Molecular profiling of TNBC has revealed recurrent activation of the PI3K/AKT/mTOR axis, driven by PTEN loss, PIK3CA mutations, and upstream receptor tyrosine kinase signaling (Koboldt et al. , 2012). Inhibition of PI3K has demonstrated pre‑clinical efficacy, yet pan‑PI3K inhibitors are limited by dose‑dependent toxicities (Huang et al. , 2020). Isoform‑selective inhibition, particularly of p110β (PI3K‑β), offers a strategy to preserve antitumor activity while sparing normal tissues that rely on p110α signaling (Samuels et al. , 2014).
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