Addition of Thalidomide to Dexamethasone Improves Responses in Multiple Myeloma

Addition of Thalidomide to Dexamethasone Improves Responses in Multiple Myeloma

According to results presented at the 2004 annual meeting of the American Society of Hematology (ASH), the addition of thalidomide (Thalomid®) to dexamethasone improves anti-cancer response rates in patients with newly diagnosed multiple myeloma.

Multiple myeloma is a cancer involving important immune (infection-fighting) cells called plasma cells. Plasma cells aid the body in fighting infection by producing specialized proteins called antibodies that have the ability to target and/or kill foreign cells. In multiple myeloma, cancerous plasma cells produce abnormal and excessive antibodies that do not have the ability to properly fight infection. In addition, the cancerous plasma cells accumulate in the bone marrow, suppressing the normal formation and function of other cells that are necessary for normal production of blood cells and immune functions. The excessive accumulation of cancer cells in the bone marrow ultimately leads to the formation of tumors in the bone and to the breakdown of bone. Standard treatment for multiple myeloma depends upon the stage, or extent, of the disease. Treatment for newly diagnosed patients with multiple myeloma may consist of the steroid dexamethasone, chemotherapy, a combination of a steroid and chemotherapy, monitoring of the disease, or a stem cell transplant.

Thalidomide is a substance known for its anti-angiogenesis properties, as well as its effects on the immune system to help fight cancer. Angiogenesis is the formation of new blood vessels in the body and is a crucial component for the development of cancer. Blood vessels are needed to supply cancer cells with essential nutrients from the blood. Anti-angiogenesis is the inhibition of the formation of new blood vessels. By stopping blood vessels from forming, cancer cells are “starved” of nutrients, ultimately inhibiting cancer development and growth. Previous clinical studies have demonstrated that thalidomide achieves significant anti-cancer responses in patients with recurrent multiple myeloma, and clinical trials are ongoing to determine its true clinical role in the treatment of multiple myeloma, as well as its effects on the immune system in fighting cancer.

Recently, researchers affiliated with the Eastern Cooperative Oncology Group (ECOG) conducted a large clinical trial directly comparing the standard treatment approach including dexamethasone to the treatment approach including thalidomide plus dexamethasone in the treatment of newly diagnosed patients with multiple myeloma. This trial included 103 patients who were treated with thalidomide/dexamethasone and 104 patients who were treated with dexamethasone alone. Interim data reported that anti-cancer responses occurred in 63% of patients treated with thalidomide/dexamethasone, compared with 41% of patients treated with dexamethasone alone. Upon analysis of M-protein (an abnormal protein measured in the urine used as a “marker” to evaluate the extent of disease), 73% of patients achieved an anti-cancer response, compared with only 50% of those treated with dexamethasone. More patients who were treated with thalidomide/dexamethasone had blood clots (deep vein thrombosis) than patients treated with dexamethasone alone.

The researchers concluded that the addition of thalidomide to dexamethasone improves anti-cancer response rates in patients with newly diagnosed multiple myeloma over treatment with dexamethasone alone. Longer follow-up may reveal progression-free survival or overall survival differences between these two treatments. Patients with newly diagnosed multiple myeloma may wish to speak with their physician about the risks and benefits of treatment with thalidomide or other promising new therapeutic approaches being evaluated in clinical trials.

Reference: Celgene Corporation. ECOG Phase III Study on Thalomid (Thalidomide) Plus Dexamethasone Reports Final Results for Newly Diagnosed Multiple Myeloma. Available at: . Accessed December 2004.

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