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Rachel Hazan, PhD
Professor of Pathology
Albert Einstein College of Medicine
Bronx, New York
- Seeking to prevent metastasis by identifying and characterizing the molecular drivers of tumor growth and survival.
Laboratory studies are conducted to test strategies to improve response to chemotherapy drugs by targeting cancer stem cells and tumor growth signals.
These studies will inform the development of targeted approaches to prevent or reduce drug resistance and improve outcomes for breast cancer patients.
Cancer stem cells are responsible for indefinitely propagating breast cancer, and are thus the underlying cause of 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.
In order to eliminate cancer stem cells and prevent metastasis, scientists need to identify the factors that drive their growth and survival. Dr. Hazan's group has shown that inhibiting a molecule called p21 kills cancer stem cells and suppresses metastasis in experimental models. They found that p21 activates a key molecular pathway called Wnt that fuels cancer stem cell renewal. Wnt signaling leads to the expression of a key factor called LEF1, which reinforces stem cell renewal.
In the coming year, Dr. Hazan's team will confirm these observations in human breast cancer cells and study ways of targeting p21 or LEF1 in cancer cells. They have identified an enzyme as a potential target and will test whether targeting this enzyme eradicates cancer stem cells and makes tumors more sensitive to chemotherapy. 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.