Abstract
Triple positive breast cancer (TPBC) overexpresses HER2 and enriches HR to estrogen and progesterone. Bidirectional cross-talk between HER2 pathways and estrogen receptor alpha (ERα) leads to tumor progression and resistance to targeted therapy for TPBC. To understand the molecular mechanisms of its antitumor response and identify ideal candidates for tailoring effective immunotherapy, we proposed a robust molecular classification of TPBC.
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