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N-ras-Oncogene

McMahon G, Davis EF, Huber LJ, Kim Y, Wogan GN. 1990. Characterization of c-Ki-ras and N-ras oncogenes in Aflatoxin Bpinduced rat liver tumors. Proc. Natl. Acad. Sci. USA 8 1104-8... [Pg.516]

Obtaining cellular RNA and DNA. Transfer of genomic DNA from human cancer or leukemic cells into NIH 3T3 cells (established from mouse embryo fibroblasts) resulted in the transformation of 3T3 cells into focus-forming cells. Such focus-forming 3T3 cells first yielded the ras family (Harvey-, Kirsten-, N-ras) oncogenes. Co-transfection of such inoculated 3T3 cells into nude mice increased the sensitivity of the assay. [Pg.181]

Mutugan AK, Munirajan AK, Tsuchida N. Ras oncogene in oral cancta- the past 20 years. Oral OncoL 2012 48 383-92. [Pg.725]

Zeytinoglu, H., Z. Incesu, and K.H.C. Baser, 2003. Inhibition of DNA synthesis by carvacrol in mouse myoblast cells bearing a human N-RAS oncogene. Phytomedicine, 10(4) 292-299. [Pg.280]

Toxicity and effectivity studies have often been performed in rodent fibroblast cells containing oncogenic H-Ras. However, prenylation of K-Ras B and N-Ras are not as effectively blocked by the farnesyltransferase inhibitors as H-Ras [48] (see below). Thus normal cells may be less sensitive to these drugs because they express K-Ras 4B and N-Ras. In this context it should be noted that H-Ras mutations are relatively uncommon in human tumors [49]. Rather, the K-Ras gene is the most frequently mutated in solid human cancers, whereas N-Ras is prevalent in leukemias. Thus the preclinical evaluation of the farnesylation inhibitors has yet to be critically re-evaluated for trials in humans. [Pg.126]

Ras, a historical proto-oncogene, is frequently mutated in many human cancers, including 90% of pancreatic cancers, 50% of colorectal cancers, 30% of lung cancers, and 15-30% of melanomas [10-12]. There are three Ras genes that encode four family members K-Ras (two alternatively spliced isoforms), H-Ras, and N-Ras. Mutations are most commonly found in K-Ras [13]. These mutations result in impaired GTP hydrolysis, which shifts the equilibrium toward GTP-bound active Ras, and results in constitutive intracellular signaling. [Pg.87]

Slebos RJ, Kibbelaar RE, Dalesio O et al. K-ras oncogene activation as a prognostic marker in adenocarcinoma of the lung. N EnglJ Med 1990 323 561-565. [Pg.124]

Ras genes are frequently mutated in chemically induced animal tumors and are the most frequently detected mutated oncogenes in human tumors. Approximately 20-30% of all human tumors contain mutated ras. The Ras subfamily includes H-ras, K-ras, and N-ra.v, and all have been found to be mutationally activated in numerous types of tumors from a large variety of species including humans. [Pg.246]

Billadeau, D., Liu, P., Jelinek, D., Shah, N., LeBien, T. W. and van Ness, B. (1997). Activating mutations in the N- and K-ras oncogenes differentially affect the growth properties of the IL-6-dependent myeloma cell line ANBL6. Cancer Res. 57, 2268-2275. [Pg.277]

Ras Regulator of gene expression and cell growth, found in mutated oncogenic forms in many human tumors H-Ras, K-Ras, N-Ras, Ral A, Rad, Rap, Rit, Anchored to plasma membrane by farnesyl, palmitoyl, or other lipid groups... [Pg.173]

The ras oncogene in Colin Tuma s malignant polyp differs from the c-ras proto-oncogene only in the region that encodes the N-terminus of the protein. This portion of the normal and mutant sequences is shown below ... [Pg.335]


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See also in sourсe #XX -- [ Pg.238 ]




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