[Advancement of subtype-based early breast cancer systematic therapy]

This article systematically reviews the latest advances in systemic therapy for early breast cancer (EBC) across different molecular subtypes-hormone receptor positive/human epidermal growth factor receptor 2 negative (HR+HER2-), HER2-positive, and triple-negative breast cancer (TNBC). It elaborates on the evolution of treatment strategies in endocrine therapy, targeted therapy, and immunotherapy. The combination of CDK4/6 inhibitors with adjuvant endocrine therapy has redefined the high-risk population in HR+HER2-breast cancer. PARP inhibitors have become an important therapeutic option for patients with germline pathogenic or likely pathogenic BRCA mutations in HER2-negative disease. Novel oral selective estrogen receptor degraders are expected to emerge as a new adjuvant treatment choice for this subtype. For HER2 positive patients, treatment is now in an era where de-escalation and escalation strategies are pursued in parallel. Antibody drug conjugates (ADC) have profoundly reshaped the treatment landscape for patients who do not achieve pathological complete response (pCR) after neoadjuvant therapy, and their role in neoadjuvant and adjuvant settings is being further explored. In TNBC, refined subtyping and the investigation of subtype-specific combination strategies have significantly improved outcomes in a subset of patients. The use of PD-1/PD-L1 inhibitors combined with chemotherapy in the neoadjuvant setting has entered the exploratory phase of de-escalation. PARP inhibitors and TROP-2 ADC have also achieved breakthrough progress in both neoadjuvant and adjuvant settings. Precision diagnostic tools, including genetic testing and liquid biopsy, are increasingly being integrated into treatment decision-making across all subtypes of breast cancer. Molecular subtype-guided precision medicine now enables individualized systemic therapy for EBC via novel agents and biomarker-driven strategies, optimizing clinical decisions and improving outcomes.