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A subset of cancer cells maintains their telomeres without telomerase through the recombination‐based alternative lengthening of telomeres (ALT) pathway. Currently, it is not yet clear in what context ALT is induced and how the pathway choice is made. Here, we show that abrogation of Brca2 reinforces break‐induced replication (BIR) and engages with ALT pathway. Brca2 depletion in telomerase‐null mouse...
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