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VCU Massey first to combine targeted agents to kill multiple myeloma cells
Date:2/10/2011

s, they experience DNA damage and, as a consequence, launch another defense mechanism by activating a protein known as ERK1/2.

"The activation of ERK1/2 explains why multiple myeloma cells are able to survive the lethal effects of Chk1 inhibitors," says Grant. "Therefore, we used Src inhibitors to block the activation of ERK1/2." The results were more promising than even the researchers had hoped.

Grant's team discovered that Src inhibitors not only blocked ERK1/2 activation, but also synergized with Chk1 inhibitors to trigger a dramatic increase in cell death. In addition, the combined treatment greatly reduced blood vessel formation, which plays an important role in the maintenance of many tumors, including multiple myeloma. Significantly, the treatment exerted virtually no effects on healthy, normal cells.

"We found tumors treated with the combined regimen were noticeably smaller and showed signs of a lack of blood supply when compared to tumors from the control group or those treated only with Chk1 inhibitors," says Grant. "This study is not only the first to demonstrate that Src inhibitors can dramatically increase the effects of Chk1 inhibitors, but it is also the first to show that preventing blood vessel formation may contribute to the effectiveness of this combination strategy."

This study builds upon more than seven years of research by Grant's team investigating cell signaling in relation to DNA damage repair and survival pathways involving Src and ERK1/2 proteins. The researchers are now developing more complex experiments as a prelude to clinical trials in multiple myeloma patients. "We're hopeful the approach of combining targeted agents will open up the possibility of developing entirely new therapies for patients with multiple myeloma and potentially other blood cancers," says Grant.


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Contact: John Wallace
wallacej@vcu.edu
804-628-1550
Virginia Commonwealth University
Source:Eurekalert

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