MYC Abrogates p53-Mediated Cell Cycle Arrest in N-(Phosphonacetyl)-l-Aspartate-Treated Cells, Permitting CAD Gene Amplification

Inhibitory effect of c-Myc on p53-induced apoptosis in leukemia cells. Microarray analysis reveals defective induction of p53 target genes and upregulation of chaperone genes

“…Thus, our data also support the hypothesis that deregulated MYC contributes to genomic instability in cells arrested by wild-type conformation p53. A previous report has described that c-Myc can overcome the p53-mediated cell cycle arrest and promotes genomic instability (Chernova et al, 1998). Altogether the results support the idea that interference with the activity of p53 as 'guardian of the genome' can be one of the tumorigenic pathways used by c-Myc.…”

Notchic-ER chimeras display hormone-dependent transformation, nuclear accumulation, phosphorylation and CBF1 activation

“…Such a mechanism has been described for MYCER oncogenes. An overexpression of MYC generates multiple genetic abnormalities that result in the acquisition of a proliferative state that can be maintained independently of MYC activation over many days (Chernova et al, 1998;Felsher and Bishop, 1999). In order to address if the mechanism of transformation mediated by Notch can follow this scheme, we cultured the clonal RKE cell lines expressing Notch ic -ER chimeras in the presence of OHT over a period of 30 days.…”

Mechanisms of apoptosis by c-Myc

“…The tight association between these properties in retroviral oncogenic myc genes, where strong selective pressures would be expected to rid death-dealing aspects, reinforces the notion that they are inseparable at the level of the protein and therefore coordinately controlled together. Investigations of the capacity of N-Myc and L-Myc to drive cell death have revealed similarities to c-Myc (Zornig et al, 1995;Ueda and Ganem, 1996;Chernova et al, 1998;Lutz et al, 1998;Nesbit et al, 1998). The antiproliferative S-Myc protein also induces apoptosis but without the need for a growth factor deprivation trigger (Asai et al, 1994).…”