Mitotic stress-induced secretome primes cancer cells to apoptosis and maximizes paclitaxel response in breast tumors when combined with BCL-xL-targeting BH3 mimetics.

We recently identified a previously unappreciated ability of antimitotics to propagate apoptotic priming across cancer cell populations. The underlying paracrine cytotoxic signal, fueled by undead cells activating the cGAS/STING pathway, is required for in vivo antitumor response and it can be further exploited by delayed, but not synchronous, BCL-xL inhibition.