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[Cancer Research 64, 3444-3451, May 15, 2004]
© 2004 American Association for Cancer Research

Regular Articles

Telomeric Recombination in Mismatch Repair Deficient Human Colon Cancer Cells after Telomerase Inhibition

Oliver E. Bechter1, Ying Zou2, William Walker2, Woodring E. Wright2 and Jerry W. Shay2

1 University of Innsbruck, Department of Internal Medicine, Innsbruck, Austria and 2 University of Texas Southwestern Medical Center, Department of Cell Biology, Dallas, Texas

The majority of human malignancies use telomerase to maintain telomere homeostasis. Antitelomerase therapy is therefore a promising approach for a cancer-specific therapy. The alternative lengthening of telomeres pathway (ALT) is a recombination-based, telomerase-independent mechanism of telomere length control. It is widely believed that ALT could be engaged when cancer cells escape from telomerase inhibition. However, no reports exist that would support this concept of therapy resistance. We inhibited telomerase in a human cancer cell line with a mismatch repair defect and observed a telomerase-independent, ALT-like telomere elongation. This is the first report of inducing a telomerase-independent telomere elongation in human cancer cells when telomerase is inhibited, thus describing a novel mechanism of resistance to antitelomerase therapy.




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