Description:
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
tzodikov@princeton.edu