Abstract
Telomerase reverse transcriptase (TERT) is a ribonucleoprotein involved in maintaining the length of telomeres. In the absence of TERT expression, differentiated cells can only divide a finite number of times before undergoing cellular senescence – often referred to as the Hayflick limit. Mutations within the promoter region of TERT that create consensus binding sequences for ETS family transcription factors are a common mechanism by which neoplastic cells increase TERT expression and overcome this limit [1]. TERT promoter mutations are common in many cancer types including 60-80% of urothelial carcinomas (UC) [2,3]. Given the high frequency of these mutations in UC and absence of these mutations in non-neoplastic/benign mimics of UC [4], TERT promoter mutations may serve as potential biomarker for monitoring patients with a history of malignancy.
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