Steinbeck Redux

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Science  30 Aug 2002:
Vol. 297, Issue 5586, pp. 1447
DOI: 10.1126/science.297.5586.1447b

Mouse models have been powerful tools for studying the molecular events that underlie cancer development. But cancer may not arise in mice in precisely the same way that it does in humans, as illustrated by two studies.

Hamad et al. present evidence that ras, one of the best-characterized oncogenes, has distinct mechanisms of action in mouse and human cells. In mice, oncogenic Ras starts a normal cell on the path to cancer by activating Raf kinases, whereas in human cells it appears to activate Ral guanine nucleotide exchange factors. In broadly analogous work, Smogorzewska and de Lange show that, in humans, both the p53 and p16/Rb pathways function to alert cells to telomere dysfunction, whereas in mice only the p53 signaling pathway is used. The cell culture systems that display these interspecies differences are themselves imperfect models of human cancer, but the work serves as an important reminder that the most accurate information about cancer is likely to come from a combination of experimental approaches. — PAK

Genes Dev. 16, 2045 (2002); EMBO J. 21, 4338 (2002).

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