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Thursday, 15 June, 2000, 10:21 GMT 11:21 UK
Cancer setback for scientists
Telomeres Geron
Telomeres cap the end of chromosomes
A protein scientists hope will help them to grow abundant supplies of human cells in the lab for transplants and other medical treatments may trigger cancer, new research has shown.

The protein, called telomerase, has been a focus of major attention since 1998, when scientists demonstrated that expressing this enzyme in cultured human cells could significantly extend their life-span.

Allied to other recent developments in areas such as cloning and stem cells, it is hoped telomerase will play a significant role in revolutionising the treatment of degenerative diseases.

But a study by Professor David Beach, of University College London, UK, and colleagues, has now revealed that telomerase expression can activate an oncogene, making cells cancerous.

Increased life-span

Telomerase's job is to maintain the integrity of telomeres. These are the caps that protect the ends of chromosomes, the large structures in the nuclei of cells that bundle up all our genetic material.

These caps will shorten each time a cell divides. And eventually, when they have become very short, the cells will stop dividing and die. It is regarded as a mechanism that stops old and damaged cells from causing problems.

However, researchers discovered they could actually maintain telomere length and extend the life-span of human cells grown in the lab if telomerase was expressed in the culture.

This trick could be extremely useful for growing large amounts of replacement human tissue.

Cautious approach

A number of experiments had sought to investigate the concern that the technique could make cells run away into a cancerous state but had come up with little evidence to support the worries.

Now, Beach and his colleagues have shown that at least one hallmark of cancer cells is observed in such cells, namely, activation of the c-myc oncogene.

They found that human mammary epithelial cells (HMEC) which had been "immortalised" by the introduction of a telomerase gene increased their levels of the c-myc protein two to three-fold.

The degree of c-myc over-expression was similar to that seen in a breast cancer cell line used as a comparison. Although the immortalised cells were not fully transformed into a cancerous state, elevated c-myc expression is a key step in the chain of events that turn cells malignant.

Appealing technologies

"There are a number of different areas in which you can imagine the utility of propagating human cells in vitro and then putting them back," Professor Beach explained. "In a way, the most graphic, if it could be achieved, would be pancreatic islets (for diabetes).

"The idea that you could take a patient's own cells, propagate them, maybe genetically modify them and put them back is very appealing."

But he said his group's findings indicated that using telomerase to develop these new treatments needed to be approached with caution.

"The previous notion that using telomerase to immortalise cells in culture and then assuming that no further genetic changes occur as a result of that is now shown to be incorrect."

The findings are reported in the journal Nature. Altered expression of c-myc is observed in about 70,000 fatal cancers a year in the United States.

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