Researchers from Sugen Inc., Duke University and New YorkUniversity Medical Center have discovered the signalingpathway between an enzyme in bone marrow cells and the cellmachinery that switches on the cell growth protein Ras.

Sugen said the Ras protein has been shown to be mutated in alarge fraction of human cancers, including leukemia.

Sugen of Redwood City, Calif., explained that the switch thatactivates the Ras protein is a molecule called GRB-2, "whichbinds to a portion of the enzyme (in bone marrow cells) andinitiates oncogenic transformation via Ras."

The company said this finding "raises the possibility of usingspecially designed molecules that can inhibit GRB-2 or otherelements, thus preventing activation of the Ras 'on' switch andpossibly arresting the cascade of events that leads touncontrolled cell growth in some cancers."

The research findings were reported in last week's issue of Cell.Researchers studied the Philadelphia chromosome, which isfound in patients with chronic myelogenous leukemia (CML)and acute lymphoblastic leukemia (ALL). The chromosome isproduced when a genetic mistake occurs in bone marrow cellsthat are destined to become white blood cells.

Sugen said it has identified lead candidates now in earlypreclinicals that may block the interaction of GRB-2 with thefaulty gene found in leukemia patients. -- Brenda Sandburg

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