Building on earlier work involving the angiogenesis inhibitor thrombospondin-1, or TSP-1, investigators say they've been able to demonstrate in animal studies that a segment of that protein acts to inhibit the growth of ovarian cancer cells. And the use of that therapeutic approach allowed for more effective use of small doses of chemotherapy in treating the deadly disease.
Co-senior author Jack Lawler at Beth Israel Deaconess Medical Center did the work with Jim Petrik, PhD, of the University of Guelph. They identified 3TSR, which interacts with CD36. After injecting animals with mouse ovarian cancer cells, they then used standard high-dose chemotherapy or bursts of low-dose chemo after the rodents were pretreated with 3TSR.
The end result was a smaller tumor with a better blood supply, making it more susceptible to low-dose chemo.
"We were able to exploit this enhanced blood supply to improve chemotherapy drug delivery to the tumor, with excellent clinical effect," said Lawler. "The benefit of this approach is that we can create an environment that increases the efficiency of drug delivery, enabling the use of significantly lower doses of the chemotherapeutic agents and thereby reducing the side effects associated with the treatment."
"The clinical implications are significant," he adds. "With this approach, patients could receive significantly smaller doses of chemotherapy drug while deriving greater clinical benefit, compared to current therapy protocols. We hope that this will soon be tested in clinical trials."
The investigators note that ovarian cancer remains a lethal threat, with 200,000 new cases and 125,000 deaths per year. New treatments are badly needed.
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