Loss of Chromosomal Integrity in Neoplasia
This extract was created in the absence of an abstract.
Excerpt
Using in vitro model systems, we have found a striking difference between normal, diploid cells and tumorigenic cells in their ability to amplify a given endogenous gene. Amplification frequency is high in tumorigenic cells (∼ 10−3), lower in nontumorigenic, preneoplastic cells (∼ 10−5), and undetectable in normal, diploid cells (< 10−9) in both the human and rodent species. To investigate the genetic control of gene amplification, amplification frequency was measured in hybrids formed between tumorigenic cells and normal, diploid cells. The ability to amplify an endogenous gene behaved as a recessive genetic trait. Amplification frequency in the hybrid cells was suppressed by more than five orders of magnitude (10−3 to < 10−8). Previously, we identified the p53 tumor suppressor gene product as one of the components of a pathway that regulates gene amplification and aneuploidy. In this paper, we discuss two points that are logical extensions of the previous work....
