Evaluation of TROP-2 expression in triple-negative breast cancer: a retrospective immunohistochemical study

Triple-negative breast cancer (TNBC) is an aggressive subtype defined by the absence of estrogen receptor (ER), progesterone receptor (PR), and HER2 expression, leaving limited targeted treatment options. In TNBC, TROP-2 (trophoblast cell surface antigen 2) is frequently overexpressed in TNBC and has been investigated as a potential biomarker and therapeutic target. This study primarily aimed to determine the prevalence and distribution of TROP-2 immunohistochemical expression in triple-negative breast cancer. Secondary exploratory analyses assessed associations between TROP-2 expression and available clinicopathological characteristics in an Egyptian cohort. In this retrospective cross-sectional study, 95 eligible TNBC cases underwent TROP-2 immunohistochemical assessment using the H-score method, with expression classified as negative (H-score = 0), low (H-score 1–99), intermediate (H-score 100–200), or high (H-score 201–300). Selected clinicopathological variables (tumour size, lymphovascular invasion, perineural invasion, pathological T/N stage, and neoadjuvant therapy) were available for 48 cases with accessible resection pathology records; extranodal extension was assessed among node-positive cases with evaluable lymph-node specimens ( n = 22). TROP-2 immunohistochemical assessment was performed on sections from the primary breast tumour; metastatic lymph-node deposits were not evaluated for TROP-2 expression. TROP-2 expression was identified in 87.4% of cases (83/95): 12.6% (12/95) were negative (H-score = 0), 16.8% (16/95) showed low expression (H-score 1–99), 25.3% (24/95) intermediate expression (H-score 100–200), and 45.3% (43/95) high expression (H-score 201–300).TROP-2 expression. TROP-2 expression categories were significantly associated with DCIS presence ( p = 0.042), Ki-67 index ( p = 0.001), extranodal extension ( p = 0.028), neoadjuvant therapy receipt ( p = 0.037), tumour-infiltrating lymphocytes (TILs; p = 0.049), and pathological T stage ( p = 0.038).Among resection cases ( n = 48), high TROP-2 expressors more frequently had T3-stage disease (34.8% vs. 0% in low expressors) and had received neoadjuvant therapy (34.8% vs. 0% in negative/low groups); extranodal extension was identified in 90.0% of node-positive high expressors vs. 25.0% of intermediate expressors ( n = 22). No significant association was observed between TROP-2 expression and lymphovascular invasion ( p = 0.056), histological grade ( p = 0.753), or nodal stage ( p = 0.432). TROP-2 expression was identified in 87.4% of TNBC cases in this Egyptian cohort and was associated with selected clinicopathological characteristics, including DCIS presence, pathological T stage, extranodal extension, Ki-67 index, tumour-infiltrating lymphocytes, and neoadjuvant therapy receipt. However, owing to the retrospective cross-sectional design, incomplete availability of selected clinicopathological variables, and absence of survival or treatment-response outcomes, these findings should be interpreted as exploratory associations and do not establish prognostic or predictive value. Larger prospective multicenter studies incorporating standardised TROP-2 immunohistochemical assessment, survival endpoints, and therapeutic-response data are needed to determine the clinical relevance of TROP-2 expression in TNBC.