Cell-cycle control of c-myc but not c-ras expression is lost following chemical transformation

c-Myc-deficient B lymphocytes are resistant to spontaneous and induced cell death

“…[1][2][3][4][5] One of its members, c-Myc, is expressed from immature stages of B-cell differentiation, and is rapidly induced upon mitogenic stimulation. [6][7][8] Overexpression of c-myc induces apoptosis in fibroblasts and myeloid cell lines in low serum conditions. 1,2,9 More recently, Hueber et al 10 have shown that c-Myc-induced apoptosis in fibroblasts requires the interaction on the cell surface of CD95, a member of the TNF receptor family, and its ligand CD95L, triggering an apoptotic pathway that activates a set of cysteine proteases, called caspases, which lead to cell death.…”

Developmentally-regulated expression of murine K-ras isoforms

“…Passage through this stage is ras-dependent unless overcome by a downstream activating mutation in raf (Yamauchi et al, 1994). While some groups found no change in H-or Kras expression in di erentiating F9 EC cells (Lockett and Sleigh, 1987;MuÈ ller, 1983), others noted a reduction in K-ras mRNA abundance following di erentiation to primitive endoderm in response to retinoic acid (Campisi et al, 1984;Sejersen et al, 1985). Quantitative analysis of H-and K-ras expression during ontogeny revealed constant mRNA abundance (MuÈ ller et al, 1982), except for a fall in K-ras in late gestation (MuÈ ller, 1983;MuÈ ller et al, 1983).…”

“…Our studies of the same cells ( SW480, Calu-1, SK-N-SH, T24, peripheral blood lymphocytes) are broadly in agreement (DJW et al, unpublished data). Subsequent reports have used a restricted range of probes which would not distinguish the K-ras isoforms: HiHi 3 (Campisi et al, 1984;Ellis et al, 1981;Lockett and Sleigh, 1987;Sejersen et al, 1985), HiHi 380 (Ellis et al, 1981(Ellis et al, , 1982Goyette et al, 1984;Yaswen et al, 1985) and pY413 (George et al, 1985;Leon et al, 1987). Where PCR has been used, primers were chosen within exons 1 and 3 (Pal et al, 1993).…”

Characterization of the rearranged tpr-met oncogene breakpoint.

“…Activated cellular oncogenes have been isolated from many tumors and tumor cell lines. In some cases, activated oncogenes have been described that contain point mutations (29) or are aberrantly regulated (5 (22). A transforming sequence, termed tpr-met, was isolated from an N-methyl-N'nitro-N-nitrosoguanidine (MNNG)-treated tumorgenic derivative cell line, MNNG-HOS, and mapped to human chromosome 7 (7,9).…”