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Experimental Drug Helps Melanoma Cells Respond to Chemotherapy

GCS-100 removes protective cell-surface proteins (Oct. 12)

Researchers at the University of California–Los Angeles (UCLA) have discovered the mechanism by which an experimental drug — GCS-100 — removes from lymphoma cells a protein that prevents the cells from responding to chemotherapy.

The discovery revives hope in the drug, which had been tested in clinical trials years before but had been delayed indefinitely. The researchers hope GCS-100 can be combined with chemotherapy to create an effective treatment for diffuse large B-cell lymphoma (DLBCL), the most common and aggressive form of non-Hodgkin lymphoma, a cancer of the immune system.

The findings were published online in Blood.

The UCLA researchers found that a protein, galectin-3, binds to CD45 enzymes on the surface of lymphoma cells. This protein–enzyme combination regulates the cancer cells' susceptibility to chemotherapy, essentially protecting them from chemotherapy drugs.

Derived from citrus pectin, GCS-100 works outside cancer cells to remove the protective galectin-3. Once galectin-3 is removed, a lymphoma cell can be killed by chemotherapy drugs — part of a chain reaction of programmed cancer-cell death, or apoptosis.

Although the researchers knew that GCS-100 had shown action against lymphoma cells, the finding that it removes the barrier to the initiation of cell death by removing galectin-3 from the cell surface was unexpected.

Early clinical trials of GCS-100 had shown no side effects of the drug other than a mild rash in some patients. Other research has demonstrated that this effect is the result of GCS-100 also promoting the development of T cells, which are created by the immune system to fight disease.

Source: UCLA, October 12, 2012.

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