Clarissa Mujacic, Maria Concetta Vitale, Rita Siino, Emilia Di Giovanni, Carla Ferrante Bannera, Enrico Di Marco, Andrea Gottardo, Tancredi Didier Bazan Russo, Nadia Barraco, Alessandro Perez, Valerio Gristina, Antonio Galvano, Giuseppe Badalamenti, Antonio Russo, Viviana Bazan, Lorena Incorvaia
Endometriosis is a benign yet debilitating condition, and its molecular complexity remains unexplored. Although clinically recognized, its genetic landscape has long been overlooked. This review analyses cancer-associated mutations (CAMs) identified in endometriotic lesions, revealing parallels with malignancy. Recurrent mutations in key oncogenic and tumour suppressor genes-PIK3CA, CTNNB1, KRAS, PTEN and ARID1A-emerge with patterns distinct from cancer, yet suggesting shared mechanisms. Despite the limited genomic data, these findings position endometriosis as a valuable model for investigating early tumour-like processes. By reframing endometriosis through the lens of molecular oncology, this study offers new insights into its pathogenesis and proposes a translational framework for advancing diagnostics and understanding disease progression at the benign-malignant interface.