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Human malignancies overcome replicative senescence either by activating the reverse‐transcriptase telomerase or by utilizing a homologous recombination‐based mechanism, referred to as alternative lengthening of telomeres ( ALT ). In budding yeast,  ALT  exhibits features of break‐induced replication ( BIR ), a repair pathway for one‐ended  DNA  double‐strand breaks ( DSB s) that requires the non‐essential subunit Pol32 of  DNA  polymerase delta and leads to conservative  DNA  replication. Here, we examined whether  ALT  in human cancers also exhibits features of  BIR . A telomeric fluorescence  in situ  hybridization protocol involving three consecutive staining steps revealed the presence of conservatively replicated telomeric  DNA  in telomerase‐negative cancer cells. Furthermore, depletion of PolD3 or PolD4, two subunits of human  DNA  polymerase delta that are essential for  BIR , reduced the frequency of conservatively replicated telomeric  DNA  ends and led to shorter telomeres and chromosome end‐to‐end fusions. Taken together, these results suggest that  BIR  is associated with conservative  DNA  replication in human cells and mediates  ALT  in cancer.

Alternative lengthening of human telomeres is a conservative DNA replication process with features of break‐induced replication