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Approximately 61,000 statements.
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The ability of CXCL12 to stimulate proliferation and survival is mediated by activation of the Erk 1/2 and phosphatidylinositol 3-kinase pathways in many cell types Taken together these data indicate that the ability of AMD 3100 to decrease tumor growth in animal models reflects direct inactivation of CXCR4 in tumor cells and consequent inhibition of Erk 1/2 and phosphatidylinositol 3-kinase pathways, resulting in increased tumor cell apoptosis and decreased proliferation.
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