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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 ongoing to test strategies to prevent metastasis by blocking new blood vessel formation.
- These studies will inform the development of targeted approaches to prevent metastasis and improve outcomes for breast cancer patients.
In order for tumors to spread to other tissues—a process called metastasis—tumor cells have to travel through the bloodstream or the lymphatic system. Advanced tumors are known to create their own rudimentary vasculature systems to facilitate this process, in many cases disguising themselves as vascular cells. Dr. Hazan is conducting studies to understand how this process occurs and identify potential strategies to block it and prevent metastasis.
Full Research Summary
Metastasis, which is the spreading of cancer cells to distant organs, is the main cause of death from breast cancer. Dr. Hazan’s team is investigating how breast cancer cells acquire the ability to spread.
Most metastatic breast cancer cells use the bloodstream to escape the tumor site and spread to distant organs. Dr. Hazan’s team previously showed that some of the most aggressive tumor cells acquire the ability to readily merge with the blood vasculature by disguising themselves as vascular cells. This process is called “vasculogenic mimicry”.
Vasculogenic mimicry has been observed in many cancers including triple negative breast cancer, where it was associated with poor prognosis and shorter patient survival. Agents that inhibit angiogenesis have not been effective at suppressing breast cancer growth. This may be due to stimulation of vasculogenic mimicry of the tumor cells, making them resistant to such a therapy.
In the coming year, Dr. Hazan will investigate how this process occurs. Elucidating the pathways that drive vasculogenic mimicry may help identify novel drugs that stop metastasis, especially in combination with anti-angiogenic therapy or chemotherapy.
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.