Published in Blood Weekly, November 29th, 2007
When these genes, Rac1 and Rac2, become hyperactive, they prompt a protein linked to leukemia to stimulate the onset and spread of CML, a cancer that originates in blood marrow stem cells. But targeted inactivation of those genes, or using a molecule to nullify their hyperactivity, inhibits the onset of leukemia due to the 'Philadelphia chromosome' fusion protein called BCR-ABL, according to David...
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