Telomere Biology

How it works

Comparisons

Where it comes from

Highlighted claims

• The modeled escape mutation is interpreted as emergence of a telomerase-positive or otherwise immortalized mutant clone. — Cellular replication limits in the Luria-Delbrück mutation model
• Escape from replicative senescence often occurs through telomerase activation or less commonly through alternative lengthening of telomeres. — Cellular replication limits in the Luria-Delbrück mutation model
• The framework connects fluctuation theory to telomere biology by treating senescence bypass as telomerase activation or another immortalization route. — Cellular replication limits in the Luria-Delbrück mutation model
• About 90% of human cancers maintain telomeres through telomerase expression. — Cellular replication limits in the Luria-Delbrück mutation model
• About 10% of human cancers maintain telomeres through ALT. — Cellular replication limits in the Luria-Delbrück mutation model
• The timing of telomerase activation varies by cancer type. — Cellular replication limits in the Luria-Delbrück mutation model