Recent data show that catastrophic events during one cell cycle can cause massive genome damage producing viable clones with unstable genomes. This is in contrast with the traditional view that tumorigenesis requires a long‐term process in which mutations gradually accumulate over decades. These sudden events are likely to result in a large increase in genomic diversity within a relatively short time, providing the opportunity for selective advantages to be gained by a subset of cells within a population. This genetic diversity (...) amplification, arising from a single aberrant cell cycle, may drive a population conversion from benign to malignant. However, there is likely a period of relative genome stability during the clonal expansion of tumors – this may provide an opportunity for therapeutic intervention, especially if mechanisms that limit tolerance of aneuploidy are exploited. (shrink)

Although alterations in Ras signalling are found in about 30% of human cancers, the transforming activity of oncogenic Ras is not fully understood. In a recent paper, a putative Ras1 effector in S. pombe, named Scd1, was reported to localize to mitotic apindies. Scd1 physically associates with Moe1, a factor that may contribute to the inherent inatability of microtubules (MTs) and appears to be needed for proper apindle function. Altered MT dynamics within the spindle are likely to affect spindle assembly (...) and chromosome capture, processes that need to be delicately controlled if cells are to guard against genome instability adn transformation. BloEssays 23: 307‐310,2001.©2001 John Willey & Sons, Inc. (shrink)