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Drug attacks prostate cancer in mouse model by destroying its blood supply

armful effects in the service of a cancer cell.

With imatinib preventing activation of PDGF-R, Fidler said, the endothelial cells died by apoptosis first, with tumor cells following suit one to two weeks later.

Fidler said the findings are a vibrant example of the "seed and soil" hypothesis in metastasis - the deadly spreading of a cancer from its organ of origin to other organs, a process that kills 90 percent of all patients who die from their disease.

In landmark findings, Fidler and colleagues demonstrated that the vast majority of cancer cells that depart a tumor die swiftly once in circulation and that metastases originate from less than 1 percent of a cancer's cells and even can arise from a single cell.

When these metastatic "seeds" enter circulation, they still need to find the exact microenvironment that permits them to grow. For prostate cancer, the second-leading cause of cancer death among men, that microenvironment is the bone.

Earlier research by Fidler and colleagues showed PDGF-R activation in metastatic prostate tumors adjacent to the bone but not in tumor cells next to muscle. PDGF-R also was activated in tumor-associated endothelial cells in the bone, but not in those blood vessel cells in neighboring muscle.

A JNCI paper by Fidler and colleagues in 2003 showed that blocking PDGF-R signaling in the mouse model of metastatic prostate cancer cut the incidence of cancer, reduced the size of tumors and incidence of metastasis.

The question was whether the combination of imatinib and paclitaxel achieved this by attacking the tumor itself or the tumor-related blood vessels. This week's JNCI paper answers that question: it kills the blood vessels first. "Here, we attack the soil. The seeds can be resistant. Kill the endothelial cell, you kill the soil," Fidler said.

Imatinib had an effect by itself, but the best result came from the pairing with paclitaxel, known commercially as Taxol,
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Contact: Scott Merville
sdmervil@mdanderson.org
713-792-0661
University of Texas M. D. Anderson Cancer Center
6-Jun-2006


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