington University in 1990. She performed her thesis work under Dr. Joseph Schlessinger, where she studied Her2 signaling in breast cancer, and was the first to map Her2 phosphorylation sites. She then joined Dr. Gerald Edelman, a Nobel laureate at Rockefeller University and Scripps Research Institute to study adhesion molecules and their regulation in neuronal and epithelial cells. This served as a basis for her ongoing work on cadherin adhesion molecules and their role in breast cancer dissemination. In 1994, she joined Memorial Sloan Kettering Cancer Center, where she initiated seminal studies on the role of cadherin switching in breast cancer progression. In 1997, she became Assistant Professor at the Mount-Sinai School of Medicine, and is presently Professor of Pathology at the Albert Einstein College of Medicine. Dr. Hazan has been studying the role of adhesion in invasion and epithelial to mesenchymal transition leading to metastasis. She showed that N-cadherin activates cancer spread by sustaining activation and signaling of the Fibroblast Growth Factor Receptor. Dr. Hazan discovered a variety of signaling pathways that contribute to metastasis and has so far elucidated key signaling modules including the MAPK, AKT and cell cycle regulators as critical promoters of metastasis. Her work uses laboratory models, cell culture systems and validation in clinical breast specimens. These models serve as a platform to elucidate mechanisms of metastatic spread with the goal of identifying pivotal targets for therapeutic application.