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• W1884954707 endingPage "1071" @default.
• W1884954707 startingPage "1071" @default.
• W1884954707 abstract "PURPOSE AND DESIGN: The purpose of this review is to provide an overview of the literature linking Ras signaling pathways and leukemia and to discuss the biologic and potential therapeutic implications of these observations. A search of MEDLINE from 1966 to October 1998 was performed. RESULTS: A wealth of data has been published on the role of Ras pathways in cancer. To be biologically active, Ras must move from the cytoplasm to the plasma membrane. Importantly, a posttranslational modification—addition of a farnesyl group to the Ras C-terminal cysteine—is a requisite for membrane localization of Ras. Farnesylation of Ras is catalyzed by an enzyme that is designated farnesyltranferase. Recently, several compounds have been developed that can inhibit farnesylation. Preclinical studies indicate that these molecules can suppress transformation and tumor growth in vitro and in animal models, with little toxicity to normal cells. CONCLUSION: An increasing body of data suggests that disruption of Ras signaling pathways, either directly through mutations or indirectly through other genetic aberrations, is important in the pathogenesis of a wide variety of cancers. Molecules such as farnesyl transferase inhibitors that interfere with the function of Ras may be exploitable in leukemia (as well as in solid tumors) as novel antitumor agents." @default.
• W1884954707 created "2016-06-24" @default.
• W1884954707 creator A5002011167 @default.
• W1884954707 creator A5053481267 @default.
• W1884954707 date "1999-03-01" @default.
• W1884954707 modified "2023-10-09" @default.
• W1884954707 title "<i>RAS</i>and Leukemia: From Basic Mechanisms to Gene-Directed Therapy" @default.
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• W1884954707 doi "https://doi.org/10.1200/jco.1999.17.3.1071" @default.
• W1884954707 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/10071302" @default.
• W1884954707 hasPublicationYear "1999" @default.
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