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Blocking telomerase kills cancer cells but provokes resistance, progression
Date:2/21/2012

hese cross-species copy number alterations included several known tumor-suppressing genes and oncogenes, suggesting that initial telomere dysfunction not only drives primary tumor development but also confers malignant traits such as invasiveness.

Telomerase extinction works - at first

The team then took tumor cells from late-generation mice with activated telomerase - the aggressive tumors - and passaged them four times through groups of mice treated with either 4-OHT to trigger telomerase production or the control vehicle that leaves the enzyme off.

During the first two rounds, survival for the two groups was about the same. In the third round, the control mice had a major improvement in survival over the telomerase arm, indicating that telomere erosion had allowed cellular defense mechanisms to pick off genomically unstable cells.

However, in the fourth passage, survival of the control-treated mice fell back toward that of mice with active telomerase. The tumors had become resistant without relying on telomerase.

Alternative lengthening of telomeres rescues cancer cells

An analysis showed that telomere lengths of tumor cells with active telomerase remained largely unchanged across the four passages. Telomeres shortened in cells lacking telomerase through the first two passages followed by a sharp increase during the third and fourth passages.

Other molecular evidence pointed to alternative lengthening of telomeres in telomerase-absent cells.

They found that ALT-positive tumors had different gene expression patterns - 891 genes with increased expression, 1,345 with decreased - compared to telomerase-positive tumors.

Key gene in mitochondrial pathway active in ALT cells

Many genes were found in networks regulating mitochondrial biology and oxidative stress regulation. PGC-1 was the only gene in both pathways with increased expression and copy number gain in
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Contact: Scott Merville
smerville@mdanderson.org
713-792-0661
University of Texas M. D. Anderson Cancer Center
Source:Eurekalert

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