The genes were hTERT, a telomerase expression regulator, and a combination of two oncogenes: the simian virus 40 large-T oncoprotein and an oncogenic allele of H-ras. By disrupting the intracellular pathways regulated by these genes, Hahn and his colleagues directly converted normal human epithelial and fibroblast cells into cancer cells. The study shows how "using these sets of genes, you can turn a normal human cell into a cancer cell in one step," Hahn says.
Because hTERT plays such a key role, it follows that telomere maintenance is also critical in forming tumors by allowing pre-cancerous cells to continue replicating longer than normal, according to Hahn. In normal human cells, hTERT is not usually found and the telomeres progressively shorten with each round of cell division, until they reach the point where they stop replicating. In contrast, telomerase is turned on in most human tumors. In fact, the difference in ...