Cell cycle-independent death of prostate adenocarcinoma is induced by the trk tyrosine kinase inhibitor CEP-751 (KT6587).

摘要: Advanced prostate cancer remains largely incurable, primarily because the very low growth fraction present in these tumors makes them generally resistant to treatment with standard chemotherapeutic agents that target cell division. Effective therapies should therefore induce death of cells, independent their rate. trkA, high-affinity tyrosine kinase-linked receptor for nerve factor, has been implicated prostatic and may represent a molecular therapeutic agents. At mg/kg doses, trk kinase inhibitor CEP-751 (KT6587) inhibits nine different animal models tumor rate, androgen sensitivity, metastatic ability, or state differentiation. is selective cancerous versus normal cells affects only limited number nonprostate tumors. Importantly, induces cycle-independent fashion and, therefore, represents novel approach management both hormone-dependent hormone-independent cancer.