Abstract

Malignant tumors are dynamic entities that evolve not only histologically but also at the molecular level. Variations in receptor expression (e.g., ER, PR, HER2) and alterations in mutation profiles observed in residual or recurrent tumor tissue after surgical resection highlight both the adaptive capacity of tumor cells and intratumoral heterogeneity. This molecular evolution is largely driven by the emergence of new genetic subclones shaped by clonal selection and microenvironmental pressures. Postoperative changes—including hypoxia, inflammation, and stromal remodeling—further promote immune evasion, epithelial–mesenchymal transition (EMT), and the development of treatment-resistant phenotypes. These processes may lead to receptor status divergence in metastatic or recurrent lesions compared to the primary tumor, necessitating reassessment of therapeutic strategies. For pathologists, repeating immunohistochemical and molecular testing on metastatic or recurrent samples is critical for optimal clinical management. This review evaluates molecular adaptation in tumor biology following surgery, with a focus on receptor conversion, mutational diversity, clonal evolution, microenvironmental interactions, and implications for pathological reporting.

Key words: Tumor biology, surgery, receptor conversion, mutation profile, heterogeneity, clonal evolution, pathology