DALLAS - December 29, 1998 - Scientists at UT Southwestern Medical Center at Dallas have shown that human cells grown in the laboratory and immortalized by the introduction of the enzyme telomerase are not transformed into cancer cells, perhaps clearing the way for safe, future medical applications.
Drs. Jerry Shay and Woodring Wright, UT Southwestern professors of cell biology and neuroscience, and their colleagues will report in the January 1999 issue of Nature Genetics that cells immortalized with telomerase, now more than 220 generations past their normal life span of 75 to 80 divisions, remain young and vigorous.
The cells exhibited none of the characteristics associated with cancer cells, such as chromosome instability, serum-independent growth, loss of contact inhibition and loss of cell-cycle checkpoint controls. In an accompanying article, collaborators at the Geron Corporation and academic colleagues demonstrate that the cells with introduced telomerase do not produce tumors in mice.
The fear that telomerase may cause cancer resulted because telomerase activity is a marker of cancer cells. While most normal cells, which have finite life spans, do not contain telomerase, more than 90 percent of cancer cells, which divide indefinitely, do.
"We clearly demonstrate that the expression of telomerase in cultured human cells does not cause cancer progression," said Wright, thereby reducing concerns that telomerase might act as an oncogene, a gene that can induce a cell to become malignant. "The abnormalities seen in cancer cells are due to other mutations; telomerase merely allows the cells to keep dividing."
A year ago the same researchers reported in Science (279:349-52, 1998) that
telomerase introduced into human cells grown in the laboratory was sufficient to
immortalize them. Their report proved that progressive shortening of telomeres -
specific short pieces of deoxyribonucleic acid (DNA) that the enzyme tel
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Contact: Heather Stieglitz
heather.stieglitz@email.swmed.edu
214-648-3404
UT Southwestern Medical Center
28-Dec-1998