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Ilan Tsarfaty, PhD
Associate Professor, Department of Human Microbiology
Sackler School of Medicine
Tel Aviv University
Tel Aviv, Israel
- Seeking to develop novel strategies to reduce drug resistance and metastasis in aggressive breast cancers.
- Laboratory studies are conducted to test a new drug target for combination therapy in triple negative breast cancers.
- This research may identify predictive biomarkers of response to targeted therapies and novel new combination approaches to counter drug resistance and prevent metastasis.
In order for a tumor to grow and spread to other tissues, it must activate cellular programs to support growth as well as the ability of tumor cells to invade and become mobile. Oncogenes are genes that drive this kind of activity and cause tumor cells to become malignant. The research team of Drs. Tsarfaty, Vande Woude and Graveel are conducting studies focused on an oncogene called MET in advanced breast cancers.
Full Research Summary
For a tumor to spread (a process called metastasis), tumor cells must be able to break through tissue barriers, enter the circulation, and become established in a new site. To achieve these steps, a tumor cell must acquire unique physical and molecular properties. This often involves the activation of a gene that is normally not active in adult tissue. The MET gene is one example. MET gene expression changes the properties of cancer cells and allows them to spread more easily.
The research team of Drs. Tsarfaty, Vande Woude, and Graveel use a combination of novel imaging techniques and mathematical models to study how MET influences breast cancer metastasis, metabolism, and drug resistance in HER2+ and triple negative breast cancers. Their recent studies have identified potential combination approaches that could reduce drug resistance and prevent metastasis in these diseases.
In the coming year, this international research team will continue to leverage the unique models to identify and characterize the modifier genes that promote MET-mediated tumorigenicity and further explore the potential of MET inhibitors in aggressive breast cancers that are resistant to other therapies.
Overall, these studies will provide new insights into the genes that influence breast cancer initiation and progression and identify potential prognostic signatures in patients who are responsive to MET-targeted therapies and lead to the development of novel combination therapies.
Dr. Ilan Tsarfaty received his BSc. (1983), MSc. (1986) and PhD (1990) from Tel Aviv University. From 1991-1994, he served as a postdoctoral research associate at the National Cancer Institute's Frederick Cancer Research and Development Center. He was a visiting scientist at the Van Andel Research Institute Grand Rapids MI as a part of the Molecular Imaging Center University of Michigan (2001 - 2003). Dr. Tsarfaty has been a member of the Department of Clinical Microbiology and Immunology, Sackler School of Medicine, Tel Aviv University since 1994. He is the author of over 50 scientific research articles and over 10 books chapters. Dr. Tsarfaty cloned the gene of the breast cancer antigen Muc1 and showed its potential use as a marker for breast cancer. He was the first to show that the Met tyrosine kinase growth factor receptor is involved in tubule formation in mammary tubule and in mesenchymal epithelial cell conversion.
Dr. Tsarfaty was the first to show that Met is a prognostic factor for breast cancer patients. He also showed that HGF/SF alters metabolic activity by induction of Mimp a novel gene that is involved in metastasis that was cloned and characterize in Dr. Tsarfaty's lab. Dr. Tsarfaty has been leading an effort to develop noninvasive breast tumor molecular imaging modalities as a powerful tool in understanding the metabolic activity induced by Met signal transduction. This technology enhances definition of tumor margins and may allow earlier detection of smaller tumor and small metastatic lesions. Currently, Dr. Tsarfaty's lab is in the process of understanding the physical, cellular and molecular mechanism of Met induced motility leading to embryo development and metastasis.