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Clinical-translational approaches to the Nm23-H1 metastasis suppressor Steeg PS; Horak CE; Miller KDClin Cancer Res 2008[Aug]; 14 (16): 5006-12Nm23-H1 significantly reduces metastasis without effects on primary tumor size and was the first discovered metastasis suppressor gene. At least three mechanisms are thought to contribute to the metastasis-suppressive effect of Nm23-H1: (a) its histidine kinase activity toward ATP-citrate lyase, aldolase C, and the kinase suppressor of ras, with the last inactivating mitogen-activated protein kinase signaling; (b) binding proteins that titer out "free" Nm23-H1 and inhibit its ability to suppress metastasis; and (c) altered gene expression downstream of Nm23-H1, particularly an inverse association with the lysophosphatidic acid receptor endothelial differentiation gene-28 (EDG2). Most metastasis suppressor genes, including Nm23-H1, affect metastatic colonization, which is the outgrowth of tumor cells in distant locations; therefore, they are of high translational interest. A phase II trial is ongoing to test the hypothesis that a compound, high-dose medroxyprogesterone acetate (MPA), used as an unconventional gluocorticoid, will stimulate breast cancer cells to reexpress Nm23-H1 and limit subsequent metastatic colonization.|Animals[MESH]|Antineoplastic Agents/pharmacology[MESH]|Clinical Trials, Phase II as Topic[MESH]|Humans[MESH]|NM23 Nucleoside Diphosphate Kinases/drug effects/*physiology[MESH]|Neoplasm Invasiveness/genetics[MESH]|Neoplasms/drug therapy/*enzymology[MESH]|Signal Transduction/drug effects/*physiology[MESH] |
