Abstract

To allow for infinite proliferation, tumor cells need to activate mechanisms for telomere maintenance, such as alternative lengthening of telomeres (ALT). ALT is linked to the loss of ATRX or DAXX. Current evidence supports that sarcomas predominantly use ALT for telomere elongation, at a prevalence rate of 20-60%. However, in our dataset, only 12.3% of sarcomas harbored ATRX/DAXX alterations. Thus, we sought to investigate genomic determinants of high telomeric content beyond the canonical ATRX/DAXX alterations.

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