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"Trojan Horse" Agent Halts Bone Metastasis in Mice

themselves do not express the Flt-1 receptor.

According to Rosenblum, the VEGF121/rGel agent entered the immature cells via the Flt-1 receptor and destroyed them, shutting down tumor growth. "This was a surprise to us," he says. "We had not expected these cells to be killed at all because we knew, through our earlier experiments, that VEGF121/rGel destroyed blood vessels by entering a different cell surface receptor, one which is not expressed on pre-osteoclasts."

Thus, in the bone, VEGF121/rGel may be working through two different VEGF receptors. It stops the bone destruction needed for the cancer to grow and may inhibit blood vessel growth to the metastasized tumor, Rosenblum says.

"The fact that this form of VEGF targeting works on different cell receptors in blood vessels and in bone cells is a unique finding that could be clinically significant, not only to treating cancer but other bone disorders," he says. "In the least, this study helps us understand more about how VEGF operates inside the body and how it is involved in bone remodeling."

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