Telomerase activation

Based on the provided sources, malignant cells and actively growing cells must maintain their telomeres [3]. Specifically, TERT promoter mutations are frequent in gliomas and subsets of tumors derived from cells with low rates of self-renewal [3]. Conversely, germ-line mutations in *hTERT* and *hTR* (encoding telomerase reverse transcriptase and RNA) cause autosomal dominant dyskeratosis congenita, which is associated with premature death and pulmonary fibrosis [5]. Additionally, transient telomerase induction in myogenic progenitor cells is investigated as a strategy to overcome stem cell exhaustion in Duchenne muscular dystrophy [9].

Open questions remain regarding the precise clinical efficacy and downstream systemic consequences of manipulating telomerase activation across different degenerative and malignant conditions, as the provided texts focus primarily on identifying mutations and the contexts of telomere maintenance [3, 5, 9].