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Experimental drug shown to block mutant protein causing blood disease

D that were treated with the oral compound PKC412 significantly outlived those given a placebo. When tested in a single patient, a 52-year-old woman with MPD, the drug reduced her dangerously high white blood cell count and shrank her enlarged spleen and lymph nodes. However, the disease wasn't cured and she underwent a bone-marrow transplant to treat the acute leukemia caused by her MPD.

PKC412 acts similarly to the pioneering drug Gleevec, one of the first drugs to treat cancers by shutting down abnormal kinase signal switches. Gleevec blocks uncontrolled growth signals in Chronic Myelogenous Leukemia and Gastrointestinal Stromal Tumor.

The Dana-Farber scientists have been testing PKC412 in patients with Acute Myeloid Leukemia, some cases of which are caused by a mutant on-off switch called FLT3. The drug specifically blocks abnormal FLT3 kinases.

MPD is caused by a different mutated kinase, FGFR1, which is inhibited by PKC412. The mutation occurs when two broken pieces of the chromosome that carries the FGFR1 gene join together abnormally.

The findings suggest, the authors write, that PKC412 may be effective in treating MPD, as well as other diseases and cancers where mutant FGFR1 is the culprit. These include human skeletal disorders such as Pfeiffer syndrome, which causes misshapen skull, face, fingers and toes, breast and pancreatic cancers, and brain tumors.


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Contact: Bill Schaller or Richard Saltus
william_schaller@dfci.harvard.edu
617-632-5357
Dana-Farber Cancer Institute
21-Sep-2004


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