EGFR Inhibitors as Therapeutic Agents for Breast Cancer Bone Metastasis

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Princeton University Invention # 09-2509

          The involvement of the EGFR signaling pathway in bone metastasis has been implicated by a number of studies. However, the therapeutic significance by targeting EGFR signaling in the tumor-stroma interface has not been evaluated. Researchers in the Molecular Biology Department at Princeton University have used a preclinical model of breast cancer bone metastasis to demonstrate that breast cancer cells resistant to the cytotoxic and cytostatic effect by the EGFR inhibitors can be targeted by these inhibitors to prevent the formation of bone metastasis. Mechanistic investigation showed that several EGF-like factors released by two metalloproteinases from tumor cells suppress the expression of osteoprotegerin (OPG) from osteoblasts. Since OPG antagonizes osteoclastogenesis which is critical for the establishment of the pro-metastatic niche in the bone, EGF-like factors ultimately promote the initiation and potentiation of osteolytic bone metastasis. By targeting the action of EGF-like factors with two clinically available EGFR inhibitors, we could inhibit the formation of bone metastasis by the breast cancer cell line MDA-MB-231. This is the first time that EGFR inhibitors are shown to inhibit bone metastasis formed by breast cancer cells that are resistant to the direct cytotoxic and cytostatic effect of these inhibitors


         Princeton is currently seeking industrial collaboration to commercialize this technology. Patent protection is pending.


For more information on Princeton University invention # 09-2509 please contact:

                        Laurie Tzodikov
                        Office of Technology Licensing and Intellectual Property
                        Princeton University
                        4 New South Building
                        Princeton, NJ 08544-0036
                        (609) 258-7256
                        (609) 258-1159 fax

Patent Information:
For Information, Contact:
Laurie Tzodikov
Licensing Associates
Princeton University
Yibin Kang
Xin Lu