Introduction: Neoadjuvant chemotherapy (NAC) has become a standard therapeutic approach in locally advanced breast cancer (LABC). Beyond tumor downstaging, NAC may induce biological alterations in tumor molecular profiles, including estrogen receptor (ER), progesterone receptor (PR), human epidermal growth factor receptor 2 (HER2), and Ki67 expression. Changes in these biomarkers may influence molecular subtype classification, prognosis, and subsequent treatment strategies.

Methods: This manuscript presents a structured literature synthesis derived from the literature review chapter, integrating current evidence regarding NAC mechanisms, immunohistochemical assessment, and biomarker modulation after systemic therapy.

Results: Anthracycline- and taxane-based regimens exert cytotoxic effects through DNA intercalation, topoisomerase II inhibition, and microtubule stabilization³. Literature demonstrates that NAC may alter ER, PR, HER2, and Ki67 expression via clonal selection, epigenetic modulation, and tumor microenvironment changes²,⁶. Biomarker conversion may result in molecular subtype shifts, particularly toward more aggressive phenotypes such as triple-negative breast cancer (TNBC)⁷.

Discussion: Changes in immunohistochemical expression following NAC have important clinical implications. Reassessment of biomarkers after treatment is essential for optimizing adjuvant therapy selection and individualized treatment planning