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Inhibition of telomerase induces alternative lengthening of telomeres during human esophageal carcinogenesis.
Queisser A, Heeg S, Thaler M, von Werder A, Opitz OG
Abstract:
.....Herein, we demonstrate that telomerase activity and ALT alternate in a cell cycle dependent fashion in human esophageal epithelial cells, and can coexist in a genetically defined model of oral-esophageal squamous carcinogenesis. Moreover, we show that immortalized premalignant cells as well as cancer cells are able to
switch from telomerase activation to ALT upon inhibition of telomerase
. This indicates that cancer cells treated with telomerase inhibitors can use alternative and adaptive ways to maintain their telomeres and thereby escape telomere-based therapeutic strategies.
switch from telomerase activation to ALT upon inhibition of telomerase
. This indicates that cancer cells treated with telomerase inhibitors can use alternative and adaptive ways to maintain their telomeres and thereby escape telomere-based therapeutic strategies.
PMID: 24331919
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