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SNM: Tumor Blood Flow, Metabolism Decrease With Increasing Anti-Angiogenesis Treatment Dose By Pippa Wysong Special to DG News TORONTO, ON -- June 26, 2001 -- The effect of anti-angiogenesis treatments are not as predictable as oncologists hoped. In a study presented at the annual meeting of the Society of Nuclear Medicine, researchers found that tumor response to the anti-angiogenesis treatment, endostatin, is not dose-dependent and that cancer cells do not die off as soon as their blood supply is cut off. Being able to see a response in tumors may take longer than with other anti-tumor agents, which target cancer cells and kill more quickly. This does not mean anti-angiogenesis angents don’t work, it just means the way they work is more complex, said Dr. Nizar Mullani from the University of Texas Medical School. Endostatin is in phase-I/phase-II safety and efficacy trials and is being tested for a variety of cancers. As an anti-angiogenesis agent, it targets cells in the endothelium to prevent tumors from creating new vascular networks that can feed the cancer. A series of imaging studies were done of 26 cancer patients taking endostatin in a phase-I study. Patients underwent magnetic resonance imagine (MRI), computed tomography (CT) blood flow imaging and positron emission tomography (PET) scans at baseline (before taking endostatin), then again at 28 and 56 days after starting treatment. The multiple scans were done to see which modality provided the best method for non-invasively measuring tumor changes. “PET gave us the best, statistically significant blood flow changes, plus gives us information about metabolism which the other two techniques don’t,” Dr. Mullani said. People in the study had a variety of cancers, ranging from melanoma to thyroid cancer and were given escalating doses of the drug. Patients were started on 30 mg/m2[ of endostatin administered intravenously, increasing the dose to 60, 120, 180 and 300 mg/m2[ over time. Overall, researchers found that tumor blood flow and metabolism decreased with increasing doses, but with some caveats. The PET studies showed that the rates at which blood flow and metabolism changed in the tumors were not directly correlated to the doses of the drug. “This was a surprise,” Dr. Mullani said. “If you look at classical chemotherapy treatment, as you increase the dose you get a linear response of cell kills. In this case we did not get that.” Tumor blood flow and glucose metabolism increase relative to baseline values at the 30 and 60 mg/m2[ doses after 28 days of treatment. When patients were given the 120 mg/m2[ doses of endostatin, there were no significant changes. At the 180 mg/m2[ dose, there was a decrease in tumor blood flow, but no change in glucose metabolism. Then, at the 300 mg/m2[ dose, both blood flow and metabolism decreased relative to baseline. There was a continued decrease in blood flow and metabolism “as a function of time of treatment with the highest doses. However these changes were not linearly related to escalating doses of endostatin,” he said. In short, the findings suggest that the mechanism of how anti-angiogenesis agents work is more complex than previously thought. E-mail this page to a friend or colleague! To print, use this version