The patient was dying of leukemia. One hundred seventy out of every 200 cells in his bone marrow had a cancer-causing mutation, and his lymph nodes were swelling, a sign the cancer was getting worse. He'd already been on multiple courses of chemotherapy, but his disease showed few signs of improvement. Then, in July 2010, he enrolled in a clinical trial for an experimental treatment, designed to turn his own immune cells against his cancer. Months later, all signs of leukemia had vanished, his physicians report today
Levine and his colleagues designed a new gene that can be inserted into T cells to trick them into attacking cancerous B cells, the cause of chronic lymphocytic leukemia (CLL). The new gene encodes a receptor that, on one end, can bind to a molecule that's unique to cancerous B cells. The other end of the receptor sets off a chain reaction when such a B cell is bound, eventually leading the T cell to destroy the cancerous cell. "Essentially, we're converting T cells that would normally recognize other types of cells to be tumor specific," Levine says. ORIGINAL ARTICLE
Levine and his colleagues designed a new gene that can be inserted into T cells to trick them into attacking cancerous B cells, the cause of chronic lymphocytic leukemia (CLL). The new gene encodes a receptor that, on one end, can bind to a molecule that's unique to cancerous B cells. The other end of the receptor sets off a chain reaction when such a B cell is bound, eventually leading the T cell to destroy the cancerous cell. "Essentially, we're converting T cells that would normally recognize other types of cells to be tumor specific," Levine says. ORIGINAL ARTICLE
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