TP53 and serous adenocarcinoma: Based on clinical and endocrine characteristics (e.g., types I and II), histopathological signatures (e.g., endometrioid, clear-cell, or serous adenocarcinoma), or molecular subtypes (e.g., microsatellite instability, TP53 mutation, POLE mutation, or high-level somatic copy number alterations, HER2 amplification), it reveals the histological heterogeneity and complexity of this neoplasm from different perspectives (27, 28).