Even the most commonly mutated tumor suppressor genes, such as p53 and Rb, malfunction in only about half of all tumor types. However, excess telomerase appears in all major cancers. So why don't more pharmaceutical strategies exist to block the enzyme that, in excess, dictates cells to divide ad infinitum?
The answer may be twofold, Serge Lichtsteiner, a researcher at Menlo Park, Calif.-based Geron Corp., reported during an interview following his presentation at a recent New York Academy of Sciences cancer meeting. Telomerase has emerged as a viable anticancer target relatively recently, so researchers know less about the basic biology behind the enzyme's activity.1 Also, many questions remain about antisense molecules, currently the leading technique for turning off telomerase.2
The ability to switch off that enzyme seems tantalizing due to telomerase's key role in cell division. Telomerase rebuilds telomeres, the chromosomal tips that dictate the number of times a cell ...
