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Rachel Hazan, PhD
Professor of Pathology
Albert Einstein College of Medicine
Bronx, New York
Goal: To understand what drives tumor growth and survival in order to prevent the spread of breast cancer.
Impact: Once breast cancer has spread to other tissues it is incurable. Dr. Hazan’s lab has shown that the loss of an enzyme that protects cells from oxidative damage—which occurs as a result of normal cell processes, but even more so in cancer cells—leads to more aggressive cell behavior and metastasis. Her lab is now focused on understanding how this occurs to identify targets that can be blocked to prevent metastasis.
What’s next: In the coming year, Dr. Hazan’s group will pursue sophisticated laboratory experiments to map out the sequence of events starting with the inactivation of the enzyme to the breast cancer metastasis.
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. Dr. Hazan has been investigating how breast cancer cells acquire the ability to spread in order to discover ways to prevent metastasis. Her research has revealed that loss of an enzyme called Glutathione Peroxidase 2 (GDx2) results in increased tumor blood vessel formation and promotes the spread of breast cancer cells. The team will now focus on the molecular pathways involved to identify new targets for prevention or treatment of metastasis.
Full Research Summary
Research area: Investigating how the spread of breast cancer (metastasis) occurs in order to discover ways to prevent it from occurring.
Impact: Metastasis is the main cause of death from breast cancer. In order to prevent breast cancer cells from invading distant tissues in the body, researchers must first determine how the cancer cells acquire the ability to spread. Advanced breast tumors are known to create their own vascular systems to facilitate this process, often disguising themselves as vascular cells. Dr. Hazan is investigating the events that lead to excessive increase in blood vessel formation that feed the cancer with oxygen and nutrients—work that could reveal strategies for blocking metastasis.
Current investigation: Dr. Hazan is studying an enzyme, glutathione peroxidase 2 (GPx2), which when lost in breast cancer cells makes them extremely metastatic (prone to spreading). Their work could lead to the discovery of novel targets that can be inhibited to fight metastasis.
What they’ve learned so far: Dr. Hazan’s team has shown that the loss of GPx2 in breast cancer cells renders tumors highly metastatic. They have determined that this involves the formation of new blood vessels that enable cancer cells to enter the bloodstream.
What’s next: The team will conduct a series of laboratory studies to further characterize the role of GPx2 in tumor cell invasion and metastasis and identify novel targets that can be inhibited to fight 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.