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According to a recent article published in the Journal of Clinical Oncology, the addition of Avastin® (bevacizumab) to the chemotherapy agent Adriamycin® (doxorubicin) may slow cancer progression in patients with metastatic soft-tissue sarcomas.

Soft-tissue sarcomas are characterized by the growth of cancer cells in the soft tissue of the body. Soft tissues include muscles, tendons, fibrous tissue, fat, blood or lymph vessels, nerves or the tissues around joints.

Treatment for these soft-tissue sarcomas varies, depending on the specific type of cancer, the place in the body where the cancer started and the extent of the disease. Treatment may include surgery to remove the cancer if possible, chemotherapy and/or radiation therapy. When this type of cancer develops in an arm or leg, amputation is sometimes necessary; however, this is always used as a last resort.

Metastatic STS refers to cancer that has spread from its site of origin to distant sites in the body, often including vital organs. Patients with this stage of disease typically have a poor prognosis following standard therapy. Therefore, research efforts have been focused on expanding effective treatment options for patients with this disease.One option for these patients involves the research surrounding the inhibition of angiogenesis.

Cancer cells require food, oxygen and growth proteins in order to grow and spread. These essential nutrients are transported to the cancer cells by blood vessels. Angiogenesis is the process of creating new blood vessels necessary to transport food to the cancer cells.

Two key proteins that are necessary for the process of angiogenesis are called matrix metalloproteinases (MMPs) and vascular endothelial growth factor (VEGF). VEGF causes endothelial cells (cells comprising the innermost layer of blood vessels) to replicate and migrate from existing blood vessels to the cancer. Endothelial cells secrete MMPs, which create an opening in existing tissues surrounding the cancer, allowing the endothelial cells to move near the cancer and form new blood vessels to feed the cancer.

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Avastin is an agent that targets VEGF so that it cannot bind to its targeted cell and stimulate angiogenesis. Avastin is currently FDA-approved in combination with 5-fluorouracil (5-FU)-based chemotherapy regimens for the initial treatment of metastatic colorectal cancer. However, researchers have been evaluating Avastin in combination with different chemotherapy agents and various scheduling for the treatment of several different types of cancer.

Researchers from several medical institutions recently conducted a clinical trial to evaluate Avastin in combination with doxorubicin for the treatment of metastatic soft-tissue sarcoma. This trial included 17 patients; the majority of whom had undergone prior therapy with either surgery, chemotherapy and/or radiation therapy. Following treatment with Avastin/doxorubicin, 12% of patients experienced a partial disappearance of cancer, and 65% experienced disease stabilization for at least 3 months. Side effects affecting the heart were observed in 6 patients.

The researchers concluded that the treatment combination consisting of Avastin and doxorubicin provides disease stabilization for a large majority of patients with metastatic soft-tissue sarcoma. These results are superior to those traditionally reported with the use of doxorubicin alone.

The authors state that future clinical trials further evaluating Avastin/doxorubicin are warranted, including different treatment schedules or combinations. Patients diagnosed with metastatic soft-tissue sarcoma may wish to speak with their physician regarding their individual risks and benefits of participating in a clinical trial further evaluating Avastin-containing combinations, or other novel therapeutic approaches. Two sources of information regarding ongoing clinical trials include the National Cancer Institute ( and

Reference: D’Adamo D, Anderson S, Albritton K, et al. Phase II Study of Doxorubicin and Bevacizumab for Patients With Metastatic Soft-Tissue Sarcomas. Journal of Clinical Oncology. 2005; 23: 7135-7142.

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